PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
16000590-9	2005	NaB radiosensitized both the A375 and MeWo melanoma cell lines, substantially reducing the surviving fraction at 2 Gy (SF2), whereas it had no effect on the normal human fibroblasts.	nab	0-3	serine and arginine rich splicing factor 1	Homo sapiens	119-122
16000590-12	2005	Moreover, NaB significantly reduced the expression of the repair-related genes Ku70 and Ku86 and DNA-dependent protein kinase catalytic subunit in melanoma cells at the protein and mRNA levels.	nab	10-13	X-ray repair cross complementing 6	Homo sapiens	79-83
16000590-12	2005	Moreover, NaB significantly reduced the expression of the repair-related genes Ku70 and Ku86 and DNA-dependent protein kinase catalytic subunit in melanoma cells at the protein and mRNA levels.	nab	10-13	X-ray repair cross complementing 5	Homo sapiens	88-92
16000590-12	2005	Moreover, NaB significantly reduced the expression of the repair-related genes Ku70 and Ku86 and DNA-dependent protein kinase catalytic subunit in melanoma cells at the protein and mRNA levels.	nab	10-13	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	97-143
15621046-11	2005	However, cells overexpressing NAB-ablating Egr-1 mutations showed four- to fivefold increased NCX1 expression.	nab	30-33	early growth response 1	Mus musculus	43-48
15905562-4	2005	Importantly, median Ad5-specific NAb titers were >10-fold higher in sub-Saharan Africa compared with the United States.	nab	33-36	Alzheimer disease, familial, type 5	Homo sapiens	20-23
15711177-11	2005	Treatment with NaB for 24 or 48 h induced no change in MRP1 and MRP2 levels, but increased MDR1 expression in 8505C and FTC 238 cell lines comparably to alkaline phosphatase activity.	nab	15-18	ATP binding cassette subfamily B member 1	Homo sapiens	91-95
15713621-3	2005	In this study, we examined the effects of two structurally different HDAC inhibitors, trichostatin A (TSA) and sodium butyrate (NaB), on the cell cycle, apoptosis, and bcl-2 expression in t(14;18) lymphoma cells.	nab	128-131	BCL2 apoptosis regulator	Homo sapiens	168-173
15713621-4	2005	We found that in addition to potent cell cycle arrest, TSA and NaB also dramatically induced apoptosis and down-regulated bcl-2 expression, and overexpression of bcl-2 inhibited TSA-induced apoptosis.	nab	63-66	BCL2 apoptosis regulator	Homo sapiens	122-127
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	nab	17-20	cyclin dependent kinase inhibitor 1A	Homo sapiens	117-120
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	nab	17-20	cyclin dependent kinase inhibitor 1A	Homo sapiens	121-125
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	nab	17-20	cyclin dependent kinase inhibitor 1A	Homo sapiens	126-130
15688418-2	2005	Sodium butyrate (NaB), a histone deacetylase inhibitor, has been shown to cause a G(1) cell cycle arrest by inducing p21(WAF1/CIP1) in a p53-independent manner.	nab	17-20	tumor protein p53	Homo sapiens	137-140
15688418-3	2005	In this report, we present evidence for activation of p53 pathway by NaB and its role in the NaB-mediated growth suppression.	nab	69-72	tumor protein p53	Homo sapiens	54-57
15688418-3	2005	In this report, we present evidence for activation of p53 pathway by NaB and its role in the NaB-mediated growth suppression.	nab	93-96	tumor protein p53	Homo sapiens	54-57
15688418-4	2005	Addition of NaB increased the levels of p53 involving a p14(ARF)-dependent post-transcriptional mechanism.	nab	12-15	tumor protein p53	Homo sapiens	40-43
15688418-4	2005	Addition of NaB increased the levels of p53 involving a p14(ARF)-dependent post-transcriptional mechanism.	nab	12-15	ribonuclease P/MRP subunit p14	Homo sapiens	56-59
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	tumor protein p53	Homo sapiens	12-15
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	tumor protein p53	Homo sapiens	46-49
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	90-93
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	94-98
15688418-5	2005	NaB induced p53 is functional as it activated p53-specific reporter, induced the level of p21(WAF1/CIP1), inhibited cellular DNA synthesis and induced apoptosis.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	99-103
15688418-6	2005	By using HPV 16 E6 stable transfectants as well as p53 null cancer cells, we show that NaB suppresses the growth of WT p53 containing cells more efficiently.	nab	87-90	tumor protein p53	Homo sapiens	51-54
15688418-6	2005	By using HPV 16 E6 stable transfectants as well as p53 null cancer cells, we show that NaB suppresses the growth of WT p53 containing cells more efficiently.	nab	87-90	tumor protein p53	Homo sapiens	119-122
15688418-7	2005	NaB inhibited DNA synthesis to similar extent both in the presence and absence of p53.	nab	0-3	tumor protein p53	Homo sapiens	82-85
15688418-8	2005	However, NaB treatment lead to a major G(2)/M arrest of cells in the presence of p53, while cells without wild-type p53 accumulated mainly in G(1) phase of the cell cycle.	nab	9-12	tumor protein p53	Homo sapiens	81-84
15688418-10	2005	These results suggest that p53 pathway mediates in part growth suppression by NaB and the p53 status may be an important determinant of chemosensitivity in HDI based cancer chemotherapy.	nab	78-81	tumor protein p53	Homo sapiens	27-30
15819885-3	2005	Remarkably, PMA and TGF-beta1 stimulation of Timp-1 show a differential response to TSA or NaB.	nab	91-94	transforming growth factor, beta 1	Mus musculus	20-29
15819885-3	2005	Remarkably, PMA and TGF-beta1 stimulation of Timp-1 show a differential response to TSA or NaB.	nab	91-94	tissue inhibitor of metalloproteinase 1	Mus musculus	45-51
15819885-4	2005	TSA or NaB potentiate PMA-induced Timp-1 expression but repress TGF-beta1-induced Timp-1 expression.	nab	7-10	tissue inhibitor of metalloproteinase 1	Mus musculus	34-40
15819885-4	2005	TSA or NaB potentiate PMA-induced Timp-1 expression but repress TGF-beta1-induced Timp-1 expression.	nab	7-10	transforming growth factor, beta 1	Mus musculus	64-73
15819885-4	2005	TSA or NaB potentiate PMA-induced Timp-1 expression but repress TGF-beta1-induced Timp-1 expression.	nab	7-10	tissue inhibitor of metalloproteinase 1	Mus musculus	82-88
15810631-6	2005	Alkaline phosphatase (ALP) activity, a marker of colonocyte differentiation, was increased 48 hr after treatment with 1 mM NaB.	nab	123-126	alkaline phosphatase, placental	Homo sapiens	0-20
15810631-6	2005	Alkaline phosphatase (ALP) activity, a marker of colonocyte differentiation, was increased 48 hr after treatment with 1 mM NaB.	nab	123-126	alkaline phosphatase, placental	Homo sapiens	22-25
15810631-9	2005	The effect of NaB on ALP activity was significantly attenuated in the presence of inhibitors of protein kinase C and JNK.	nab	14-17	alkaline phosphatase, placental	Homo sapiens	21-24
15810631-9	2005	The effect of NaB on ALP activity was significantly attenuated in the presence of inhibitors of protein kinase C and JNK.	nab	14-17	mitogen-activated protein kinase 8	Homo sapiens	117-120
15621046-11	2005	However, cells overexpressing NAB-ablating Egr-1 mutations showed four- to fivefold increased NCX1 expression.	nab	30-33	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	94-98
15621046-13	2005	Thus, the in vitro results indicate that Egr-1/NAB interactions are critical for NCX1 repression at the NCX1 promoter.	nab	47-50	early growth response 1	Mus musculus	41-46
15621046-13	2005	Thus, the in vitro results indicate that Egr-1/NAB interactions are critical for NCX1 repression at the NCX1 promoter.	nab	47-50	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	81-85
15621046-13	2005	Thus, the in vitro results indicate that Egr-1/NAB interactions are critical for NCX1 repression at the NCX1 promoter.	nab	47-50	solute carrier family 8 (sodium/calcium exchanger), member 1	Mus musculus	104-108
15498118-1	2004	The study was purposed to explore the molecular mechanisms of sodium butyrate (NaB) action on SKM-1 cell proliferation/differentiation and to study its synergistic effect with all-trans retinoic acid (ATRA).	nab	79-82	sodium voltage-gated channel alpha subunit 4	Homo sapiens	94-99
15520174-4	2004	Down-regulation of HDAC1 by an antisense vector sensitized the cells to NaB-induced apoptosis, whereas its overexpression conferred resistance to this agent.	nab	72-75	histone deacetylase 1	Homo sapiens	19-24
15520174-5	2004	Increased HDAC1 levels and activity impaired NaB-mediated activation of Bax promoter and Bax protein levels.	nab	45-48	histone deacetylase 1	Homo sapiens	10-15
15520174-5	2004	Increased HDAC1 levels and activity impaired NaB-mediated activation of Bax promoter and Bax protein levels.	nab	45-48	BCL2 associated X, apoptosis regulator	Homo sapiens	72-75
15520174-5	2004	Increased HDAC1 levels and activity impaired NaB-mediated activation of Bax promoter and Bax protein levels.	nab	45-48	BCL2 associated X, apoptosis regulator	Homo sapiens	89-92
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	tumor protein p53	Homo sapiens	15-18
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	tumor protein p53	Homo sapiens	94-97
15520174-6	2004	Finally, using p53-null melanoma cell line and RNA interference in cells expressing wild-type p53 protein, we show that Bax induction and NaB-mediated apoptosis is p53 dependent.	nab	138-141	tumor protein p53	Homo sapiens	94-97
15489637-6	2004	Expression of a hypoxia-responsive gene encoding intestinal trefoil factor (ITF) in Caco-2 cells after NaB treatment was assessed using reverse-transcription PCR.	nab	103-106	trefoil factor 3	Homo sapiens	49-74
15489637-6	2004	Expression of a hypoxia-responsive gene encoding intestinal trefoil factor (ITF) in Caco-2 cells after NaB treatment was assessed using reverse-transcription PCR.	nab	103-106	trefoil factor 3	Homo sapiens	76-79
15489637-8	2004	NaB suppressed up-regulation of HIF-1 transcriptional activity under hypoxic conditions in Caco-2 and IEC-6 cells.	nab	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	32-37
15489637-10	2004	Furthermore, NaB down-regulated enhanced transcription of ITF gene.	nab	13-16	trefoil factor 3	Homo sapiens	58-61
15489637-12	2004	These findings indicate that NaB suppresses HIF-1 transcriptional activity on hypoxia-responsive genes by reducing the HRE DNA binding activity under hypoxic conditions in intestinal epithelial cells.	nab	29-32	hypoxia inducible factor 1 subunit alpha	Homo sapiens	44-49
15235103-2	2004	Exposure (24 h) of U937 human leukemia cells to NaB (1 mM) or SAHA (1.5 microM) resulted in a marked increase in NF-kappaB DNA binding, effects that were essentially abrogated by coadministration of flavopiridol (100 nM).	nab	48-51	nuclear factor kappa B subunit 1	Homo sapiens	113-122
15498118-4	2004	It is concluded that the NaB effect on cell proliferation/differentiation may be linked to its ability to induce expression of p21 mRNA and inhibit the cyclin D-CDK complexes.	nab	25-28	H3 histone pseudogene 16	Homo sapiens	127-130
15184610-7	2004	During IFNbeta treatment, both NAb+ and NAb- patients showed a reduction in relapse rate; this reduction (25%) was not significant in NAb+ patients but was significant (67%; p < 0.0001) in NAb- patients.	nab	31-34	interferon beta 1	Homo sapiens	7-14
15314118-6	2004	The two remaining IFN beta biological non-responders were NAb-.	nab	58-61	interferon beta 1	Homo sapiens	18-26
15318170-6	2004	Closer view at the expression profile of NaB-treated cells revealed the downregulation of a total of 16 genes associated with cytokine signaling, in particular, interferon gamma (IFNgamma) pathway.	nab	41-44	interferon gamma	Homo sapiens	179-187
15318170-10	2004	Upregulation of metastatic suppressor Kangai 1 (KAI1) by NaB in a time-dependent manner was confirmed by RT-PCR analysis.	nab	57-60	CD82 molecule	Homo sapiens	38-46
15318170-10	2004	Upregulation of metastatic suppressor Kangai 1 (KAI1) by NaB in a time-dependent manner was confirmed by RT-PCR analysis.	nab	57-60	CD82 molecule	Homo sapiens	48-52
15265702-2	2004	We have previously demonstrated that an inhibitor of HDAC, sodium butyrate (NaB), induces apoptosis of breast cancer cells in a P53-independent and P21(waf1)-dependent manner.	nab	76-79	tumor protein p53	Homo sapiens	128-131
15265702-2	2004	We have previously demonstrated that an inhibitor of HDAC, sodium butyrate (NaB), induces apoptosis of breast cancer cells in a P53-independent and P21(waf1)-dependent manner.	nab	76-79	cyclin dependent kinase inhibitor 1A	Homo sapiens	148-156
15265702-3	2004	In this study, we showed that tumor necrosis factor-alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and anti-Fas agonist antibody potentiated NaB-induced growth inhibition through synergistic induction of apoptosis in breast cancer cell lines (MCF-7, T47-D, and BT-20).	nab	160-163	tumor necrosis factor	Homo sapiens	30-57
15265702-3	2004	In this study, we showed that tumor necrosis factor-alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and anti-Fas agonist antibody potentiated NaB-induced growth inhibition through synergistic induction of apoptosis in breast cancer cell lines (MCF-7, T47-D, and BT-20).	nab	160-163	tumor necrosis factor	Homo sapiens	59-68
15265702-3	2004	In this study, we showed that tumor necrosis factor-alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and anti-Fas agonist antibody potentiated NaB-induced growth inhibition through synergistic induction of apoptosis in breast cancer cell lines (MCF-7, T47-D, and BT-20).	nab	160-163	TNF superfamily member 10	Homo sapiens	71-108
15265702-3	2004	In this study, we showed that tumor necrosis factor-alpha (TNF-alpha), TNF-related apoptosis-inducing ligand (TRAIL), and anti-Fas agonist antibody potentiated NaB-induced growth inhibition through synergistic induction of apoptosis in breast cancer cell lines (MCF-7, T47-D, and BT-20).	nab	160-163	TNF superfamily member 10	Homo sapiens	110-115
15265702-4	2004	In MCF-7 cells, NaB increased the expression of death receptors; NaB alone or in combination with TNF-alpha, TRAIL, and anti-Fas agonist antibody increased the levels of Bid, tBid, and that of cytosolic cytochrome c.	nab	65-68	BH3 interacting domain death agonist	Homo sapiens	170-173
15265702-4	2004	In MCF-7 cells, NaB increased the expression of death receptors; NaB alone or in combination with TNF-alpha, TRAIL, and anti-Fas agonist antibody increased the levels of Bid, tBid, and that of cytosolic cytochrome c.	nab	65-68	cytochrome c, somatic	Homo sapiens	203-215
15265702-6	2004	Moreover, cotreatment of NaB and ligands of death receptors up-regulated the levels of P21(waf1) and that of proliferating cell nuclear antigen (PCNA) associated with P21(waf1).	nab	25-28	cyclin dependent kinase inhibitor 1A	Homo sapiens	87-95
15265702-6	2004	Moreover, cotreatment of NaB and ligands of death receptors up-regulated the levels of P21(waf1) and that of proliferating cell nuclear antigen (PCNA) associated with P21(waf1).	nab	25-28	proliferating cell nuclear antigen	Homo sapiens	109-143
15265702-6	2004	Moreover, cotreatment of NaB and ligands of death receptors up-regulated the levels of P21(waf1) and that of proliferating cell nuclear antigen (PCNA) associated with P21(waf1).	nab	25-28	proliferating cell nuclear antigen	Homo sapiens	145-149
15265702-6	2004	Moreover, cotreatment of NaB and ligands of death receptors up-regulated the levels of P21(waf1) and that of proliferating cell nuclear antigen (PCNA) associated with P21(waf1).	nab	25-28	cyclin dependent kinase inhibitor 1A	Homo sapiens	167-175
15184610-7	2004	During IFNbeta treatment, both NAb+ and NAb- patients showed a reduction in relapse rate; this reduction (25%) was not significant in NAb+ patients but was significant (67%; p < 0.0001) in NAb- patients.	nab	40-43	interferon beta 1	Homo sapiens	7-14
15184610-7	2004	During IFNbeta treatment, both NAb+ and NAb- patients showed a reduction in relapse rate; this reduction (25%) was not significant in NAb+ patients but was significant (67%; p < 0.0001) in NAb- patients.	nab	40-43	interferon beta 1	Homo sapiens	7-14
15184610-7	2004	During IFNbeta treatment, both NAb+ and NAb- patients showed a reduction in relapse rate; this reduction (25%) was not significant in NAb+ patients but was significant (67%; p < 0.0001) in NAb- patients.	nab	40-43	interferon beta 1	Homo sapiens	7-14
14557628-3	2003	We show that the ORF50 promoter is highly responsive to sodium butyrate (NaB) and trichostatin A (TSA), two chemicals known to inhibit histone deacetylases.	nab	73-76	ORF50	Human gammaherpesvirus 8	17-22
15253685-6	2004	Data from clinical trials of IFNbeta products indicate that clinical efficacy of IFNbeta is reduced in NAb-positive patients.	nab	103-106	interferon beta 1	Homo sapiens	29-36
15253685-6	2004	Data from clinical trials of IFNbeta products indicate that clinical efficacy of IFNbeta is reduced in NAb-positive patients.	nab	103-106	interferon beta 1	Homo sapiens	81-88
14750171-2	2004	The mechanism by which sodium butyrate (NaB) induces p21WAF1/CIP1, a critical gene involved in the antiproliferative effect of NaB, was studied at the chromatin level.	nab	40-43	cyclin dependent kinase inhibitor 1A	Homo sapiens	53-65
14750171-2	2004	The mechanism by which sodium butyrate (NaB) induces p21WAF1/CIP1, a critical gene involved in the antiproliferative effect of NaB, was studied at the chromatin level.	nab	127-130	cyclin dependent kinase inhibitor 1A	Homo sapiens	53-65
14750171-6	2004	NaB stimulated recruitment of the transcription factors ZBP89 and Sp1 as well as GCN5, but did not influence recruitment of Sp3, HDAC1, p300, or CBP.	nab	0-3	zinc finger protein 148	Homo sapiens	56-61
14750171-6	2004	NaB stimulated recruitment of the transcription factors ZBP89 and Sp1 as well as GCN5, but did not influence recruitment of Sp3, HDAC1, p300, or CBP.	nab	0-3	lysine acetyltransferase 2A	Homo sapiens	81-85
15264109-3	2004	This article reviews the long-term data from large phase III clinical trials showing that NAbs can reduce the clinical efficacy of IFNbeta in patients with MS; patients who have a positive result on NAb testing have a higher relapse rate and more disease activity, as measured by brain MRI, than do patients with a negative result.	nab	90-93	interferon beta 1	Homo sapiens	131-138
15048829-4	2004	In addition to improving the energy balance between folded and unfolded conformers, the algorithm (available in the AMBER-7 and NAB molecular modeling packages) is shown to perform well in more than 50 ns of native-state molecular dynamics (MD) simulations of thioredoxin, protein-A, and ubiquitin, as well as in a simulation of Barnase/Barstar complex formation.	nab	128-131	thioredoxin	Homo sapiens	260-271
15047174-7	2004	In human cells the MVP promoter was potently stimulated by the histone deacetylase (HDAC) inhibitors butyrate (NaB) and trichostatin A (TSA), resulting in enhanced MVP expression.	nab	111-114	major vault protein	Homo sapiens	19-22
15047174-7	2004	In human cells the MVP promoter was potently stimulated by the histone deacetylase (HDAC) inhibitors butyrate (NaB) and trichostatin A (TSA), resulting in enhanced MVP expression.	nab	111-114	major vault protein	Homo sapiens	164-167
15161018-5	2004	MATERIALS AND METHODS: We used human colon carcinoma cell lines treated with sodium butyrate (NaB) in order to induce LRP expression.	nab	94-97	major vault protein	Homo sapiens	118-121
14712207-3	2004	Here, we showed that NaB-induced cell cycle arrest and apoptosis were associated with an increase of P21(waf1/cip1) in MCF-7 breast cancer cells.	nab	21-24	cyclin dependent kinase inhibitor 1A	Homo sapiens	101-114
14712207-5	2004	Transient transfections of MCF-7 cells with p21 deficient for interaction with CDK, but not with p21 deficient for interaction with PCNA (p21PCNA-), abrogated NaB-induced cell cycle arrest.	nab	159-162	cyclin dependent kinase inhibitor 1A	Homo sapiens	44-47
14712207-8	2004	On the other hand, NaB-induced apoptosis was abolished by p21 antisense or p21PCNA-.	nab	19-22	cyclin dependent kinase inhibitor 1A	Homo sapiens	58-61
14712207-8	2004	On the other hand, NaB-induced apoptosis was abolished by p21 antisense or p21PCNA-.	nab	19-22	proliferating cell nuclear antigen	Homo sapiens	75-83
14712207-9	2004	In addition, NaB decreased PCNA levels, but increased the association of PCNA with P21(waf1/cip1).	nab	13-16	cyclin dependent kinase inhibitor 1A	Homo sapiens	83-96
14712207-10	2004	These results suggested that NaB-induced apoptosis required P21(waf1/cip1) and its interaction with PCNA.	nab	29-32	cyclin dependent kinase inhibitor 1A	Homo sapiens	60-73
14709802-5	2003	Treatment of cells with 1 mM NaB or 1 nM TGF 1 for 4 d decreased cell proliferation with a concomitant increase in the cell cycle protein p21.	nab	29-32	H3 histone pseudogene 16	Homo sapiens	138-141
14709802-10	2003	These results indicated that NaB and TGFbeta1 inhibit pituitary cell proliferation and regulate the expression of 7B2, PC1, and PC2 in a cell culture model of pituitary tumors.	nab	29-32	secretogranin V	Homo sapiens	114-117
14709802-10	2003	These results indicated that NaB and TGFbeta1 inhibit pituitary cell proliferation and regulate the expression of 7B2, PC1, and PC2 in a cell culture model of pituitary tumors.	nab	29-32	chromobox 4	Homo sapiens	128-131
14557628-4	2003	The NaB and TSA responsive element was mapped to a 70-bp minimal promoter containing an essential GC box that binds Sp1/Sp3 in vitro and in vivo.	nab	4-7	Sp3 transcription factor	Homo sapiens	120-123
14557628-6	2003	Stimulation with NaB or TSA increased histone acetylation and restriction enzyme accessibility of the ORF50 promoter transcription initiation site.	nab	17-20	ORF50	Human gammaherpesvirus 8	102-107
14557628-8	2003	NaB treatment led to the rapid association of Ini1/Snf5, a component of the Swi/Snf family of chromatin remodeling proteins, with the ORF50 promoter.	nab	0-3	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	46-50
14557628-8	2003	NaB treatment led to the rapid association of Ini1/Snf5, a component of the Swi/Snf family of chromatin remodeling proteins, with the ORF50 promoter.	nab	0-3	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily b, member 1	Homo sapiens	51-55
14557628-8	2003	NaB treatment led to the rapid association of Ini1/Snf5, a component of the Swi/Snf family of chromatin remodeling proteins, with the ORF50 promoter.	nab	0-3	ORF50	Human gammaherpesvirus 8	134-139
12902981-3	2003	Here, we report that NaB specifically represses the expression of the MUC2 gene, a differentiation marker of the secretory goblet cell lineage, in forskolin- and 12-O-tetradecanoylphorbol 13-acetate-induced HT29 cells, and Cl.16E cells, a clonal derivative of HT29 cells that spontaneously differentiates into goblet cells.	nab	21-24	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	70-74
12963846-2	2003	Cells stably transfected with an IkappaBalpha "super-repressor" lacking phosphorylation sites necessary for proteasomal degradation exhibited diminished IkBa phosphorylation and NF-kappaB DNA binding upon exposure to TNFalpha When exposed to NaB (1 mM; 48 hr) or PMA (5 nM; 24 hr), IkappaBalphaM cells displayed a marked reduction in G1 arrest compared to Neo controls.	nab	242-245	nuclear factor kappa B subunit 1	Homo sapiens	178-187
12963846-2	2003	Cells stably transfected with an IkappaBalpha "super-repressor" lacking phosphorylation sites necessary for proteasomal degradation exhibited diminished IkBa phosphorylation and NF-kappaB DNA binding upon exposure to TNFalpha When exposed to NaB (1 mM; 48 hr) or PMA (5 nM; 24 hr), IkappaBalphaM cells displayed a marked reduction in G1 arrest compared to Neo controls.	nab	242-245	tumor necrosis factor	Homo sapiens	217-225
12963846-5	2003	In contrast to impairment in NaB- or PMA-induced NF-kappaB DNA binding, stable expression of the IkappaBalphaM did not modify DNA binding of SP1 or AP2 transcription factors.	nab	29-32	nuclear factor kappa B subunit 1	Homo sapiens	49-58
12963846-6	2003	IkappaBalphaM cells also displayed impairment in NaB- and PMA-mediated induction of p21CIP1 and phosphorylation (inactivation) of p34cdc2, as well as diminished levels of pRb-bound E2F1.	nab	49-52	cyclin dependent kinase inhibitor 1A	Homo sapiens	84-91
12963846-6	2003	IkappaBalphaM cells also displayed impairment in NaB- and PMA-mediated induction of p21CIP1 and phosphorylation (inactivation) of p34cdc2, as well as diminished levels of pRb-bound E2F1.	nab	49-52	cyclin dependent kinase 1	Homo sapiens	130-137
12963846-7	2003	Finally, the NF-kappaB inhibitor CAPE antagonized NaB- and PMA-related NF-kappaB DNA binding as well as induction of p21CIP1.	nab	50-53	nuclear factor kappa B subunit 1	Homo sapiens	13-22
12963846-7	2003	Finally, the NF-kappaB inhibitor CAPE antagonized NaB- and PMA-related NF-kappaB DNA binding as well as induction of p21CIP1.	nab	50-53	nuclear factor kappa B subunit 1	Homo sapiens	71-80
12963846-8	2003	Together, these findings suggest that NF-kappaB plays an important functional role in mediating NaB-induced p21CIP1 induction, G1 arrest, and maturation in human myelomonocytic leukemia cells, and that disruption of the NF-kappaB pathway causes cells to engage an alternative, apoptotic program.	nab	96-99	nuclear factor kappa B subunit 1	Homo sapiens	38-47
12963846-8	2003	Together, these findings suggest that NF-kappaB plays an important functional role in mediating NaB-induced p21CIP1 induction, G1 arrest, and maturation in human myelomonocytic leukemia cells, and that disruption of the NF-kappaB pathway causes cells to engage an alternative, apoptotic program.	nab	96-99	cyclin dependent kinase inhibitor 1A	Homo sapiens	108-115
12963846-8	2003	Together, these findings suggest that NF-kappaB plays an important functional role in mediating NaB-induced p21CIP1 induction, G1 arrest, and maturation in human myelomonocytic leukemia cells, and that disruption of the NF-kappaB pathway causes cells to engage an alternative, apoptotic program.	nab	96-99	nuclear factor kappa B subunit 1	Homo sapiens	220-229
12963846-1	2003	The role of NFkappaB in regulating G1 arrest and maturation induced by the histone deacetylase inhibitor sodium butyrate (NaB) was examined in human myelomonocytic leukemia cells (U937).	nab	122-125	nuclear factor kappa B subunit 1	Homo sapiens	12-20
12963846-2	2003	Cells stably transfected with an IkappaBalpha "super-repressor" lacking phosphorylation sites necessary for proteasomal degradation exhibited diminished IkBa phosphorylation and NF-kappaB DNA binding upon exposure to TNFalpha When exposed to NaB (1 mM; 48 hr) or PMA (5 nM; 24 hr), IkappaBalphaM cells displayed a marked reduction in G1 arrest compared to Neo controls.	nab	242-245	NFKB inhibitor alpha	Homo sapiens	153-157
12511413-8	2003	TSA and NaB also inhibited osteoclast formation and osteoclast-specific mRNA expression in RAW264 cells stimulated with receptor activator of nuclear factor-kappa B (NF-kappa B) ligand (RANKL).	nab	8-11	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	166-176
12865274-5	2003	METHODS: The effect of sodium butyrate (NaB), a histone deacetylase inhibitor, on rescuing RET expression was tested by one round of reverse transcription- polymerase chain reaction from total RNA of treated lymphoblasts from both HSCR patients and control individuals.	nab	40-43	ret proto-oncogene	Homo sapiens	91-94
12865274-6	2003	RESULTS: Analysis of RET expression was possible by NaB treatment of RET negative cells, such as lymphoblasts.	nab	52-55	ret proto-oncogene	Homo sapiens	21-24
12865274-6	2003	RESULTS: Analysis of RET expression was possible by NaB treatment of RET negative cells, such as lymphoblasts.	nab	52-55	ret proto-oncogene	Homo sapiens	69-72
12820170-1	2003	We examined the effect of histone deacetylase inhibitors (HDIs), trichostatin A (TSA), valproic acid (VPA), and sodium butyrate (NaB) on heat shock protein (hsp) gene expression during early Xenopus laevis development.	nab	129-132	heat shock 70kDa protein L homeolog	Xenopus laevis	137-155
12820170-1	2003	We examined the effect of histone deacetylase inhibitors (HDIs), trichostatin A (TSA), valproic acid (VPA), and sodium butyrate (NaB) on heat shock protein (hsp) gene expression during early Xenopus laevis development.	nab	129-132	heat shock 70kDa protein L homeolog	Xenopus laevis	157-160
12917027-2	2003	This study was designed to investigate the effect of sodium butyrate (NaB) on LRP expression level and the function of LRP in K562 cells.	nab	70-73	major vault protein	Homo sapiens	78-81
12917027-4	2003	The LRP mRNA expression and protein levels in the cells before and after NaB treatment were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and flow cytometry indirect immunofluorescence method,respectively.	nab	73-76	major vault protein	Homo sapiens	4-7
12917027-6	2003	RESULTS: Compared with untreated K562 cells, the LRP mRNA level in the cells treated with 2 mmol/L NaB was increased obviously; the protein expression were turned from negative result to positive result and the ratios of positive cells were increased from 1.68% to 35.81%.	nab	99-102	major vault protein	Homo sapiens	49-52
12917027-9	2003	CONCLUSION: Both the mRNA level and the protein expression of LRP in K562 cells can be increased by NaB induction.	nab	100-103	major vault protein	Homo sapiens	62-65
12917027-10	2003	LRP induced by NaB is involved in the decreasing anti-cancer drug accumulation and transporting the drugs from the nucleus to the cytoplasm in K562 cells.	nab	15-18	major vault protein	Homo sapiens	0-3
12511413-8	2003	TSA and NaB also inhibited osteoclast formation and osteoclast-specific mRNA expression in RAW264 cells stimulated with receptor activator of nuclear factor-kappa B (NF-kappa B) ligand (RANKL).	nab	8-11	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	186-191
12511413-9	2003	Transient transfection assay revealed that TSA and NaB dose dependently reduced the sRANKL-stimulated or tumor necrosis factor alpha (TNF-alpha)-stimulated transactivation of NF-kappa B-dependent reporter genes.	nab	51-54	tumor necrosis factor	Mus musculus	134-143
12511413-9	2003	Transient transfection assay revealed that TSA and NaB dose dependently reduced the sRANKL-stimulated or tumor necrosis factor alpha (TNF-alpha)-stimulated transactivation of NF-kappa B-dependent reporter genes.	nab	51-54	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	175-185
12511413-10	2003	The treatment of RAW264 cells with TSA and NaB inhibited TNF-alpha-induced nuclear translocation of NF-kappa B and sRANKL-induced activation of p38 mitogen-activated protein kinase (MAPK) signals.	nab	43-46	tumor necrosis factor	Mus musculus	57-66
12511413-10	2003	The treatment of RAW264 cells with TSA and NaB inhibited TNF-alpha-induced nuclear translocation of NF-kappa B and sRANKL-induced activation of p38 mitogen-activated protein kinase (MAPK) signals.	nab	43-46	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-110
12603604-7	2003	We examined the inhibitory effects of various caspase inhibitors on the expression of CD86 in cells treated with NaB, because NaB also induced apoptosis with slow kinetics.	nab	113-116	caspase 1	Homo sapiens	46-53
12603604-1	2003	To investigate the underlying mechanism for induction of CD86 molecules, we analysed the ability of the histone deacetylase (HDAC) inhibitor, sodium butyrate (NaB), to induce CD86 at the transcriptional level in HL60 cells.	nab	159-162	CD86 molecule	Homo sapiens	57-61
12603604-7	2003	We examined the inhibitory effects of various caspase inhibitors on the expression of CD86 in cells treated with NaB, because NaB also induced apoptosis with slow kinetics.	nab	113-116	CD86 molecule	Homo sapiens	86-90
12603604-1	2003	To investigate the underlying mechanism for induction of CD86 molecules, we analysed the ability of the histone deacetylase (HDAC) inhibitor, sodium butyrate (NaB), to induce CD86 at the transcriptional level in HL60 cells.	nab	159-162	CD86 molecule	Homo sapiens	175-179
12603604-7	2003	We examined the inhibitory effects of various caspase inhibitors on the expression of CD86 in cells treated with NaB, because NaB also induced apoptosis with slow kinetics.	nab	126-129	CD86 molecule	Homo sapiens	86-90
12603604-2	2003	Our studies showed that the expression of CD86 on the cell surface was increased by 24 hr of NaB treatment, and the enhancement of CD86 mRNA expression was observed by real-time polymerase chain reaction.	nab	93-96	CD86 molecule	Homo sapiens	42-46
12603604-10	2003	These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB.	nab	245-248	CD86 molecule	Homo sapiens	74-78
12603604-10	2003	These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB.	nab	245-248	cAMP responsive element binding protein 1	Homo sapiens	163-167
12603604-10	2003	These results suggested that butyrate not only acetylates histones on the CD86 promoter through the suppression of HDAC activity, but that butyrate also regulates CREB-mediated transcription, possibly through the caspase activities triggered by NaB.	nab	245-248	caspase 1	Homo sapiens	213-220
12937835-5	2003	The analysis involves the separation of fragments amplified with primers that flank altered sites in the BRCA1 gene on non-denaturing polyacrylamide gels containing Spreadex Polymer NAB.	nab	182-185	BRCA1 DNA repair associated	Homo sapiens	105-110
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	93-96	angiotensin I converting enzyme	Homo sapiens	101-129
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	93-96	angiotensin I converting enzyme	Homo sapiens	131-134
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	93-96	angiotensin I converting enzyme	Homo sapiens	231-234
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	224-227	angiotensin I converting enzyme	Homo sapiens	101-129
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	224-227	angiotensin I converting enzyme	Homo sapiens	131-134
14598588-1	2003	The results of the analysis of diagnostic significance of examination of natural antibodies (Nab) to agiotensin-converting enzyme (ACE) and its substrates in the serum of hypertensive patients indicate that concentration of Nab to ACE differ from this mean concentration in donors.	nab	224-227	angiotensin I converting enzyme	Homo sapiens	231-234
14598588-2	2003	An elevated level of Nab to ACE may be considered as a compensatory reaction to increased content of the enzyme in vascular endothelium and blood flow.	nab	21-24	angiotensin I converting enzyme	Homo sapiens	28-31
14598588-5	2003	The same patients had also high Nab to ACE.	nab	32-35	angiotensin I converting enzyme	Homo sapiens	39-42
14598588-10	2003	Thus, the proposed method of solid phase enzyme immunoassay quantifies Nab to ACE and its substrates in the patients.	nab	71-74	angiotensin I converting enzyme	Homo sapiens	78-81
14690797-6	2003	A second objective was to determine whether NaB similarly affected the cyclin-dependent kinase inhibitor, p21WAF1/CIP1.	nab	44-47	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-118
14690797-7	2003	In all cell lines, p21 mRNA levels were immediately elevated after NaB exposure, and p21 protein levels were increased within 6 h. NaB increased p21 promoter activity in both Caco2 and Lovo, suggesting p53 independence.	nab	131-134	tumor protein p53	Homo sapiens	202-205
14690797-9	2003	Although three DNase I hypersensitivity sites were identified in the region of the p21 gene, induction of p21 mRNA by NaB was not accompanied by relaxation of the chromatin in the region of the p21 gene.	nab	118-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-109
14690797-9	2003	Although three DNase I hypersensitivity sites were identified in the region of the p21 gene, induction of p21 mRNA by NaB was not accompanied by relaxation of the chromatin in the region of the p21 gene.	nab	118-121	cyclin dependent kinase inhibitor 1A	Homo sapiens	106-109
12123817-3	2002	Here we show that the histone deacetylase inhibitor sodium butyrate (NaB) increases RET transcription in cells displaying low levels of its mRNA, while it has no effect in cells expressing at high levels.	nab	69-72	ret proto-oncogene	Homo sapiens	84-87
14989149-3	2003	By means of RT-PCR and immunoblotting, we found that NaB significantly changed the expression of genes involved in proliferation: cyclins D1, A, E and cyclin-dependent kinases Cdk2 and Cdk4, whereas the amount of p21Waf1 and p27Kip1 inhibitors greatly increased.	nab	53-56	cyclin D1	Rattus norvegicus	130-146
14989149-3	2003	By means of RT-PCR and immunoblotting, we found that NaB significantly changed the expression of genes involved in proliferation: cyclins D1, A, E and cyclin-dependent kinases Cdk2 and Cdk4, whereas the amount of p21Waf1 and p27Kip1 inhibitors greatly increased.	nab	53-56	cyclin dependent kinase 2	Rattus norvegicus	176-180
14989149-3	2003	By means of RT-PCR and immunoblotting, we found that NaB significantly changed the expression of genes involved in proliferation: cyclins D1, A, E and cyclin-dependent kinases Cdk2 and Cdk4, whereas the amount of p21Waf1 and p27Kip1 inhibitors greatly increased.	nab	53-56	cyclin-dependent kinase 4	Rattus norvegicus	185-189
14989149-3	2003	By means of RT-PCR and immunoblotting, we found that NaB significantly changed the expression of genes involved in proliferation: cyclins D1, A, E and cyclin-dependent kinases Cdk2 and Cdk4, whereas the amount of p21Waf1 and p27Kip1 inhibitors greatly increased.	nab	53-56	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	225-232
12433635-1	2002	OBJECTIVE: To investigate the effect of sodium butyrate (NaB) on the expression level of lung resistance-related protein (LRP) in K562 cells.	nab	57-60	major vault protein	Homo sapiens	89-120
12433635-1	2002	OBJECTIVE: To investigate the effect of sodium butyrate (NaB) on the expression level of lung resistance-related protein (LRP) in K562 cells.	nab	57-60	major vault protein	Homo sapiens	122-125
12433635-4	2002	RESULTS: A 1-day treatment with 2 mmol/L NaB induced the gene expression of LRP to increase to the maximum in the cells, and a 3-day treatment caused the corresponding protein level to increase to the maximum.	nab	41-44	major vault protein	Homo sapiens	76-79
12433635-5	2002	CONCLUSION: Both the mRNA level and the protein expression of LRP can be induced by NaB in K562 cells.	nab	84-87	major vault protein	Homo sapiens	62-65
12433376-6	2002	The injection of BDNF+CNTF+forskolin also increases the numbers of regenerated beta and NAB cells, but only slightly enhances axonal regeneration of alpha cells.	nab	88-91	brain derived neurotrophic factor	Homo sapiens	17-21
12433376-6	2002	The injection of BDNF+CNTF+forskolin also increases the numbers of regenerated beta and NAB cells, but only slightly enhances axonal regeneration of alpha cells.	nab	88-91	ciliary neurotrophic factor	Homo sapiens	22-26
12366693-6	2002	5AC and NaB each markedly increased expression of SPRR1/2 and involucrin in NHK.	nab	8-11	small proline rich protein 1B	Homo sapiens	50-57
12123817-4	2002	Chromatin immunoprecipitation (ChIP) experiments showed increased histone acetylation within the 5" flanking [corrected] region, in particular the Sox10-Pax3 enhancer site, due to NaB.	nab	180-183	SRY-box transcription factor 10	Homo sapiens	147-152
12123817-4	2002	Chromatin immunoprecipitation (ChIP) experiments showed increased histone acetylation within the 5" flanking [corrected] region, in particular the Sox10-Pax3 enhancer site, due to NaB.	nab	180-183	paired box 3	Homo sapiens	153-157
11807787-7	2002	In LNCaP cells, hTERT mRNA expression was suppressed at 1 and 3 hr after treatment with 1 microM TSA and 4 mM NaB, respectively, followed by inhibition of telomerase activity.	nab	110-113	telomerase reverse transcriptase	Homo sapiens	16-21
12184915-6	2002	The BAb and NAb positivity rate in IFN-beta1a-treated patients was significantly lower than in the group submitted to IFN-beta1b therapy (7% vs. 84% and 0% vs. 30%, respectively).	nab	12-15	interferon alpha 1	Homo sapiens	35-38
12184915-10	2002	IFN-beta1a treatment was associated with a significantly lower prevalence of both BAb and NAb-positive titers than was IFN-beta1b.	nab	90-93	interferon alpha 1	Homo sapiens	0-3
12016145-3	2002	NaB treatment had a different effect on VEGF165 and HIF-1alpha expression.	nab	0-3	hypoxia inducible factor 1 subunit alpha	Homo sapiens	52-62
12016145-5	2002	Conversely, after 24 h of treatment all the tested NaB concentrations reduced the HIF-1alpha protein level, whereas after a longer time of exposure HIF-1alpha level increased in the presence of a high NaB concentration (2 mM) with a concomitant increase in HIF-1alpha mRNA.	nab	51-54	hypoxia inducible factor 1 subunit alpha	Homo sapiens	82-92
12016145-5	2002	Conversely, after 24 h of treatment all the tested NaB concentrations reduced the HIF-1alpha protein level, whereas after a longer time of exposure HIF-1alpha level increased in the presence of a high NaB concentration (2 mM) with a concomitant increase in HIF-1alpha mRNA.	nab	201-204	hypoxia inducible factor 1 subunit alpha	Homo sapiens	148-158
12016145-5	2002	Conversely, after 24 h of treatment all the tested NaB concentrations reduced the HIF-1alpha protein level, whereas after a longer time of exposure HIF-1alpha level increased in the presence of a high NaB concentration (2 mM) with a concomitant increase in HIF-1alpha mRNA.	nab	201-204	hypoxia inducible factor 1 subunit alpha	Homo sapiens	148-158
11956160-4	2002	Treatment with NaB (0-10 mM) caused a dose-dependent stimulation of IGFBP-3 mRNA expression and parallel increases in protein levels.	nab	15-18	insulin like growth factor binding protein 3	Homo sapiens	68-75
11956160-6	2002	To investigate the molecular mechanism of NaB-regulated IGFBP-3 expression, 1.87 kb of the human IGFBP-3 gene promoter was cloned into the pGL2-basic luciferase reporter vector.	nab	42-45	insulin like growth factor binding protein 3	Homo sapiens	56-63
11956160-6	2002	To investigate the molecular mechanism of NaB-regulated IGFBP-3 expression, 1.87 kb of the human IGFBP-3 gene promoter was cloned into the pGL2-basic luciferase reporter vector.	nab	42-45	insulin like growth factor binding protein 3	Homo sapiens	97-104
11956160-6	2002	To investigate the molecular mechanism of NaB-regulated IGFBP-3 expression, 1.87 kb of the human IGFBP-3 gene promoter was cloned into the pGL2-basic luciferase reporter vector.	nab	42-45	succinate dehydrogenase complex assembly factor 2	Homo sapiens	139-143
11956160-8	2002	However, using 5" sequential deletion constructs of the IGFBP-3 promoter, the NaB response sequences in the IGFBP-3 promoter were different in PC-3 and LNCaP cells.	nab	78-81	insulin like growth factor binding protein 3	Homo sapiens	56-63
11956160-8	2002	However, using 5" sequential deletion constructs of the IGFBP-3 promoter, the NaB response sequences in the IGFBP-3 promoter were different in PC-3 and LNCaP cells.	nab	78-81	insulin like growth factor binding protein 3	Homo sapiens	108-115
11956160-12	2002	These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.	nab	186-189	glutaminyl-tRNA amidotransferase subunit QRSL1	Homo sapiens	58-62
11956160-12	2002	These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.	nab	186-189	tumor protein p53	Homo sapiens	149-152
11956160-12	2002	These regions contain consensus binding sites for p53 and GATA, respectively, but mutational analyses and gel shift assays suggested that, while the p53 response element is required for NaB responsiveness, neither p53 nor GATA are involved.	nab	186-189	tumor protein p53	Homo sapiens	149-152
11956160-13	2002	In summary, we have demonstrated that 1) NaB significantly up-regulates IGFBP-3 mRNA and protein levels in PC-3 and LNCaP prostate cancer cells; and 2) novel butyrate- responsive elements lacking consensus Sp1 sites are used in LNCaP cells.	nab	41-44	insulin like growth factor binding protein 3	Homo sapiens	72-79
11956160-3	2002	In this study, we investigated the effects of NaB on the expression of IGF binding protein (IGFBP)-3, a known growth regulator, in two human prostate cancer cell lines (PC-3 and LNCaP).	nab	46-49	insulin like growth factor binding protein 3	Homo sapiens	71-100
11889074-1	2002	BACKGROUND: The transcription factor encoded by the intestinal Cdx2 homeobox gene and treatment with sodium butyrate (NaB), a byproduct of fibre fermentation by colonic bacteria, exert similar effects on colon cancer cell lines as they both inhibit cell growth and stimulate cell differentiation and apoptosis.	nab	118-121	caudal type homeobox 2	Homo sapiens	63-67
11889074-2	2002	AIM: To investigate whether NaB regulates expression of the Cdx2 gene in colon cancer cell lines.	nab	28-31	caudal type homeobox 2	Homo sapiens	60-64
11889074-6	2002	Stimulation of the activity of the Cdx2 promoter by NaB was dose and time dependent.	nab	52-55	caudal type homeobox 2	Homo sapiens	35-39
11889074-7	2002	The Cdx2 promoter contains discrete regions that participate in or inversely that blunt the stimulatory effect exerted by NaB.	nab	122-125	caudal type homeobox 2	Homo sapiens	4-8
11889074-8	2002	In addition, NaB stimulated the transcriptional activity of the Cdx2 promoter downregulated by oncogenic ras.	nab	13-16	caudal type homeobox 2	Homo sapiens	64-68
12030330-4	2002	This mutation abolishes the interaction of EGR2 with the NAB corepressors and thereby increases transcriptional activity.	nab	57-60	early growth response 2	Homo sapiens	43-47
11830487-5	2002	The Gly289Arg mutation in the clinical responder produced the most defective PML-RARalpha function in the presence of RA with or without sodium butyrate (NaB) or trichostatin A.	nab	154-157	PML nuclear body scaffold	Homo sapiens	77-80
11830487-5	2002	The Gly289Arg mutation in the clinical responder produced the most defective PML-RARalpha function in the presence of RA with or without sodium butyrate (NaB) or trichostatin A.	nab	154-157	retinoic acid receptor alpha	Homo sapiens	81-89
11807787-9	2002	In PC-3 cells, TSA and NaB also inhibited cell proliferation, hTERT mRNA expression and telomerase activity.	nab	23-26	telomerase reverse transcriptase	Homo sapiens	62-67
12136943-7	2002	They appeared to undergo a change in the phenotype induced by NaB, as indicated by reduced proliferation, enhanced differentiation, stimulation of apoptosis leading to decreased viability of cells, and stimulation of interleukin-8 secretion.	nab	62-65	C-X-C motif chemokine ligand 8	Homo sapiens	217-230
11668507-8	2001	This suggested that NaB had the potential to elicit SLPs through p21-mediated withdrawal from cell cycle progression.	nab	20-23	H3 histone pseudogene 16	Homo sapiens	65-68
11668507-3	2001	NaB-mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation.	nab	0-3	RB transcriptional corepressor 1	Homo sapiens	99-102
11713097-2	2001	Sodium butyrate (NaB) is a histone deacetylase inhibitor capable of alteration of bcl-2 family protein expression in other tumor types.	nab	17-20	BCL2 apoptosis regulator	Homo sapiens	82-87
11713097-7	2001	Cells were sensitive to NaB at low IC(50) (REN, 0.3 mM; I-45, 1 mM) and demonstrated apoptosis (percentage of cells below G1 phase by flow cytometry [sub-G1]: REN, 38.5%; I-45, 30.9%).	nab	24-27	renin	Homo sapiens	43-46
11713097-11	2001	Stable overexpressing BCL-XL clones were proportionally resistant to the NaB effect.	nab	73-76	BCL2 like 1	Homo sapiens	22-28
11668507-3	2001	NaB-mediated p21 might arrest endometrial and ovarian cancer cells at the G0/G1 phase by eliciting pRb unphosphorylation.	nab	0-3	H3 histone pseudogene 16	Homo sapiens	13-16
11668507-11	2001	NaB was effective even in the cancer cells with mutant p53 and/or Rb genes by eliciting cell senescence.	nab	0-3	tumor protein p53	Homo sapiens	55-58
11327726-3	2001	Egr-1 protein binds to a family of corepressor proteins called NAB which function to block or limit Egr-1 trans-activation of cognate target genes.	nab	63-66	early growth response 1	Homo sapiens	0-5
11557515-2	2001	NaB induces NHE3 activity and protein and mRNA expression both in vivo and in vitro.	nab	0-3	solute carrier family 9 member A3	Rattus norvegicus	12-16
11557515-6	2001	NaB effects on the NHE3 promoter depended on the activity of Ser/Thr kinases, in particular, protein kinase A (PKA).	nab	0-3	solute carrier family 9 member A3	Rattus norvegicus	19-23
11557515-6	2001	NaB effects on the NHE3 promoter depended on the activity of Ser/Thr kinases, in particular, protein kinase A (PKA).	nab	0-3	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	93-109
11557515-6	2001	NaB effects on the NHE3 promoter depended on the activity of Ser/Thr kinases, in particular, protein kinase A (PKA).	nab	0-3	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	111-114
11557515-9	2001	The putative NaB-responsive elements were localized within -320/-34 bp of the NHE3 promoter.	nab	13-16	solute carrier family 9 member A3	Rattus norvegicus	78-82
11557515-10	2001	These findings suggest that PKA mediates NaB effects on NHE3 gene transcription and that the mechanism of NaB action is different from that of TSA.	nab	41-44	protein kinase cAMP-activated catalytic subunit alpha	Rattus norvegicus	28-31
11557515-10	2001	These findings suggest that PKA mediates NaB effects on NHE3 gene transcription and that the mechanism of NaB action is different from that of TSA.	nab	41-44	solute carrier family 9 member A3	Rattus norvegicus	56-60
11587480-1	2001	PURPOSE: To examine the changes in expression levels of CYP3A4 and efflux transporters in CYP3A4-transfected Caco-2 (colon carcinoma) cells in the presence of the inducers sodium butyrate (NaB) and 12-O-tetradecanoylphorbol-13-acetate (TPA).	nab	189-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	56-62
11587480-1	2001	PURPOSE: To examine the changes in expression levels of CYP3A4 and efflux transporters in CYP3A4-transfected Caco-2 (colon carcinoma) cells in the presence of the inducers sodium butyrate (NaB) and 12-O-tetradecanoylphorbol-13-acetate (TPA).	nab	189-192	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	90-96
11587480-9	2001	CONCLUSIONS: The present study characterized CYP3A4-Caco-2 cell monolayers when induced for 24 h in the presence of both NaB and TPA.	nab	121-124	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	45-51
11327726-3	2001	Egr-1 protein binds to a family of corepressor proteins called NAB which function to block or limit Egr-1 trans-activation of cognate target genes.	nab	63-66	early growth response 1	Homo sapiens	100-105
11283848-5	2001	The mean volume of ascites, number of tumor cells in ascites, and the peritoneal capillary permeability were significantly suppressed by VEGF-A nAb and KDR/Flk-1 nAb treatment.	nab	144-147	vascular endothelial growth factor A	Mus musculus	137-143
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	176-179	kinase insert domain protein receptor	Mus musculus	27-30
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	176-179	kinase insert domain protein receptor	Mus musculus	32-37
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	176-179	vascular endothelial growth factor A	Mus musculus	169-175
11283848-9	2001	Furthermore, in the therapeutic experiment, although both VEGF-A nAb and KDR/Flk-1 nAb prolonged the survival rate of ascites-bearing mice, the latter showed a more significant impact on the survival of animals.	nab	65-68	vascular endothelial growth factor A	Mus musculus	58-64
11283848-9	2001	Furthermore, in the therapeutic experiment, although both VEGF-A nAb and KDR/Flk-1 nAb prolonged the survival rate of ascites-bearing mice, the latter showed a more significant impact on the survival of animals.	nab	83-86	kinase insert domain protein receptor	Mus musculus	73-76
11283848-9	2001	Furthermore, in the therapeutic experiment, although both VEGF-A nAb and KDR/Flk-1 nAb prolonged the survival rate of ascites-bearing mice, the latter showed a more significant impact on the survival of animals.	nab	83-86	kinase insert domain protein receptor	Mus musculus	77-82
11283848-5	2001	The mean volume of ascites, number of tumor cells in ascites, and the peritoneal capillary permeability were significantly suppressed by VEGF-A nAb and KDR/Flk-1 nAb treatment.	nab	162-165	kinase insert domain protein receptor	Mus musculus	152-155
11283848-5	2001	The mean volume of ascites, number of tumor cells in ascites, and the peritoneal capillary permeability were significantly suppressed by VEGF-A nAb and KDR/Flk-1 nAb treatment.	nab	162-165	kinase insert domain protein receptor	Mus musculus	156-161
11283848-6	2001	These inhibitory effects of KDR/Flk-1 nAb were more potent than those of VEGF-A nAb.	nab	38-41	kinase insert domain protein receptor	Mus musculus	28-31
11283848-6	2001	These inhibitory effects of KDR/Flk-1 nAb were more potent than those of VEGF-A nAb.	nab	38-41	kinase insert domain protein receptor	Mus musculus	32-37
11283848-6	2001	These inhibitory effects of KDR/Flk-1 nAb were more potent than those of VEGF-A nAb.	nab	80-83	vascular endothelial growth factor A	Mus musculus	73-79
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	107-110	kinase insert domain protein receptor	Mus musculus	27-30
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	107-110	kinase insert domain protein receptor	Mus musculus	32-37
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	107-110	kinase insert domain protein receptor	Mus musculus	96-99
11283848-7	2001	The autophosphorylation of KDR/ Flk-1 in the peritoneal wall was almost completely abolished by KDR/ Flk-1 nAb, whereas a certain level of activation was still shown by VEGF-A nAb treatment.	nab	107-110	kinase insert domain protein receptor	Mus musculus	101-106
11149411-2	2001	The levels of expression of LRP mRNA and LRP in a human colon carcinoma cell line, SW-620, were increased by the differentiation-inducing agent, sodium butyrate (NaB).	nab	162-165	major vault protein	Homo sapiens	28-31
11267976-1	2001	To elucidate the mechanism of action of sodium butyrate (NaB), we examined its effect on the expression of some cell cycle-related proteins (cyclins D1 and E, p16(ink4), p21(waf1), p27(kip1)) in 2 human non-small cell lung cancer cell lines (NCI-460 and NCI-H23) characterized by wild- type and mutant TP53, respectively.	nab	57-60	cyclin dependent kinase inhibitor 1A	Homo sapiens	170-178
11267976-3	2001	In NCI-H460, the p27(kip1) and p16(ink4) protein levels were markedly increased following NaB treatment, whereas p21(waf1) was only slightly elevated, with a peak at 2 mM NaB, and p53 was unaffected by any concentration.	nab	90-93	interferon alpha inducible protein 27	Homo sapiens	17-20
11267976-3	2001	In NCI-H460, the p27(kip1) and p16(ink4) protein levels were markedly increased following NaB treatment, whereas p21(waf1) was only slightly elevated, with a peak at 2 mM NaB, and p53 was unaffected by any concentration.	nab	90-93	cyclin dependent kinase inhibitor 1B	Homo sapiens	21-25
11267976-3	2001	In NCI-H460, the p27(kip1) and p16(ink4) protein levels were markedly increased following NaB treatment, whereas p21(waf1) was only slightly elevated, with a peak at 2 mM NaB, and p53 was unaffected by any concentration.	nab	90-93	cyclin dependent kinase inhibitor 2A	Homo sapiens	31-34
11267976-3	2001	In NCI-H460, the p27(kip1) and p16(ink4) protein levels were markedly increased following NaB treatment, whereas p21(waf1) was only slightly elevated, with a peak at 2 mM NaB, and p53 was unaffected by any concentration.	nab	90-93	cyclin dependent kinase inhibitor 2A	Homo sapiens	35-39
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	cyclin dependent kinase inhibitor 1A	Homo sapiens	133-136
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	interferon alpha inducible protein 27	Homo sapiens	158-161
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	cyclin dependent kinase inhibitor 1B	Homo sapiens	162-166
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	cyclin dependent kinase inhibitor 2A	Homo sapiens	172-175
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	cyclin dependent kinase inhibitor 2A	Homo sapiens	176-180
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	tumor protein p53	Homo sapiens	205-208
11267976-5	2001	The results suggest that NaB blocks the growth of both cell lines by induction of cyclin-dependent kinase inhibitors (in particular, p21(waf1) in NCI-H23 and p27(kip1) and p16(ink4) in NCI-H460) through a p53-dependent or p53-independent mechanism, and open up interesting perspectives for the use of NaB as an alternative or additional strategy in the treatment of non-small cell lung carcinoma.	nab	25-28	tumor protein p53	Homo sapiens	222-225
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	46-49
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	50-54
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	0-3	cyclin dependent kinase inhibitor 1A	Homo sapiens	55-59
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	0-3	interferon alpha inducible protein 27	Homo sapiens	123-126
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	0-3	cyclin dependent kinase inhibitor 1B	Homo sapiens	127-131
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	158-161	cyclin dependent kinase inhibitor 1A	Homo sapiens	50-54
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	158-161	cyclin dependent kinase inhibitor 1A	Homo sapiens	55-59
11250651-8	2001	NaB treatment resulted in increased levels of p21(Waf1/Cip1) mRNA and protein in Hs578T cells and distinct upregulation of p27(Kip1) in HMEC, suggesting that NaB activates different genes involved in cell cycle arrest, depending upon the cell type.	nab	158-161	cyclin dependent kinase inhibitor 1B	Homo sapiens	127-131
11250651-9	2001	In the same context, among the IGFBP superfamily members tested, NaB specifically upregulated the expression of IGFBP-3 and IGFBP-rP2.	nab	65-68	insulin like growth factor binding protein 3	Homo sapiens	31-36
11250651-9	2001	In the same context, among the IGFBP superfamily members tested, NaB specifically upregulated the expression of IGFBP-3 and IGFBP-rP2.	nab	65-68	insulin like growth factor binding protein 3	Homo sapiens	112-119
11250651-11	2001	Northern blot analysis showed that NaB treatment at 1-10 mM concentrations caused a dose-dependent stimulation of IGFBP-3 mRNA expression in cancerous cells and IGFBP-rP2 mRNA expression in both cancerous and non-cancerous cells.	nab	35-38	insulin like growth factor binding protein 3	Homo sapiens	114-121
11250651-13	2001	In summary, we have demonstrated that NaB (i) uniformly suppresses DNA synthesis in both cancerous and non-cancerous mammary cells, and (ii) upregulates IGFBP-3 and IGFBP-rP2 mRNA and protein levels in cancerous and non-cancerous mammary cells.	nab	38-41	insulin like growth factor binding protein 3	Homo sapiens	153-160
11267976-1	2001	To elucidate the mechanism of action of sodium butyrate (NaB), we examined its effect on the expression of some cell cycle-related proteins (cyclins D1 and E, p16(ink4), p21(waf1), p27(kip1)) in 2 human non-small cell lung cancer cell lines (NCI-460 and NCI-H23) characterized by wild- type and mutant TP53, respectively.	nab	57-60	cyclin D1	Homo sapiens	141-157
11149411-2	2001	The levels of expression of LRP mRNA and LRP in a human colon carcinoma cell line, SW-620, were increased by the differentiation-inducing agent, sodium butyrate (NaB).	nab	162-165	major vault protein	Homo sapiens	41-44
11149411-9	2001	PAK-104P and an antibody against LRP increased the accumulation of ADM in the isolated nuclei from NaB-treated cells, and inhibited the enhanced efflux of ADM from the nuclei.	nab	99-102	major vault protein	Homo sapiens	33-36
10734128-5	2000	Furthermore, we report that NAB-activated promoters such as LHbeta contain EGR consensus sites that are fewer in number and lower in binding affinity than those found at NAB-repressed promoters such as basic fibroblast growth factor.	nab	28-31	luteinizing hormone beta	Mus musculus	60-66
11111043-2	2000	To test their roles in cell physiology, we constructed adenoviral recombinants encoding NGFI-A binding protein 2 (NAB2, a repressor of EGR1, EGR2, and EGR3), EGR1, NAB-insensitive EGR1(I293F) (EGR1*), EGR2, and the NAB-binding, repressive domain 1 (R1) of EGR1.	nab	114-117	early growth response 1	Homo sapiens	135-139
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	cyclin D1	Homo sapiens	60-69
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	tumor protein p53	Homo sapiens	74-77
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	cyclin dependent kinase inhibitor 1A	Homo sapiens	142-154
10959623-4	2000	At inhibitory concentrations (higher than 1 mM) NaB reduced cyclin D1 and p53 level in a dose-dependent manner and sustained the synthesis of p21waf1/cip1, probably in a p53-independent way, accounting for the G0/G1 block observed by flow cytometry.	nab	48-51	tumor protein p53	Homo sapiens	170-173
10734128-4	2000	NAB coactivation requires the conserved NCD2 protein domain, previously implicated in NAB corepression, is strictly dependent upon EGR binding to the LHbeta proximal promoter and is independent of EGR activation domains.	nab	0-3	early growth response 1	Mus musculus	131-134
10734128-4	2000	NAB coactivation requires the conserved NCD2 protein domain, previously implicated in NAB corepression, is strictly dependent upon EGR binding to the LHbeta proximal promoter and is independent of EGR activation domains.	nab	0-3	luteinizing hormone beta	Mus musculus	150-156
10734128-4	2000	NAB coactivation requires the conserved NCD2 protein domain, previously implicated in NAB corepression, is strictly dependent upon EGR binding to the LHbeta proximal promoter and is independent of EGR activation domains.	nab	0-3	early growth response 1	Mus musculus	197-200
11122449-2	2000	Flow cytometry revealed an instability of syngeneic NAb binding to C3H 10T1/2 fibroblast variants at 37 degrees, which could be partially reduced by H7, an inhibitor of the pivotal signalling serine/threonine kinase, protein kinase C (PKC).	nab	52-55	protein kinase C, alpha	Rattus norvegicus	235-238
11122449-3	2000	Cells coated with purified NAb at 4 degrees followed by a rise in temperature to 37 degrees showed an increase in membrane expression of introduced rat PKC-beta 1 and endogenous PKC-alpha, in the PKC-beta 1-overexpressing PKC-4 and v-H-ras-producing I3T2.1, respectively.	nab	27-30	protein kinase C, beta	Rattus norvegicus	152-160
11122449-3	2000	Cells coated with purified NAb at 4 degrees followed by a rise in temperature to 37 degrees showed an increase in membrane expression of introduced rat PKC-beta 1 and endogenous PKC-alpha, in the PKC-beta 1-overexpressing PKC-4 and v-H-ras-producing I3T2.1, respectively.	nab	27-30	protein kinase C, alpha	Rattus norvegicus	178-187
11122449-3	2000	Cells coated with purified NAb at 4 degrees followed by a rise in temperature to 37 degrees showed an increase in membrane expression of introduced rat PKC-beta 1 and endogenous PKC-alpha, in the PKC-beta 1-overexpressing PKC-4 and v-H-ras-producing I3T2.1, respectively.	nab	27-30	protein kinase C, beta	Rattus norvegicus	196-204
11122449-5	2000	In addition, both the precoated NAb and numerous membrane molecules ranging from 20,000 to 220,000 MW were released into the supernatant, including the receptor-like protein tyrosine phosphatase alpha (RPTP-alpha).	nab	32-35	protein tyrosine phosphatase receptor type A	Homo sapiens	202-212
10734128-5	2000	Furthermore, we report that NAB-activated promoters such as LHbeta contain EGR consensus sites that are fewer in number and lower in binding affinity than those found at NAB-repressed promoters such as basic fibroblast growth factor.	nab	28-31	early growth response 1	Mus musculus	75-78
10734128-6	2000	Analysis of mutant and synthetic promoters confirms that both the strength and multiplicity of EGR-binding sites influence the transcriptional outcome of NAB recruitment.	nab	154-157	early growth response 1	Mus musculus	95-98
10808411-3	2000	A 5"-32P-labeled primer with a photoreactive group at the 3"-terminus was derived from NAB-ddUTP and used for photoaffinity labeling of the human replication protein A (RPA).	nab	87-90	replication protein A1	Homo sapiens	146-167
10808411-3	2000	A 5"-32P-labeled primer with a photoreactive group at the 3"-terminus was derived from NAB-ddUTP and used for photoaffinity labeling of the human replication protein A (RPA).	nab	87-90	replication protein A1	Homo sapiens	169-172
10657000-4	2000	When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression.	nab	42-45	transglutaminase 2	Homo sapiens	158-181
10657000-4	2000	When RA was used in combination with 2 mM NaB, the treatment induced substantial morphological changes, apoptosis-independent growth arrest, up-regulation of tissue transglutaminase (tTGase), and down-regulation of beta and gamma RA receptor (RAR) mRNA expression.	nab	42-45	transglutaminase 2	Homo sapiens	183-189
10534117-6	1999	In transient transfection assays, PMA and NaB both stimulate transcription of the luciferase reporter gene placed under the control of ctsb promoter fragments.	nab	42-45	cathepsin B	Homo sapiens	135-139
10695015-8	1999	Two LRP-specific ribozymes inhibited the NaB-induced expression of LRP in SW-620 cells and almost completely abolished their acquisition of the MDR phenotype.	nab	41-44	major vault protein	Homo sapiens	4-7
10695015-8	1999	Two LRP-specific ribozymes inhibited the NaB-induced expression of LRP in SW-620 cells and almost completely abolished their acquisition of the MDR phenotype.	nab	41-44	major vault protein	Homo sapiens	67-70
10695015-7	1999	Treatment of human colorectal carcinoma SW-620 cells with sodium butyrate(NaB) induced LRP in the cells and conferred resistance to Adrianycin(ADM), VCR, VP-16, gramicidin D and taxol.	nab	74-77	major vault protein	Homo sapiens	87-90
10695015-12	1999	Efflux of ADM from nuclei isolated from NaB-treated cells was enhanced compared with those from untreated cells and NaB-treated cells transfected with a LRP-specific ribozyme.	nab	40-43	major vault protein	Homo sapiens	153-156
10695015-7	1999	Treatment of human colorectal carcinoma SW-620 cells with sodium butyrate(NaB) induced LRP in the cells and conferred resistance to Adrianycin(ADM), VCR, VP-16, gramicidin D and taxol.	nab	74-77	host cell factor C1	Homo sapiens	154-159
10695015-12	1999	Efflux of ADM from nuclei isolated from NaB-treated cells was enhanced compared with those from untreated cells and NaB-treated cells transfected with a LRP-specific ribozyme.	nab	116-119	major vault protein	Homo sapiens	153-156
10695015-13	1999	The polyclonal antibody against LRP inhibited the enhanced efflux of ADM from nuclei isolated from NaB-treated cells.	nab	99-102	major vault protein	Homo sapiens	32-35
9851863-4	1998	Sodium butyrate (NaB), which inhibits NBEC as well as cancer cell proliferation, induced an increase in 35S incorporation into HSPG in all cell types studied.	nab	17-20	syndecan 2	Homo sapiens	127-131
9927752-1	1999	We have investigated by electrophoretic mobility shift assay (EMSA) the level of GATA-1 DNA-binding activity in nuclear extracts prepared from the human erythroleukaemic cell line, K562, after erythroid induction by hemin, sodium butyrate (NaB) or Trichostatin A or treatment with N -acetylcysteine (NAC).	nab	240-243	GATA binding protein 1	Homo sapiens	81-87
9927752-5	1999	When the mouse erythroleukaemic cell line MEL was induced with dimethylsulphoxide (DMSO), NaB or NAC, GATA-1 binding activity fell with DMSO, rose significantly with NaB and remained at about the same level in NAC-induced cells.	nab	90-93	GATA binding protein 1	Mus musculus	102-108
9927752-5	1999	When the mouse erythroleukaemic cell line MEL was induced with dimethylsulphoxide (DMSO), NaB or NAC, GATA-1 binding activity fell with DMSO, rose significantly with NaB and remained at about the same level in NAC-induced cells.	nab	166-169	GATA binding protein 1	Mus musculus	102-108
10219763-3	1999	Now a rat PKC-beta1-overexpressing 10T 1/2 clone, PKC-4, with an 11-fold increase in PKC activity and an activated, partially transformed phenotype, links higher susceptibility to transformation through v-Ha-ras infection with an 80% increase in NAb binding assayed by flow cytometry.	nab	246-249	protein kinase C alpha	Homo sapiens	10-13
10219763-4	1999	H7 and E-64d inhibition and phorbol ester depletion of PKC reduced NAb binding.	nab	67-70	protein kinase C alpha	Homo sapiens	55-58
10219763-6	1999	Thus, expression of NAb-binding structures appears to be elevated by constitutive increases in the basal activation of PKC in both the ras-transformation and the PKC-beta1-preneoplasia models.	nab	20-23	protein kinase C alpha	Homo sapiens	119-122
10219763-7	1999	This, coupled with corresponding decreases in membrane PKC-alpha and NAb binding in confluent 10T 1/2 cells raises the possibility that in general, cells activated through PKC are NAb sensitive.	nab	180-183	protein kinase C alpha	Homo sapiens	55-64
10219763-7	1999	This, coupled with corresponding decreases in membrane PKC-alpha and NAb binding in confluent 10T 1/2 cells raises the possibility that in general, cells activated through PKC are NAb sensitive.	nab	180-183	protein kinase C alpha	Homo sapiens	55-58
9851863-6	1998	Modification of HSPG induced by TGFbeta-1 or NaB treatments in normal and breast cancer epithelial cells resulted in an increase in 125I-fibroblast growth factor-2 (FGF-2) binding on HSPG.	nab	45-48	fibroblast growth factor 2	Homo sapiens	165-170
9851863-6	1998	Modification of HSPG induced by TGFbeta-1 or NaB treatments in normal and breast cancer epithelial cells resulted in an increase in 125I-fibroblast growth factor-2 (FGF-2) binding on HSPG.	nab	45-48	syndecan 2	Homo sapiens	183-187
9851863-7	1998	More importantly, NaB pretreatment resulted in an inhibition of the MCF-7 cell responsiveness to FGF-2, even though these cells remained sensitive to growth stimulation induced by serum or epidermal growth factor.	nab	18-21	fibroblast growth factor 2	Homo sapiens	97-102
9851863-6	1998	Modification of HSPG induced by TGFbeta-1 or NaB treatments in normal and breast cancer epithelial cells resulted in an increase in 125I-fibroblast growth factor-2 (FGF-2) binding on HSPG.	nab	45-48	syndecan 2	Homo sapiens	16-20
9851863-6	1998	Modification of HSPG induced by TGFbeta-1 or NaB treatments in normal and breast cancer epithelial cells resulted in an increase in 125I-fibroblast growth factor-2 (FGF-2) binding on HSPG.	nab	45-48	fibroblast growth factor 2	Homo sapiens	132-163
9774344-2	1998	Using a novel adaptation of the yeast two-hybrid screen, we have identified several point mutations in NAB corepressors that interfere with their ability to bind to the Egr1 R1 domain.	nab	103-106	early growth response 1	Homo sapiens	169-173
9703983-4	1998	In this report, we demonstrate that NaB stimulates PKC activation by 3-fold and induces differential expression of several PKC isoforms.	nab	36-39	protein kinase C beta	Homo sapiens	51-54
9734851-9	1998	The DMI and ADG were increased (P < .05) by FM and NaB supplementation.	nab	54-57	ADG	Ovis aries	12-15
9734851-10	1998	Interactions (P < .05) revealed that NaB increased DMI, ADG, gain per feed (g/kg of DMI), and plasma urea N concentration in the absence of FM but not in the presence of FM in the diet.	nab	40-43	ADG	Ovis aries	59-62
9774344-6	1998	To examine NAB repression of a native Egr target gene, we show that NAB2 represses Egr2/Krox20-mediated activation of the bFGF/FGF-2 promoter, and that repression is reversed by coexpression of dominant negative NAB2.	nab	11-14	NGFI-A binding protein 2	Homo sapiens	68-72
9703983-4	1998	In this report, we demonstrate that NaB stimulates PKC activation by 3-fold and induces differential expression of several PKC isoforms.	nab	36-39	protein kinase C beta	Homo sapiens	123-126
9581847-7	1998	Northern blot analysis and cytofluorometry revealed that NaB-treated cells showed a lower expression of MUC1 than did untreated cells.	nab	57-60	mucin 1, cell surface associated	Homo sapiens	104-108
9464250-2	1998	We used doxorubicin (DOX) and sodium butyrate (NaB) to accumulate p53 protein.	nab	47-50	tumor protein p53	Homo sapiens	66-69
8956976-9	1996	We found that cAMP or sodium butyrate (NaB) were also effective at inhibiting growth of the NHL cells; this was a profound inhibition (approaching 100%) compared to the 50% inhibition seen with anti-CD40 treatment.	nab	39-42	CD40 molecule	Homo sapiens	199-203
9200472-6	1997	Growth of the LYNAb+ from a threshold s.c. inoculum in syngeneic DBA/2 mice yielded more tumorigenic cells which bound less NAb, anti-CD45RA, and anti-CD45RC; the same very low anti-CD45RB; and more anti-pan CD45.	nab	16-19	protein tyrosine phosphatase, receptor type, C	Mus musculus	134-138
9200472-9	1997	The consistent correspondence between CD45RA and CD45RC determinant expression, CD45 isoform expression, tumorigenicity, and NAb binding exhibited by T lymphoma cells selected for high NAb binding in vitro or through tumor progression in vivo suggests that asialo high m.w.	nab	185-188	protein tyrosine phosphatase receptor type C	Homo sapiens	38-42
9200472-10	1997	isoforms of the cell surface-signaling molecule CD45 are differentially expressed during tumor development and furthermore that they participate in NAb-mediated antitumor mechanisms.	nab	148-151	protein tyrosine phosphatase receptor type C	Homo sapiens	48-52
9275119-1	1997	BACKGROUND: The cell surface carbohydrate moiety, Gal(alpha1,3)Galactose (alphaGal), has been implicated as the major determinant recognized by more than 80% of human anti-porcine natural antibodies (NAb).	nab	200-203	galanin and GMAP prepropeptide	Homo sapiens	50-72
9275119-2	1997	An ELISA system was developed for the detection of this subpopulation of porcine cell-reactive NAb using synthetic alphaGal conjugated to bovine serum albumin.	nab	95-98	albumin	Homo sapiens	145-158
8995352-5	1997	Truncated HERG proteins containing NAB(HERG), including one that resulted from the delta1261 human mutation, inhibit the functional expression of the HERG channel in transfected cells.	nab	35-38	potassium voltage-gated channel subfamily H member 2	Homo sapiens	10-14
8995352-5	1997	Truncated HERG proteins containing NAB(HERG), including one that resulted from the delta1261 human mutation, inhibit the functional expression of the HERG channel in transfected cells.	nab	35-38	potassium voltage-gated channel subfamily H member 2	Homo sapiens	39-43
8995352-5	1997	Truncated HERG proteins containing NAB(HERG), including one that resulted from the delta1261 human mutation, inhibit the functional expression of the HERG channel in transfected cells.	nab	35-38	potassium voltage-gated channel subfamily H member 2	Homo sapiens	39-43
8892860-5	1996	To address this question, we characterized the activity of LAT promoter fusion constructs in PC12 cells following treatment with nerve growth factor (NGF) and/or sodium butyrate (NaB), agents that affect expression of cell cycle-associated genes.	nab	179-182	linker for activation of T cells	Rattus norvegicus	59-62
8892860-6	1996	Expression from the LAT promoter was induced 8- to 12-fold by either NGF or NaB alone and 40- to 60-fold when the two agents were added simultaneously.	nab	76-79	linker for activation of T cells	Homo sapiens	20-23
8892860-10	1996	To identify pathways leading to LAT activation in vitro, we characterized the response of the LAT promoter to NGF and/or NaB in PC12-derived cell lines containing mutations in specific signal transduction pathways.	nab	121-124	linker for activation of T cells	Homo sapiens	94-97
8892861-3	1996	Consistent with this hypothesis, we have recently demonstrated that LAT expression is significantly enhanced by nerve growth factor (NGF) and sodium butyrate (NaB) in neurally derived PC12 cells.	nab	159-162	linker for activation of T cells	Homo sapiens	68-71
8857714-3	1996	First, we validated the IFNB NAB assay used in the multicenter trial by having representative stored serum samples reanalyzed by an independent laboratory.	nab	29-32	interferon beta 1	Homo sapiens	24-28
8892861-8	1996	In contrast to basal expression, maximum induction of the LAT promoter by NGF and NaB requires sequences between -159 and -81.	nab	82-85	linker for activation of T cells	Homo sapiens	58-61
8892861-13	1996	These regions were critical for complex formation in vitro and for maximum induction of the LAT promoter by NGF and NaB in transient expression assays.	nab	116-119	linker for activation of T cells	Homo sapiens	92-95
7827091-3	1995	Sites of in vivo glycation of rat liver aldehyde reductase were identified by sequencing of digested peptides labeled with NaB[3H]4 and by mass spectrometry.	nab	123-126	aldo-keto reductase family 1, member B7	Rattus norvegicus	40-58
8695921-2	1996	We previously observed that treatment with NaB in association with interleukin 2 (IL2), cures 60% of peritoneal carcinomatosis induced by injection of DHDK12/TRb cells in syngenic rats [15].	nab	43-46	interleukin 2	Rattus norvegicus	67-80
8695921-2	1996	We previously observed that treatment with NaB in association with interleukin 2 (IL2), cures 60% of peritoneal carcinomatosis induced by injection of DHDK12/TRb cells in syngenic rats [15].	nab	43-46	interleukin 2	Rattus norvegicus	82-85
8695921-9	1996	These in vitro data were confirmed in vivo showing a significant expression of apoptotic tumour cells in NaB- or NaB/IL2-treated tumours.	nab	113-116	interleukin 2	Rattus norvegicus	117-120
8695921-10	1996	Thus, the present results in the rat peritoneal carcinomatosis treatment show that combination of apoptotic process induced by NaB with immunostimulation by IL2 has powerful therapeutic properties.	nab	127-130	interleukin 2	Rattus norvegicus	157-160
7767986-2	1995	The mRNA of the growth related proto-oncogene c-myc, constitutively expressed in N.1 cells decreased significantly within 24 h of NaB treatment and remained suppressed until the NaB block was released.	nab	178-181	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	46-51
7767986-4	1995	We demonstrated that NaB blocked general mechanisms in signal transduction, such as the release of Ca2+ from intracellular stores, and modulated the activity of serine/threonine kinases.	nab	21-24	carbonic anhydrase 2	Homo sapiens	99-102
7772641-7	1995	NaB enhanced the expression of AP three-fold and CEA five-fold.	nab	0-3	CEA cell adhesion molecule 3	Homo sapiens	49-52
7697745-4	1995	Unexpectedly, both sodium barbital (NaB) and phorone (PHR) moderately induce CYP2B1 isoforms in rat, the extent being highest in female kidney (PHR, 14-fold increase) and male lung (NaB, 4.5-fold).	nab	36-39	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	77-83
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	nab	206-209	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	22-25
7887903-1	1995	Expression of the rat p52(PAI-1) gene is positively regulated by agents that influence cellular microfilament organization and/or cell-to-substrate adhesion [e.g. cytochalasin D (CD) and sodium n-butyrate (NaB)] [Higgins, Chaudhari and Ryan (1991) Biochem.	nab	206-209	serpin family E member 1	Rattus norvegicus	26-31
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	nab	0-3	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	37-40
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	nab	0-3	serpin family E member 1	Rattus norvegicus	41-46
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	nab	0-3	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	92-95
7887903-8	1995	NaB and/or CD effectively stimulated p52(PAI-1) run-off transcription and augmented de novo p52(PAI-1) mRNA and protein synthesis in KNRK cells; induction at both the mRNA and protein levels was inhibited by actinomycin D.	nab	0-3	serpin family E member 1	Rattus norvegicus	96-101
8881765-4	1996	The antigen-biding activity of IgM NAb increased after isolation of the serum immunoglobulins on a Staphylococcus Protein A (SPA)-Sepharose column.	nab	35-38	pulmonary surfactant-associated protein A	Sus scrofa	125-128
8713125-8	1996	Furthermore, NaB induces tyrosine phosphorylation and rapid activation of MAP kinase (ERK-1).	nab	13-16	mitogen-activated protein kinase 3	Homo sapiens	86-91
8693544-2	1996	Previous studies have implicated xenoreactive IgM natural antibody (nAb) as the predominant immunoglobulin involved in HAR.	nab	68-71	Ig kappa chain	Sus scrofa	46-49
8693544-11	1996	Organ survival was negatively associated with xenoreactive IgM nAb levels measured immediately before perfusion (r=-0.83; P=0.01), and not with IgG nAb levels (r=-0.21; P=0.62).	nab	63-66	Ig kappa chain	Sus scrofa	59-62
8693544-12	1996	The ability of plasma from IgM-depleted blood to elicit complement activation, measured by iC3b binding to porcine aortic endothelial cells in vitro, was also strongly associated with IgM xenoreactive nAb levels (r=0.92; P<0.0001).	nab	201-204	Ig kappa chain	Sus scrofa	27-30
8693544-12	1996	The ability of plasma from IgM-depleted blood to elicit complement activation, measured by iC3b binding to porcine aortic endothelial cells in vitro, was also strongly associated with IgM xenoreactive nAb levels (r=0.92; P<0.0001).	nab	201-204	Ig kappa chain	Sus scrofa	184-187
8928764-6	1996	On the other hand, 6-OHDA injection into the PVN or NAB not only decreased the extracellular NPY level, the amount of food intake was not change by the 6-OHDA treatment.	nab	52-55	neuropeptide Y	Rattus norvegicus	93-96
8928764-7	1996	It is concluded that the NAB is involved in the prefeeding NPY release in rats under RF but not in the deprivation-induced NPY release.	nab	25-28	neuropeptide Y	Rattus norvegicus	59-62
8595156-2	1996	The differentiation inducer sodium butyrate (NaB) arrested growth of N.1 ovarian carcinoma cells and repressed expression of cyclin D1/prad1 and the invasiveness-related protease plasminogen activator-urokinase (plau).	nab	45-48	cyclin D1	Homo sapiens	125-134
8595156-2	1996	The differentiation inducer sodium butyrate (NaB) arrested growth of N.1 ovarian carcinoma cells and repressed expression of cyclin D1/prad1 and the invasiveness-related protease plasminogen activator-urokinase (plau).	nab	45-48	cyclin D1	Homo sapiens	135-140
8595156-2	1996	The differentiation inducer sodium butyrate (NaB) arrested growth of N.1 ovarian carcinoma cells and repressed expression of cyclin D1/prad1 and the invasiveness-related protease plasminogen activator-urokinase (plau).	nab	45-48	plasminogen activator, urokinase	Homo sapiens	212-216
8595156-5	1996	Recently, it was shown that NaB represses the transcription factor c-myc by blocking Ca2+ signals and modulating serine threonine kinase activity.	nab	28-31	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	67-72
8595156-6	1996	We wanted to investigate NaB-mediated interference on signals contributing to the expression on prad1, plau and growth arrest-specific 6 (gas6).	nab	25-28	cyclin D1	Homo sapiens	96-101
8595156-6	1996	We wanted to investigate NaB-mediated interference on signals contributing to the expression on prad1, plau and growth arrest-specific 6 (gas6).	nab	25-28	plasminogen activator, urokinase	Homo sapiens	103-107
8595156-6	1996	We wanted to investigate NaB-mediated interference on signals contributing to the expression on prad1, plau and growth arrest-specific 6 (gas6).	nab	25-28	growth arrest specific 6	Homo sapiens	112-136
8595156-6	1996	We wanted to investigate NaB-mediated interference on signals contributing to the expression on prad1, plau and growth arrest-specific 6 (gas6).	nab	25-28	growth arrest specific 6	Homo sapiens	138-142
8595156-11	1996	Constitutive plau expression was insensitive to additional Ca2+-mediated signals, but it became responsive upon NaB treatment.	nab	112-115	plasminogen activator, urokinase	Homo sapiens	13-17
8527478-7	1995	The production of retrovirus vectors containing genes other than CFTR could also be increased by NaB treatment, although the enhancement in titer was modest (2-fold to 10-fold).	nab	97-100	CF transmembrane conductance regulator	Homo sapiens	65-69
7767986-2	1995	The mRNA of the growth related proto-oncogene c-myc, constitutively expressed in N.1 cells decreased significantly within 24 h of NaB treatment and remained suppressed until the NaB block was released.	nab	130-133	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	46-51
7887903-9	1995	Pretreatment with cycloheximide (CX) markedly attenuated NaB- and/or CD-stimulated p52(PAI-1) expression.	nab	57-60	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	83-86
7887903-9	1995	Pretreatment with cycloheximide (CX) markedly attenuated NaB- and/or CD-stimulated p52(PAI-1) expression.	nab	57-60	serpin family E member 1	Rattus norvegicus	87-92
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	nab	92-95	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	20-23
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	nab	92-95	serpin family E member 1	Rattus norvegicus	24-29
7887903-12	1995	Full stimulation of p52(PAI-1) expression in KNRK cells in response to the shape modulators NaB and/or CD involves transcriptional activation of the p52(PAI-1) gene, requires de novo RNA synthesis and occurs through a secondary-response (i.e. protein-synthesis-dependent) pathway.	nab	92-95	serpin family E member 1	Rattus norvegicus	153-158
7913275-4	1994	The strong induction of HIV expression by NaB or HMBA in J delta K cells clearly demonstrates the existence of NF-kappa B-independent mechanisms of HIV activation in chronically infected cells.	nab	42-45	nuclear factor kappa B subunit 1	Homo sapiens	111-121
7908296-1	1994	We investigated the mechanism of sodium butyrate (NaB)-mediated induction of mdr1 mRNA in parental (wild type) and multidrug-resistant (Ad1000) SW620 colon cancer cell lines.	nab	50-53	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
7908296-2	1994	NaB treatment resulted in reversible, time-dependent increases in nuclear run-on transcription of endogenous mdr1 in these cell lines that paralleled the reversible increases of mdr1 mRNA in both timing and magnitude.	nab	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	109-113
7908296-2	1994	NaB treatment resulted in reversible, time-dependent increases in nuclear run-on transcription of endogenous mdr1 in these cell lines that paralleled the reversible increases of mdr1 mRNA in both timing and magnitude.	nab	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	178-182
7908296-4	1994	Thus, the effects of NaB on mdr1 mRNA levels are fully attributable to altered mdr1 transcription.	nab	21-24	ATP binding cassette subfamily B member 1	Homo sapiens	28-32
7908296-4	1994	Thus, the effects of NaB on mdr1 mRNA levels are fully attributable to altered mdr1 transcription.	nab	21-24	ATP binding cassette subfamily B member 1	Homo sapiens	79-83
7908296-5	1994	Furthermore, NaB induces the expression of transiently transfected chloramphenicol acetyltransferase reporter plasmids that are under the transcriptional control of the mdr1 promoter (mdrCAT vectors).	nab	13-16	ATP binding cassette subfamily B member 1	Homo sapiens	169-173
7908296-6	1994	Transfections using mdrCAT vectors modified by deletion and site-directed mutagenesis of the mdr1 promoter indicate that NaB-mediated induction of these vectors is at least partially dependent upon sequences present in the basal mdr1 promoter between -89 and +11 relative to the start site of transcription.	nab	121-124	ATP binding cassette subfamily B member 1	Homo sapiens	93-97
7908296-6	1994	Transfections using mdrCAT vectors modified by deletion and site-directed mutagenesis of the mdr1 promoter indicate that NaB-mediated induction of these vectors is at least partially dependent upon sequences present in the basal mdr1 promoter between -89 and +11 relative to the start site of transcription.	nab	121-124	ATP binding cassette subfamily B member 1	Homo sapiens	229-233
8217487-3	1993	NaB, RA and VD3 increased CA125 release per cell and 125I-labeled anti-CA125 MoAb binding to the cells.	nab	0-3	mucin 16, cell surface associated	Homo sapiens	26-31
8103760-3	1993	In 4 colon carcinoma cell lines (SW 620, HCT-15, DLD-1, LS 180), MDR1 expression was reported in an earlier study to be elevated after exposure to a differentiating agent, sodium butyrate (NaB).	nab	189-192	ATP binding cassette subfamily B member 1	Homo sapiens	65-69
8103760-5	1993	We have re-examined the effect of NaB on MDR1/P-glycoprotein expression and function in the same colon carcinoma cell lines.	nab	34-37	ATP binding cassette subfamily B member 1	Homo sapiens	41-45
8103760-5	1993	We have re-examined the effect of NaB on MDR1/P-glycoprotein expression and function in the same colon carcinoma cell lines.	nab	34-37	ATP binding cassette subfamily B member 1	Homo sapiens	46-60
8103760-6	1993	NaB treatment induced differentiation-related changes and increased expression of MDR1 mRNA in all 4 cell lines.	nab	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	82-86
8103760-9	1993	NaB treatment caused a relatively minor increase in MDR1 mRNA expressed in the other 3 cell lines.	nab	0-3	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
8103760-11	1993	The magnitude of MDR1 induction by NaB showed no apparent correlation with differentiation-related changes induced by this agent.	nab	35-38	ATP binding cassette subfamily B member 1	Homo sapiens	17-21
8375477-6	1993	Although c-jun expression was induced with RA, rapid and predominant induction of junB expression was specifically observed with NaB, which is regulated by both transcriptional and post-transcriptional mechanisms.	nab	129-132	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	82-86
8375477-7	1993	These results suggest that the mechanism of differentiation induced with NaB differs from that of RA; the former may be mediated by the junB gene and the latter by c-jun.	nab	73-76	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-140
8375477-7	1993	These results suggest that the mechanism of differentiation induced with NaB differs from that of RA; the former may be mediated by the junB gene and the latter by c-jun.	nab	73-76	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	164-169
8217487-3	1993	NaB, RA and VD3 increased CA125 release per cell and 125I-labeled anti-CA125 MoAb binding to the cells.	nab	0-3	mucin 16, cell surface associated	Homo sapiens	71-76
8500547-1	1993	Expression of SPARC (secreted protein acidic and rich in cysteine), a 43-kDa extracellular matrix-associated glycoprotein involved in tissue remodeling, was quantitated during normal human keratinocyte (NHK) growth in culture and as a function of sodium n-butyrate (NaB)-induced differentiation to mature enucleate cornified envelopes (CEs).	nab	266-269	secreted protein acidic and cysteine rich	Homo sapiens	14-19
8019883-6	1993	The survival median of IL-2 treated rats significantly increased versus those of untreated ones, and was much higher with NaB in supplement.	nab	122-125	interleukin 2	Rattus norvegicus	23-27
8500547-12	1993	NHKs cultured on fibronectin (FN), an established modulator of epidermal cell maturation in vitro, showed a similar response to NaB.	nab	128-131	fibronectin 1	Homo sapiens	17-28
8500547-12	1993	NHKs cultured on fibronectin (FN), an established modulator of epidermal cell maturation in vitro, showed a similar response to NaB.	nab	128-131	fibronectin 1	Homo sapiens	30-32
8500547-13	1993	In general, however, the level of NaB-induced SPARC expression was considerably reduced in FN cultures correlating with a lower efficiency of CE formation.	nab	34-37	secreted protein acidic and cysteine rich	Homo sapiens	46-51
8500547-13	1993	In general, however, the level of NaB-induced SPARC expression was considerably reduced in FN cultures correlating with a lower efficiency of CE formation.	nab	34-37	fibronectin 1	Homo sapiens	91-93
8500547-14	1993	Induced SPARC expression was, in large part, dependent on autocrine transforming growth factor-beta (TGF-beta) production since incubation in the presence of NaB+neutralizing antibodies to TGF-beta inhibited both the expression of SPARC by 72% and development of mature CEs.	nab	158-161	secreted protein acidic and cysteine rich	Homo sapiens	8-13
8500547-14	1993	Induced SPARC expression was, in large part, dependent on autocrine transforming growth factor-beta (TGF-beta) production since incubation in the presence of NaB+neutralizing antibodies to TGF-beta inhibited both the expression of SPARC by 72% and development of mature CEs.	nab	158-161	transforming growth factor beta 1	Homo sapiens	68-99
8500547-14	1993	Induced SPARC expression was, in large part, dependent on autocrine transforming growth factor-beta (TGF-beta) production since incubation in the presence of NaB+neutralizing antibodies to TGF-beta inhibited both the expression of SPARC by 72% and development of mature CEs.	nab	158-161	transforming growth factor beta 1	Homo sapiens	101-109
8500547-14	1993	Induced SPARC expression was, in large part, dependent on autocrine transforming growth factor-beta (TGF-beta) production since incubation in the presence of NaB+neutralizing antibodies to TGF-beta inhibited both the expression of SPARC by 72% and development of mature CEs.	nab	158-161	secreted protein acidic and cysteine rich	Homo sapiens	231-236
8500547-3	1993	After addition of NaB, SPARC expression increased and the pattern of expression shifted to one involving predominantly suprabasal cells (i.e., spinous cells, pre-CEs, and mature CEs).	nab	18-21	secreted protein acidic and cysteine rich	Homo sapiens	23-28
8500547-10	1993	During NaB-induced NHK differentiation, SPARC intracellular content increased prior to the onset of CE formation (i.e., 2 days after its addition) followed by a period of extracellular accumulation which coincided with the time of maximal CE generation (i.e., Days 4 and 5 after NaB addition).	nab	7-10	secreted protein acidic and cysteine rich	Homo sapiens	40-45
8500547-10	1993	During NaB-induced NHK differentiation, SPARC intracellular content increased prior to the onset of CE formation (i.e., 2 days after its addition) followed by a period of extracellular accumulation which coincided with the time of maximal CE generation (i.e., Days 4 and 5 after NaB addition).	nab	279-282	secreted protein acidic and cysteine rich	Homo sapiens	40-45
1639037-2	1992	Treatment of mammary carcinoma cells with the differentiating agent sodium butyrate (NaB) is known to reduce PRLR binding activity and PRLR gene expression, however the mechanism which mediates these changes is unknown, prompting this investigation.	nab	85-88	prolactin receptor	Homo sapiens	109-113
1639037-5	1992	These results indicate that NaB inhibits PRLR gene expression by a transcriptional mechanism that does not require continuing protein synthesis.	nab	28-31	prolactin receptor	Homo sapiens	41-45
8497896-8	1993	Eluates contained NAb of predominantly IgM and IgG2 isotypes.	nab	18-21	Ig kappa chain	Sus scrofa	39-42
8419178-12	1993	Sera of H-2b, H-2d and H-2k mice of different ages and microflora possess NAb against human erythrocytes of blood group type A and occasionally demonstrate weak titers against erythrocytes of blood groups B and O (H) and the Rhesus factor.	nab	74-77	histocompatibility 2, D region	Mus musculus	14-18
1639037-2	1992	Treatment of mammary carcinoma cells with the differentiating agent sodium butyrate (NaB) is known to reduce PRLR binding activity and PRLR gene expression, however the mechanism which mediates these changes is unknown, prompting this investigation.	nab	85-88	prolactin receptor	Homo sapiens	135-139
1639037-3	1992	Using MCF-7 human breast cancer cells, assay of the rate of PRLR gene transcription by the nuclear run-on technique indicated that 3 mM NaB reduced PRLR gene transcription by 50% after 3 h of treatment and that this effect was maintained for at least 24 h. The protein synthesis inhibitor cycloheximide failed to abrogate this effect, which indicated that NaB did not require continuing protein synthesis to reduce the rate of PRLR transcription.	nab	136-139	prolactin receptor	Homo sapiens	60-64
1639037-3	1992	Using MCF-7 human breast cancer cells, assay of the rate of PRLR gene transcription by the nuclear run-on technique indicated that 3 mM NaB reduced PRLR gene transcription by 50% after 3 h of treatment and that this effect was maintained for at least 24 h. The protein synthesis inhibitor cycloheximide failed to abrogate this effect, which indicated that NaB did not require continuing protein synthesis to reduce the rate of PRLR transcription.	nab	136-139	prolactin receptor	Homo sapiens	148-152
1639037-3	1992	Using MCF-7 human breast cancer cells, assay of the rate of PRLR gene transcription by the nuclear run-on technique indicated that 3 mM NaB reduced PRLR gene transcription by 50% after 3 h of treatment and that this effect was maintained for at least 24 h. The protein synthesis inhibitor cycloheximide failed to abrogate this effect, which indicated that NaB did not require continuing protein synthesis to reduce the rate of PRLR transcription.	nab	136-139	prolactin receptor	Homo sapiens	148-152
1555205-1	1992	The effects of sodium butyrate (NaB) on the response of the RCA human colon carcinoma cell line to transforming growth factor-beta 1 (TGF-beta 1) were examined.	nab	32-35	transforming growth factor beta 1	Homo sapiens	99-132
1341266-8	1992	NaB stimulated ODC activity in a dose-dependent manner.	nab	0-3	ornithine decarboxylase, structural 1	Mus musculus	15-18
1341266-10	1992	The increase in ODC activity led to an increase in polyamine biosynthesis; putrescine, spermidine, and spermine levels in MC-26 cells were significantly elevated by 24 h after treatment with NaB.	nab	191-194	ornithine decarboxylase, structural 1	Mus musculus	16-19
1584790-2	1992	Reaction of insulin (which contains no sulfhydryl groups) with HNE leads to the generation of HNE-protein adducts, which are converted to radioactive derivatives upon subsequent treatment with NaB[3H]H4.	nab	193-196	insulin	Homo sapiens	12-19
1555205-5	1992	Addition of TGF-beta 1 to cells grown in the presence of NaB resulted in a stimulation of growth.	nab	57-60	transforming growth factor beta 1	Homo sapiens	12-22
1555205-6	1992	Cells pretreated with TGF-beta 1 remained sensitive to the growth inhibitory and differentiation inducing effects of NaB.	nab	117-120	transforming growth factor beta 1	Homo sapiens	22-32
1555205-7	1992	These results suggest that NaB may alter the expression of proteins responsible for a stimulatory signal response to TGF-beta 1 in RCA cells.	nab	27-30	transforming growth factor beta 1	Homo sapiens	117-127
1652685-5	1991	Clonal analysis of this population demonstrated that the increased NAb binding was associated with tumorigenic conversion and ras-p21 expression.	nab	67-70	H3 histone pseudogene 16	Homo sapiens	130-133
1735612-7	1992	The results show that NAb binding and susceptibility to NK cells increased following ras oncogene expression in 10T 1/2 cells and that both parameters were regulated by p21 expression.	nab	22-25	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	169-172
1735612-10	1992	In contrast, small but statistically significant reductions in NAb binding were observed following v-H-ras transformation of NIH 3T3 cells or v-src transformation of 10T 1/2.	nab	63-66	Harvey rat sarcoma virus oncogene	Mus musculus	101-106
1727055-3	1992	NaB also induces TGF-beta mRNA in the maturing suprabasal compartment, suggesting that TGF-beta may play a role in NaB-initiated NHEK differentiation.	nab	0-3	transforming growth factor beta 1	Homo sapiens	17-25
1727055-3	1992	NaB also induces TGF-beta mRNA in the maturing suprabasal compartment, suggesting that TGF-beta may play a role in NaB-initiated NHEK differentiation.	nab	0-3	transforming growth factor beta 1	Homo sapiens	87-95
1727055-3	1992	NaB also induces TGF-beta mRNA in the maturing suprabasal compartment, suggesting that TGF-beta may play a role in NaB-initiated NHEK differentiation.	nab	115-118	transforming growth factor beta 1	Homo sapiens	87-95
1727055-5	1992	TGF-beta 1 was quite effective in inducing significant levels of CE expression when used simultaneously with suboptimal concentrations of NaB.	nab	138-141	transforming growth factor beta 1	Homo sapiens	0-10
1727055-6	1992	The cooperative action of suboptimal NaB and TGF-beta 1 generated numbers of CEs which, in fact, exceeded the incidence of mature CEs formed in response to optimal levels of NaB alone.	nab	174-177	transforming growth factor beta 1	Homo sapiens	45-55
1727055-7	1992	Neutralizing antibodies to TGF-beta, moreover, effectively reduced the incidence of CE formation in cultures treated with optimal NaB concentrations, further implicating endogenous TGF-beta activity in the NaB-initiated NHEK differentiation model.	nab	130-133	transforming growth factor beta 1	Homo sapiens	27-35
1727055-7	1992	Neutralizing antibodies to TGF-beta, moreover, effectively reduced the incidence of CE formation in cultures treated with optimal NaB concentrations, further implicating endogenous TGF-beta activity in the NaB-initiated NHEK differentiation model.	nab	206-209	transforming growth factor beta 1	Homo sapiens	27-35
1727055-7	1992	Neutralizing antibodies to TGF-beta, moreover, effectively reduced the incidence of CE formation in cultures treated with optimal NaB concentrations, further implicating endogenous TGF-beta activity in the NaB-initiated NHEK differentiation model.	nab	206-209	transforming growth factor beta 1	Homo sapiens	181-189
1727055-8	1992	It is suggested, therefore, that within the NaB-induced pathway of NHEK differentiation, TGF-beta can positively modulate expression of the differentiated phenotype but alone is insufficient for generation of mature CEs.	nab	44-47	transforming growth factor beta 1	Homo sapiens	89-97
1608202-1	1992	Coagulation in angina pectoris has been analyzed in a normal and elevated level of natural antibodies (nAb) to thrombin.	nab	103-106	coagulation factor II, thrombin	Homo sapiens	111-119
1608202-2	1992	A correlation was found between the level of nAb to thrombin and hemostatic shifts.	nab	45-48	coagulation factor II, thrombin	Homo sapiens	52-60
1608202-6	1992	It is concluded that nAb to thrombin levels have prognostic potential as an indicator of coagulation activity and efficacy of anticoagulant therapy in extracorporeal interventions.	nab	21-24	coagulation factor II, thrombin	Homo sapiens	28-36
1730582-3	1992	The pyridoxal 5"-phosphate binding lysine in mouse ODC was identified as lysine 69 of the mouse sequence by reduction of the purified holoenzyme form with NaB[3H]4 followed by digestion of the carboxymethylated protein with endoproteinase Lys-C, radioactive peptide mapping using reversed-phase high pressure liquid chromatography and gas-phase peptide sequencing.	nab	155-158	ornithine decarboxylase, structural 1	Mus musculus	51-54
1953684-1	1991	Flat revertants of v-ras-transformed (KNRK) rat kidney cells, which express elevated levels of p21ras protein, were generated to high efficiencies with sodium butyrate (NaB).	nab	169-172	HRas proto-oncogene, GTPase	Rattus norvegicus	95-101
1953684-8	1991	NaB-induced p52(PAI-1) synthesis and generation of early morphological reversion in KNRK cells required ongoing RNA synthesis, since exposure to actinomycin D before addition of NaB inhibited both events.	nab	0-3	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	12-15
1953684-8	1991	NaB-induced p52(PAI-1) synthesis and generation of early morphological reversion in KNRK cells required ongoing RNA synthesis, since exposure to actinomycin D before addition of NaB inhibited both events.	nab	0-3	serpin family E member 2	Rattus norvegicus	16-21
1953684-9	1991	p52(PAI-1) induction by NaB was regulated at the level of mRNA abundance; in contrast, actin mRNA levels were the same in parental and revertant cells, suggesting that the increased actin content which typified the revertant phenotype was due to augmented actin microfilament stability.	nab	24-27	similar to Mitochondrial processing peptidase beta subunit, mitochondrial precursor (Beta-MPP; P-52)	Rattus norvegicus	0-3
1953684-9	1991	p52(PAI-1) induction by NaB was regulated at the level of mRNA abundance; in contrast, actin mRNA levels were the same in parental and revertant cells, suggesting that the increased actin content which typified the revertant phenotype was due to augmented actin microfilament stability.	nab	24-27	serpin family E member 2	Rattus norvegicus	4-9
1656587-3	1991	Immunofluorescence staining, gel electrophoresis, and Northern blot analysis revealed that TPC-1 cells are nonpermissive for expression of HCMV major immediate early (IE1) functions, but many of the cells become permissive after being treated with NaB.	nab	248-251	two pore segment channel 1	Homo sapiens	91-96
2110861-4	1990	Following RA treatment, cell-surface sialic acid residues on gp160 were also more intensely labeled by NaIO4 oxidation and subsequent NaB[3H]4 reduction than were those on gp160 of untreated cells.	nab	134-137	leucyl/cystinyl aminopeptidase	Mus musculus	61-66
2257881-3	1990	NaB induced a four-fold increase in TGF-beta mRNA transcript levels.	nab	0-3	transforming growth factor beta 1	Homo sapiens	36-44
2257881-4	1990	This increase in TGF-beta mRNA abundance occurred only within the nonbasal keratinocyte subpopulation which maximally responds to NaB treatment by progression to cornified envelopes.	nab	130-133	transforming growth factor beta 1	Homo sapiens	17-25
1698477-2	1990	GM-CSF exerted a stronger proliferative stimulus than G-CSF for marrow myeloid clonal growth (CFU-GM) in these patients (44 v 12 colonies per 10(5) nonadherent buoyant bone marrow cells [NAB], respectively, P less than .025).	nab	187-190	colony stimulating factor 2	Homo sapiens	0-6
1698477-3	1990	GM-CSF stimulated increased CFU-GM growth in the 16 patients with abnormal marrow cytogenetics in comparison with the 20 patients who had normal cytogenetics (52 and 30 colonies per 10(5) NAB, respectively, P less than .05), whereas no such difference could be demonstrated with G-CSF (11 and 16 colonies per 10(5) NAB, respectively).	nab	188-191	colony stimulating factor 2	Homo sapiens	0-6
1698477-3	1990	GM-CSF stimulated increased CFU-GM growth in the 16 patients with abnormal marrow cytogenetics in comparison with the 20 patients who had normal cytogenetics (52 and 30 colonies per 10(5) NAB, respectively, P less than .05), whereas no such difference could be demonstrated with G-CSF (11 and 16 colonies per 10(5) NAB, respectively).	nab	315-318	colony stimulating factor 2	Homo sapiens	0-6
34635391-9	2022	Additionally, in the absence of vaccination, HLA associations were observed between the presence of DPB1*03:01 and increased NAb log GMT levels (beta: 1.24; p = 0.005, q = 0.17), and between DPB1*05:01 and reduced NAb log GMT levels (beta: -1.1; p = 0.001, q = 0.07).	nab	125-128	major histocompatibility complex, class II, DR beta 1	Homo sapiens	45-48
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	interleukin 1 alpha	Rattus norvegicus	117-125
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	interleukin 6	Rattus norvegicus	127-131
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	transforming growth factor alpha	Rattus norvegicus	137-145
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	tight junction protein 1	Rattus norvegicus	222-226
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	claudin 5	Rattus norvegicus	228-237
34470077-4	2022	We found that NaB significantly decreased the levels of blood pressure, 24-h protein urine and inflammatory factors (IL-1beta, IL-6, and TGF-beta), increased the fetal and placental weights and intestinal barrier markers (ZO-1, claudin-5, and occludin) expression.	nab	14-17	occludin	Rattus norvegicus	243-251
34470077-5	2022	In addition, NaB intervention reduced the levels of soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) and increased placental growth factor (PlGF) level.	nab	13-16	Fms related receptor tyrosine kinase 1	Rattus norvegicus	60-86
34470077-5	2022	In addition, NaB intervention reduced the levels of soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) and increased placental growth factor (PlGF) level.	nab	13-16	endoglin	Rattus norvegicus	107-115
34470077-5	2022	In addition, NaB intervention reduced the levels of soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) and increased placental growth factor (PlGF) level.	nab	13-16	placental growth factor	Rattus norvegicus	137-160
34470077-5	2022	In addition, NaB intervention reduced the levels of soluble fms-like tyrosine kinase 1 (sFlt1) and soluble endoglin (sEng) and increased placental growth factor (PlGF) level.	nab	13-16	placental growth factor	Rattus norvegicus	162-166
34635391-9	2022	Additionally, in the absence of vaccination, HLA associations were observed between the presence of DPB1*03:01 and increased NAb log GMT levels (beta: 1.24; p = 0.005, q = 0.17), and between DPB1*05:01 and reduced NAb log GMT levels (beta: -1.1; p = 0.001, q = 0.07).	nab	214-217	major histocompatibility complex, class II, DR beta 1	Homo sapiens	45-48
34896331-9	2022	NaB activated autophagy pathway and reduced rotenone-induced alpha-synuclein expression through the activation of autophagy.	nab	0-3	synuclein alpha	Rattus norvegicus	61-76
34896331-10	2022	Notably, NaB activated autophagy pathway through upregulating PGC-1alpha expression.	nab	9-12	PPARG coactivator 1 alpha	Rattus norvegicus	62-72
34896331-11	2022	More importantly, NaB promoted the levels of histone 3 lysine 9 acetylation (H3K9Ac) and histone 3 lysine 27 acetylation (H3K27Ac) at PGC-1alpha promoter region, indicating that NaB promotes PGC-1alpha expression via histone acetylation modification.	nab	18-21	PPARG coactivator 1 alpha	Rattus norvegicus	134-144
34896331-11	2022	More importantly, NaB promoted the levels of histone 3 lysine 9 acetylation (H3K9Ac) and histone 3 lysine 27 acetylation (H3K27Ac) at PGC-1alpha promoter region, indicating that NaB promotes PGC-1alpha expression via histone acetylation modification.	nab	18-21	PPARG coactivator 1 alpha	Rattus norvegicus	191-201
34896331-11	2022	More importantly, NaB promoted the levels of histone 3 lysine 9 acetylation (H3K9Ac) and histone 3 lysine 27 acetylation (H3K27Ac) at PGC-1alpha promoter region, indicating that NaB promotes PGC-1alpha expression via histone acetylation modification.	nab	178-181	PPARG coactivator 1 alpha	Rattus norvegicus	134-144
34896331-11	2022	More importantly, NaB promoted the levels of histone 3 lysine 9 acetylation (H3K9Ac) and histone 3 lysine 27 acetylation (H3K27Ac) at PGC-1alpha promoter region, indicating that NaB promotes PGC-1alpha expression via histone acetylation modification.	nab	178-181	PPARG coactivator 1 alpha	Rattus norvegicus	191-201
34896331-12	2022	In conclusion, NaB can protect against rotenone-induced toxicity through activation of the autophagy pathway by upregulating PGC-1alpha expression via epigenetic modification.	nab	15-18	PPARG coactivator 1 alpha	Rattus norvegicus	125-135
34890760-5	2022	We found that NaB restored bodyweight and attenuated P-53, Bcl-2-associated X protein (BAX), and caspase cascades in the brains of HFD-fed mice.	nab	14-17	transformation related protein 53, pseudogene	Mus musculus	53-57
34890760-5	2022	We found that NaB restored bodyweight and attenuated P-53, Bcl-2-associated X protein (BAX), and caspase cascades in the brains of HFD-fed mice.	nab	14-17	BCL2-associated X protein	Mus musculus	59-85
34890760-5	2022	We found that NaB restored bodyweight and attenuated P-53, Bcl-2-associated X protein (BAX), and caspase cascades in the brains of HFD-fed mice.	nab	14-17	BCL2-associated X protein	Mus musculus	87-90
34890760-8	2022	NaB treatment upregulated the expression of the growth factor-related factors PPARgamma, CREB, and BDNF in the brain tissues of HFD-fed mice.	nab	0-3	peroxisome proliferator activated receptor gamma	Mus musculus	78-87
34890760-8	2022	NaB treatment upregulated the expression of the growth factor-related factors PPARgamma, CREB, and BDNF in the brain tissues of HFD-fed mice.	nab	0-3	cAMP responsive element binding protein 1	Mus musculus	89-93
34890760-8	2022	NaB treatment upregulated the expression of the growth factor-related factors PPARgamma, CREB, and BDNF in the brain tissues of HFD-fed mice.	nab	0-3	brain derived neurotrophic factor	Mus musculus	99-103
34890760-9	2022	Furthermore, we found that NaB significantly ameliorated glucocorticoid receptor and NLRP3 inflammasome expression.	nab	27-30	nuclear receptor subfamily 3, group C, member 1	Mus musculus	57-80
34890760-9	2022	Furthermore, we found that NaB significantly ameliorated glucocorticoid receptor and NLRP3 inflammasome expression.	nab	27-30	NLR family, pyrin domain containing 3	Mus musculus	85-90
34946164-5	2021	Interestingly cellular transcription factors (TFs), activators for EBV lytic reactivation, such as MEF2D and SP1, were significantly abolished in AGS-EBV cells treated with andrographolide and sodium butyrate (NaB) compared with NaB-treated cells.	nab	210-213	myocyte enhancer factor 2D	Homo sapiens	99-104
34974029-0	2022	SPARC-mediated long-term retention of nab-paclitaxel in pediatric sarcomas.	nab	38-41	secreted protein acidic and cysteine rich	Homo sapiens	0-5
34974029-5	2022	Then, we used SPARC-edited Ewing sarcoma cells (A673 line) to demonstrate that SPARC knocked down (KD) cells accumulated significantly less amount of nab-paclitaxel in vitro than SPARC wild type (WT) cells.	nab	150-153	secreted protein acidic and cysteine rich	Homo sapiens	79-84
34974029-6	2022	In vivo, SPARC KD and SPARC WT subcutaneous xenografts in mice achieved similar maximum intratumoral concentrations of nab-paclitaxel, though drug clearance from SPARC WT tumors was significantly slower.	nab	119-122	secreted acidic cysteine rich glycoprotein	Mus musculus	9-14
34974029-7	2022	We confirmed such SPARC-mediated long-term intratumoral accumulation of nab-paclitaxel in Ewing sarcoma PDX with high expression of SPARC, which accumulated significantly more nab-paclitaxel than SPARC-low PDX.	nab	72-75	secreted acidic cysteine rich glycoprotein	Mus musculus	18-23
34974029-7	2022	We confirmed such SPARC-mediated long-term intratumoral accumulation of nab-paclitaxel in Ewing sarcoma PDX with high expression of SPARC, which accumulated significantly more nab-paclitaxel than SPARC-low PDX.	nab	176-179	secreted acidic cysteine rich glycoprotein	Mus musculus	18-23
34974029-7	2022	We confirmed such SPARC-mediated long-term intratumoral accumulation of nab-paclitaxel in Ewing sarcoma PDX with high expression of SPARC, which accumulated significantly more nab-paclitaxel than SPARC-low PDX.	nab	176-179	secreted acidic cysteine rich glycoprotein	Mus musculus	132-137
34974029-8	2022	SPARC-high PDX responded better to nab-paclitaxel than SPARC-low tumors, although these results should be taken cautiously, given that the PDXs were established from different patients that could have specific determinants predisposing response to paclitaxel.	nab	35-38	secreted protein acidic and cysteine rich	Homo sapiens	0-5
34974029-9	2022	In addition, SPARC KD Ewing sarcoma xenografts responded better to soluble docetaxel and paclitaxel than to nab-paclitaxel, while SPARC WT ones showed similar response to soluble and albumin-carried drugs.	nab	108-111	secreted protein acidic and cysteine rich	Homo sapiens	13-18
34974029-10	2022	Overall, our results show that pediatric sarcomas expressing SPARC accumulate nab-paclitaxel for longer periods of time, which could have clinical implications for chemotherapy efficacy.	nab	78-81	secreted protein acidic and cysteine rich	Homo sapiens	61-66
34946164-6	2021	In contrast, the suppressors of EBV lytic reactivation, such as EZH2 and HDAC6, were significantly up-regulated in cells treated with both andrographolide and NaB compared with NaB treatment alone.	nab	159-162	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	64-68
34946164-6	2021	In contrast, the suppressors of EBV lytic reactivation, such as EZH2 and HDAC6, were significantly up-regulated in cells treated with both andrographolide and NaB compared with NaB treatment alone.	nab	159-162	histone deacetylase 6	Homo sapiens	73-78
34946164-6	2021	In contrast, the suppressors of EBV lytic reactivation, such as EZH2 and HDAC6, were significantly up-regulated in cells treated with both andrographolide and NaB compared with NaB treatment alone.	nab	177-180	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	64-68
34946164-6	2021	In contrast, the suppressors of EBV lytic reactivation, such as EZH2 and HDAC6, were significantly up-regulated in cells treated with both andrographolide and NaB compared with NaB treatment alone.	nab	177-180	histone deacetylase 6	Homo sapiens	73-78
34882068-11	2021	These results demonstrate that the FGFR/VEGFR/PDGFR inhibitor, dovitinib, has the potential to augment the antitumor effects of nab-paclitaxel, with implications for use in the advancement of clinical GAC therapy.	nab	128-131	kinase insert domain receptor	Homo sapiens	40-45
34882068-0	2021	Targeted FGFR/VEGFR/PDGFR inhibition with dovitinib enhances the effects of nab-paclitaxel in preclinical gastric cancer models.	nab	76-79	kinase insert domain receptor	Homo sapiens	14-19
34403723-6	2021	In this study, we found that hSVCT1 expression and function were significantly decreased in intestinal epithelial cells by the histone deacetylase inhibitors (HDACi), valproic acid (VPA) and sodium butyrate (NaB).	nab	208-211	solute carrier family 23 member 1	Homo sapiens	29-35
34637337-2	2021	To our knowledge, this phase II, single-arm, registration trial is the first prospective clinical trial in this disease, investigating the safety and efficacy of the mammalian target of rapamycin inhibitor nab-sirolimus (AMPECT, NCT02494570).	nab	206-209	mechanistic target of rapamycin kinase	Homo sapiens	166-195
34903409-9	2021	The combination of NaB and PROB exerted protective effects against severe burn-induced intestinal barrier injury by reducing the levels of diamine oxidase and intestinal fatty acid binding protein.	nab	19-22	amine oxidase, copper containing 1	Rattus norvegicus	139-154
34903409-9	2021	The combination of NaB and PROB exerted protective effects against severe burn-induced intestinal barrier injury by reducing the levels of diamine oxidase and intestinal fatty acid binding protein.	nab	19-22	fatty acid binding protein 2	Rattus norvegicus	159-196
34903409-10	2021	Combined NaB and PROB treatment inhibited severe burn-induced oxidative stress by increasing superoxide dismutase levels and decreasing those of malondialdehyde and myeloperoxidase levels.	nab	9-12	myeloperoxidase	Rattus norvegicus	165-180
34903409-11	2021	Severe burn-induced inflammation was suppressed by combined NaB and PROB administration, as demonstrated by the decreased mRNA expression of tumor necrosis factor-alpha, interleukin-6, interleukin-1beta, and high mobility group box-1 in the small intestine.	nab	60-63	tumor necrosis factor	Rattus norvegicus	141-168
34903409-11	2021	Severe burn-induced inflammation was suppressed by combined NaB and PROB administration, as demonstrated by the decreased mRNA expression of tumor necrosis factor-alpha, interleukin-6, interleukin-1beta, and high mobility group box-1 in the small intestine.	nab	60-63	interleukin 6	Rattus norvegicus	170-183
34903409-11	2021	Severe burn-induced inflammation was suppressed by combined NaB and PROB administration, as demonstrated by the decreased mRNA expression of tumor necrosis factor-alpha, interleukin-6, interleukin-1beta, and high mobility group box-1 in the small intestine.	nab	60-63	interleukin 1 beta	Rattus norvegicus	185-202
34903409-11	2021	Severe burn-induced inflammation was suppressed by combined NaB and PROB administration, as demonstrated by the decreased mRNA expression of tumor necrosis factor-alpha, interleukin-6, interleukin-1beta, and high mobility group box-1 in the small intestine.	nab	60-63	high mobility group box 1	Rattus norvegicus	208-233
34903409-12	2021	In addition, this study showed that combined NaB and PROB administration increased nuclear factor-erythroid 2-related factor 2 (Nrf2) protein expression and decreased the phosphorylation of nuclear factor (NF)-kappaB and extracellular signal-regulated kinase 1/2 (ERK 1/2).	nab	45-48	NFE2 like bZIP transcription factor 2	Rattus norvegicus	83-126
34903409-12	2021	In addition, this study showed that combined NaB and PROB administration increased nuclear factor-erythroid 2-related factor 2 (Nrf2) protein expression and decreased the phosphorylation of nuclear factor (NF)-kappaB and extracellular signal-regulated kinase 1/2 (ERK 1/2).	nab	45-48	NFE2 like bZIP transcription factor 2	Rattus norvegicus	128-132
34903409-12	2021	In addition, this study showed that combined NaB and PROB administration increased nuclear factor-erythroid 2-related factor 2 (Nrf2) protein expression and decreased the phosphorylation of nuclear factor (NF)-kappaB and extracellular signal-regulated kinase 1/2 (ERK 1/2).	nab	45-48	mitogen activated protein kinase 3	Rattus norvegicus	221-262
34903409-12	2021	In addition, this study showed that combined NaB and PROB administration increased nuclear factor-erythroid 2-related factor 2 (Nrf2) protein expression and decreased the phosphorylation of nuclear factor (NF)-kappaB and extracellular signal-regulated kinase 1/2 (ERK 1/2).	nab	45-48	mitogen activated protein kinase 3	Rattus norvegicus	264-271
34903409-13	2021	In conclusion, our findings indicate that combined NaB and PROB treatment may inhibit severe burn-induced inflammation and oxidative stress in the small intestine by regulating HMGB1/NF-kappaB and ERK1/2/Nrf2 signaling, thereby providing a new therapeutic strategy for intestinal injury induced by severe burn.	nab	51-54	high mobility group box 1	Rattus norvegicus	177-182
34903409-13	2021	In conclusion, our findings indicate that combined NaB and PROB treatment may inhibit severe burn-induced inflammation and oxidative stress in the small intestine by regulating HMGB1/NF-kappaB and ERK1/2/Nrf2 signaling, thereby providing a new therapeutic strategy for intestinal injury induced by severe burn.	nab	51-54	mitogen activated protein kinase 3	Rattus norvegicus	197-203
34903409-13	2021	In conclusion, our findings indicate that combined NaB and PROB treatment may inhibit severe burn-induced inflammation and oxidative stress in the small intestine by regulating HMGB1/NF-kappaB and ERK1/2/Nrf2 signaling, thereby providing a new therapeutic strategy for intestinal injury induced by severe burn.	nab	51-54	NFE2 like bZIP transcription factor 2	Rattus norvegicus	204-208
34502057-6	2021	Supplementation of sodium butyrate (NaB) inhibited the activations of IRE1alpha/XBP1 and PERK/eIF2alpha pathways caused by cereulide exposure in mice, and reduced the cell apoptosis in liver and kidney.	nab	36-39	X-box binding protein 1	Mus musculus	80-84
34638252-0	2021	Pharmacological Inhibition of PP2A Overcomes Nab-Paclitaxel Resistance by Downregulating MCL1 in Esophageal Squamous Cell Carcinoma (ESCC).	nab	45-48	protein phosphatase 2 phosphatase activator	Homo sapiens	30-34
34638252-5	2021	Additionally, we discovered the elevated activity of protein phosphatase 2A (PP2A), the phosphatase that dephosphorylates and stabilizes MCL1, in nab-PTX resistant cell lines.	nab	146-149	protein phosphatase 2 phosphatase activator	Homo sapiens	61-75
34638252-5	2021	Additionally, we discovered the elevated activity of protein phosphatase 2A (PP2A), the phosphatase that dephosphorylates and stabilizes MCL1, in nab-PTX resistant cell lines.	nab	146-149	protein phosphatase 2 phosphatase activator	Homo sapiens	77-81
34638252-6	2021	Pharmacological inhibition of PP2A with small molecule compound LB-100 decreased MCL1 protein level, caused more apoptosis in nab-PTX resistant ESCC cell lines than in the parental cells in vitro, and significantly inhibited the tumor growth of nab-PTX resistant xenografts in vivo.	nab	126-129	protein phosphatase 2 phosphatase activator	Homo sapiens	30-34
34638252-6	2021	Pharmacological inhibition of PP2A with small molecule compound LB-100 decreased MCL1 protein level, caused more apoptosis in nab-PTX resistant ESCC cell lines than in the parental cells in vitro, and significantly inhibited the tumor growth of nab-PTX resistant xenografts in vivo.	nab	245-248	protein phosphatase 2 phosphatase activator	Homo sapiens	30-34
34638252-8	2021	In summary, our study identifies a novel mechanism whereby elevated PP2A activity stabilizes MCL1 protein, increases OXPHOS, and confers nab-PTX resistance, suggesting that targeting PP2A is a potential strategy for reversing nab-PTX resistance in patients with advanced ESCC.	nab	137-140	protein phosphatase 2 phosphatase activator	Homo sapiens	68-72
34638252-8	2021	In summary, our study identifies a novel mechanism whereby elevated PP2A activity stabilizes MCL1 protein, increases OXPHOS, and confers nab-PTX resistance, suggesting that targeting PP2A is a potential strategy for reversing nab-PTX resistance in patients with advanced ESCC.	nab	226-229	protein phosphatase 2 phosphatase activator	Homo sapiens	68-72
34101131-9	2021	NaB significantly decreased the CVS-induced anxiety level by elevating acetyl-H3K9 and BDNF expression.	nab	0-3	brain derived neurotrophic factor	Mus musculus	87-91
34106394-9	2021	NaB notably ameliorated apoptotic regulatory proteins p-53, Caspase-3 and caspase-1 level, and reversed phosphorylation of extracellular signal-regulated kinases and p-38 proteins.	nab	0-3	caspase 3	Homo sapiens	60-69
34106394-9	2021	NaB notably ameliorated apoptotic regulatory proteins p-53, Caspase-3 and caspase-1 level, and reversed phosphorylation of extracellular signal-regulated kinases and p-38 proteins.	nab	0-3	caspase 1	Homo sapiens	74-83
34106394-10	2021	NaB ameliorated Glucocorticoid receptor and NLRP3 inflammasome expressions.	nab	0-3	nuclear receptor subfamily 3 group C member 1	Homo sapiens	16-39
34106394-10	2021	NaB ameliorated Glucocorticoid receptor and NLRP3 inflammasome expressions.	nab	0-3	NLR family pyrin domain containing 3	Homo sapiens	44-49
34106394-11	2021	NaB also suppressed the BAX nuclear translocation and modulated Nrf-2, HO-1 and MnSOD expression in neuroblastoma cells.	nab	0-3	BCL2 associated X, apoptosis regulator	Homo sapiens	24-27
34106394-11	2021	NaB also suppressed the BAX nuclear translocation and modulated Nrf-2, HO-1 and MnSOD expression in neuroblastoma cells.	nab	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	64-69
34106394-11	2021	NaB also suppressed the BAX nuclear translocation and modulated Nrf-2, HO-1 and MnSOD expression in neuroblastoma cells.	nab	0-3	heme oxygenase 1	Homo sapiens	71-75
34106394-11	2021	NaB also suppressed the BAX nuclear translocation and modulated Nrf-2, HO-1 and MnSOD expression in neuroblastoma cells.	nab	0-3	superoxide dismutase 2	Homo sapiens	80-85
34502057-6	2021	Supplementation of sodium butyrate (NaB) inhibited the activations of IRE1alpha/XBP1 and PERK/eIF2alpha pathways caused by cereulide exposure in mice, and reduced the cell apoptosis in liver and kidney.	nab	36-39	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	70-79
34076963-9	2021	NAB samples were classified as high for K17 when >=80% of tumor cells showed strong (2+) staining.	nab	0-3	keratin 17	Homo sapiens	40-43
34076963-11	2021	CONCLUSIONS: K17 has been identified as a robust and independent prognostic biomarker that stratifies clinical outcomes for cases that are diagnosed by NAB.	nab	152-155	keratin 17	Homo sapiens	13-16
34453881-2	2021	Here, we applied live bioluminescence imaging (BLI) to monitor the real-time effects of NAb treatment during prophylaxis and therapy of K18-hACE2 mice intranasally infected with SARS-CoV-2-nanoluciferase.	nab	88-91	angiotensin converting enzyme 2	Homo sapiens	140-145
34590611-2	2021	Furthermore, Cav-1 is critical for the uptake of albumin as well as nab-paclitaxel in PDAC cells.	nab	68-71	caveolin 1	Homo sapiens	13-18
34502057-6	2021	Supplementation of sodium butyrate (NaB) inhibited the activations of IRE1alpha/XBP1 and PERK/eIF2alpha pathways caused by cereulide exposure in mice, and reduced the cell apoptosis in liver and kidney.	nab	36-39	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	89-93
34502057-6	2021	Supplementation of sodium butyrate (NaB) inhibited the activations of IRE1alpha/XBP1 and PERK/eIF2alpha pathways caused by cereulide exposure in mice, and reduced the cell apoptosis in liver and kidney.	nab	36-39	eukaryotic translation initiation factor 2A	Mus musculus	94-103
34452170-2	2021	Nanoparticle albumin-bound (nab)-technology, such as nab-paclitaxel (Abraxane ), has attracted significant interest in drug delivery research.	nab	53-56	albumin	Homo sapiens	13-20
34113786-7	2021	Results: NaB increased the mRNA and protein expression of TH to produce DA in mouse MN9D dopaminergic neuronal cells.	nab	9-12	tyrosine hydroxylase	Mus musculus	58-60
34359638-0	2021	Gemcitabine Plus Nab-Paclitaxel Induces PD-L1 mRNA Expression in Plasma-Derived Microvesicles in Pancreatic Cancer.	nab	17-20	CD274 molecule	Homo sapiens	40-45
34066839-0	2021	Heme Oxygenase-1 Inhibition Potentiates the Effects of Nab-Paclitaxel-Gemcitabine and Modulates the Tumor Microenvironment in Pancreatic Ductal Adenocarcinoma.	nab	55-58	heme oxygenase 1	Mus musculus	0-16
34066839-3	2021	We present evidence that nab-paclitaxel-gemcitabine (NPG) and/or a hypoxic tumor microenvironment (TME) up-regulate heme oxygenase-1 (HO-1), providing a survival advantage for tumors.	nab	25-28	heme oxygenase 1	Mus musculus	116-132
34066839-3	2021	We present evidence that nab-paclitaxel-gemcitabine (NPG) and/or a hypoxic tumor microenvironment (TME) up-regulate heme oxygenase-1 (HO-1), providing a survival advantage for tumors.	nab	25-28	heme oxygenase 1	Mus musculus	134-138
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	70-73	cAMP responsive element binding protein 1	Homo sapiens	19-48
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	70-73	cAMP responsive element binding protein 1	Homo sapiens	50-54
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	70-73	cAMP responsive element binding protein 1	Homo sapiens	263-267
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	196-199	cAMP responsive element binding protein 1	Homo sapiens	19-48
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	196-199	cAMP responsive element binding protein 1	Homo sapiens	50-54
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	196-199	cAMP responsive element binding protein 1	Homo sapiens	178-182
34113786-9	2021	Rapid induction of cAMP response element binding (CREB) activation by NaB in dopaminergic neuronal cells and the abrogation of NaB-induced expression of TH by siRNA knockdown of CREB suggest that NaB stimulates the transcription of TH in dopaminergic neurons via CREB.	nab	196-199	cAMP responsive element binding protein 1	Homo sapiens	263-267
35619841-5	2022	We report a case of a 74-year-old male with stage four (IV) BSCC of the lung who experienced a complete metabolic with partial anatomic response to combined chemotherapy and immunotherapy with carboplatin/nab-paclitaxel/pembrolizumab and has continued to be in partial remission on maintenance immunotherapy with pembrolizumab despite PD-L1-negative status.	nab	205-208	CD274 molecule	Homo sapiens	335-340
34118789-0	2021	A Phase II study of nab-Paclitaxel (nab-P) in patients with advanced non-small cell lung cancer with EGFR mutations after frontline tyrosine kinase inhibitor therapy.	nab	20-23	epidermal growth factor receptor	Homo sapiens	101-105
35263013-8	2022	In conclusion, our study showed that HLA class II genotype is associated with the risk of developing ADA, and specifically NAb, in patients treated with atezolizumab, but the effect estimates suggest that immunogenetic factors are not sufficient as clinically meaningful predictors.	nab	123-126	major histocompatibility complex, class II, DR beta 1	Homo sapiens	37-40
35634239-8	2022	And HOXB9 expression regulated the resistance to chemotherapy (Gemcitabine and nab-Paclitaxel) and stem cell population.	nab	79-82	homeobox B9	Homo sapiens	4-9
35365420-7	2022	Of 100 patients who received neoadjuvant chemotherapy (NAC), high ADAM12 expression was significantly associated with poor DFS in a subset of patients treated with the nab-paclitaxel (PTX) neoadjuvant regimen (P = 0.03), whereas the prognostic value of ADAM12 was not evident in patients not treated with nab-PTX (P = 0.12).	nab	168-171	ADAM metallopeptidase domain 12	Homo sapiens	66-72
35365420-7	2022	Of 100 patients who received neoadjuvant chemotherapy (NAC), high ADAM12 expression was significantly associated with poor DFS in a subset of patients treated with the nab-paclitaxel (PTX) neoadjuvant regimen (P = 0.03), whereas the prognostic value of ADAM12 was not evident in patients not treated with nab-PTX (P = 0.12).	nab	168-171	ADAM metallopeptidase domain 12	Homo sapiens	253-259
35263013-6	2022	The top-associated alleles were HLA-DRB1*01:01 in a comparison of ADA-positive versus ADA-negative patients (p=3.4*10-5 , odds ratio=1.96, 95% confidence interval=1.64-2.28), and HLA-DQA1*01:01 when comparing NAb-positive with ADA-negative patients (p=2.8 x 10-7 , OR=2.31, 95% CI=1.98-2.66).	nab	209-212	major histocompatibility complex, class II, DR beta 1	Homo sapiens	32-40
35617963-5	2022	The tetravalent nAb binds to the spike protein trimer at least 100-fold more tightly than bivalent IgGs (apparent KD < 1 pM) and neutralizes a broad array of SARS-CoV-2 pseudoviruses, chimeric viruses, and authentic viral variants with high potency.	nab	16-19	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	33-38
35365420-7	2022	Of 100 patients who received neoadjuvant chemotherapy (NAC), high ADAM12 expression was significantly associated with poor DFS in a subset of patients treated with the nab-paclitaxel (PTX) neoadjuvant regimen (P = 0.03), whereas the prognostic value of ADAM12 was not evident in patients not treated with nab-PTX (P = 0.12).	nab	305-308	ADAM metallopeptidase domain 12	Homo sapiens	66-72
35365420-8	2022	CONCLUSIONS: A negative prognostic value of high ADAM12 expression was observed in patients with PDAC treated with surgical resection, which was enhanced in patients treated with NAC, including nab-PTX.	nab	194-197	ADAM metallopeptidase domain 12	Homo sapiens	49-55
35365420-9	2022	These results suggested that ADAM12 expression can predict nab-PTX chemosensitivity in PDAC and reflect PDAC progression.	nab	59-62	ADAM metallopeptidase domain 12	Homo sapiens	29-35
35508100-3	2022	This study aimed to determine the frequency of transient and fluctuating NAb positivity in a real-world clinical routine setting using a large retrospective international cohort of IFNbeta-treated MS patients collected as a part of the ABIRISK consortium (n = 9657).	nab	73-76	IFN1@	Homo sapiens	181-188
35051615-3	2022	Herein, we showed that the immunotherapeutic HCW9218, comprising TGF-beta receptor II and IL-15/IL-15 receptor alpha domains, enhanced metabolic and cytotoxic activities of immune cells and reduced TIS tumor cells in vivo to improve the efficacy of docetaxel and gemcitabine plus nab-paclitaxel against B16F10 melanoma and SW1990 pancreatic tumors, respectively.	nab	280-283	interleukin 15	Mus musculus	90-95
35429118-4	2022	NaB inhibited NRF2/NRF2-target genes and blocked NRF2-ARE signaling.	nab	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
35429118-4	2022	NaB inhibited NRF2/NRF2-target genes and blocked NRF2-ARE signaling.	nab	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	19-23
35429118-4	2022	NaB inhibited NRF2/NRF2-target genes and blocked NRF2-ARE signaling.	nab	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	49-53
35429118-5	2022	NaB increased NRF2 negative regulator KEAP1 expression through inhibiting its promoter methylation.	nab	0-3	NFE2 like bZIP transcription factor 2	Homo sapiens	14-18
35429118-5	2022	NaB increased NRF2 negative regulator KEAP1 expression through inhibiting its promoter methylation.	nab	0-3	kelch like ECH associated protein 1	Homo sapiens	38-43
35386224-11	2022	In addition, NaB prevented the increase in intracellular reactive oxygen species (ROS) generation and inducible nitric-oxide synthase expression in LPS-stimulated primary microglia.	nab	13-16	nitric oxide synthase 2, inducible	Mus musculus	102-133
35372004-13	2022	These results suggest that low-dose nab-paclitaxel plus tislelizumab is well tolerated and effective in elderly patients with advanced NSCLC, including those with EGFR/ALK variations.	nab	36-39	ALK receptor tyrosine kinase	Homo sapiens	168-171
35322444-4	2022	In addition, elevated levels of indicators of kidney damage creatinine and blood urine nitrogen, inflammatory mediators TNF-alpha, and IL-6 dropped after NaB administration.	nab	154-157	tumor necrosis factor	Rattus norvegicus	120-129
35322444-4	2022	In addition, elevated levels of indicators of kidney damage creatinine and blood urine nitrogen, inflammatory mediators TNF-alpha, and IL-6 dropped after NaB administration.	nab	154-157	interleukin 6	Rattus norvegicus	135-139
35322444-5	2022	Rat beta-defensin 2 (rBD2), as estimated by mRNA level, was significantly higher in LPS-treated kidneys, whereas the changes of rBD2 reduced in NaB-treated kidneys.	nab	144-147	defensin beta 4	Rattus norvegicus	4-19
35322444-5	2022	Rat beta-defensin 2 (rBD2), as estimated by mRNA level, was significantly higher in LPS-treated kidneys, whereas the changes of rBD2 reduced in NaB-treated kidneys.	nab	144-147	defensin beta 4	Rattus norvegicus	128-132
35322444-7	2022	Mechanistically, the present study indicates that NaB has nephroprotective activity resulting from modulation of TLR2/4 to regulate rBD2 expression hence curbing inflammation.	nab	50-53	toll-like receptor 2	Rattus norvegicus	113-119
35322444-7	2022	Mechanistically, the present study indicates that NaB has nephroprotective activity resulting from modulation of TLR2/4 to regulate rBD2 expression hence curbing inflammation.	nab	50-53	defensin beta 4	Rattus norvegicus	132-136
35313798-18	2022	CONCLUSIONS: The effect of a polymorphism in the TLR1A gene on IgTotal and IgM NAb was confirmed.	nab	79-82	toll-like receptor 1 family member A	Gallus gallus	49-54
35172762-13	2022	The addition of chemotherapy was associated with reduced number of myeloid and lymphoid cell types, except for CD4 + cells whose levels were largely unaltered only in tumors treated with gemcitabine/nab-paclitaxel.	nab	199-202	CD4 antigen	Mus musculus	111-114
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	59-62	tumor protein p53	Homo sapiens	22-25
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	59-62	caspase 3	Homo sapiens	30-39
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	108-111	tumor protein p53	Homo sapiens	22-25
35007916-16	2022	The protein levels of P53 and Caspase 3 increased with BA, NaB and SPT treatment for 72 h. CONCLUSIONS: BA, NaB and SPT show anti-cancer activity in the DMS-114 cell line without damaging MRC-5 cells, and some of the molecular mechanisms are involved in apoptosis and cell cycle arrest.	nab	108-111	caspase 3	Homo sapiens	30-39
35223210-10	2022	Further mechanistic investigation demonstrated that NaB induced EMT by increasing the expression of Vimentin and SNAI1, decreasing the expression of membrane-bound E-cadherin, and correspondingly promoting E-cadherin translocation from the membrane to the cytoplasm.	nab	52-55	vimentin	Homo sapiens	100-108
35223210-10	2022	Further mechanistic investigation demonstrated that NaB induced EMT by increasing the expression of Vimentin and SNAI1, decreasing the expression of membrane-bound E-cadherin, and correspondingly promoting E-cadherin translocation from the membrane to the cytoplasm.	nab	52-55	snail family transcriptional repressor 1	Homo sapiens	113-118
35223210-10	2022	Further mechanistic investigation demonstrated that NaB induced EMT by increasing the expression of Vimentin and SNAI1, decreasing the expression of membrane-bound E-cadherin, and correspondingly promoting E-cadherin translocation from the membrane to the cytoplasm.	nab	52-55	cadherin 1	Homo sapiens	164-174
35223210-10	2022	Further mechanistic investigation demonstrated that NaB induced EMT by increasing the expression of Vimentin and SNAI1, decreasing the expression of membrane-bound E-cadherin, and correspondingly promoting E-cadherin translocation from the membrane to the cytoplasm.	nab	52-55	cadherin 1	Homo sapiens	206-216
35223210-11	2022	In addition, the overexpression of MMP1/2/9/13 was closely related to NaB treatment.	nab	70-73	matrix metallopeptidase 1	Homo sapiens	35-46
35087749-1	2021	Background: Nanoparticle albumin-bound paclitaxel (nab-paclitaxel) as neoadjuvant chemotherapy (NAC) for breast cancer remains controversial.	nab	51-54	albumin	Homo sapiens	25-32
35499412-12	2022	In November 2021, the FDA approved nab-sirolimus (mTOR inhibitor) for PEComas.	nab	35-38	mechanistic target of rapamycin kinase	Homo sapiens	50-54
35044411-5	2022	NaB supplementation decreased the mRNA levels of toll-like receptor (TLR)-4, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and the trend was most pronounced in the jejunum.	nab	0-3	toll-like receptor 4	Rattus norvegicus	49-75
35044411-5	2022	NaB supplementation decreased the mRNA levels of toll-like receptor (TLR)-4, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and the trend was most pronounced in the jejunum.	nab	0-3	tumor necrosis factor	Rattus norvegicus	77-104
35044411-5	2022	NaB supplementation decreased the mRNA levels of toll-like receptor (TLR)-4, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and the trend was most pronounced in the jejunum.	nab	0-3	tumor necrosis factor	Rattus norvegicus	106-115
35044411-5	2022	NaB supplementation decreased the mRNA levels of toll-like receptor (TLR)-4, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and the trend was most pronounced in the jejunum.	nab	0-3	interleukin 6	Rattus norvegicus	121-134
35044411-5	2022	NaB supplementation decreased the mRNA levels of toll-like receptor (TLR)-4, tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6), and the trend was most pronounced in the jejunum.	nab	0-3	interleukin 6	Rattus norvegicus	136-140
35415672-16	2022	Flow cytometry studies revealed significantly increased M2 (CD206+ ) macrophages and Tregs (CD25+ ) relative to the M1 macrophage population and CD4+ T cells respectively in NaB treated mice, suggesting its potential role in alleviating the inflammatory profile.	nab	174-177	mannose receptor, C type 1	Mus musculus	60-65
35415672-16	2022	Flow cytometry studies revealed significantly increased M2 (CD206+ ) macrophages and Tregs (CD25+ ) relative to the M1 macrophage population and CD4+ T cells respectively in NaB treated mice, suggesting its potential role in alleviating the inflammatory profile.	nab	174-177	interleukin 2 receptor, alpha chain	Mus musculus	92-96
35415672-16	2022	Flow cytometry studies revealed significantly increased M2 (CD206+ ) macrophages and Tregs (CD25+ ) relative to the M1 macrophage population and CD4+ T cells respectively in NaB treated mice, suggesting its potential role in alleviating the inflammatory profile.	nab	174-177	CD4 antigen	Mus musculus	145-148
2822731-3	1987	GFAP levels decreased by about 50% in the RF cell line, and S-100 protein levels decreased protein levels decreased by about 40% after treatment with 1 mM NaB for 48 h. In the C6 rat glioma cell line, isoproterenol with theophylline was found to increase S-100 levels by two-fold over basal levels.	nab	155-158	S100 calcium binding protein A1	Homo sapiens	60-65
34996504-3	2022	METHODS: We performed RNA sequencing (RNA-seq) on samples from patients who were resistant or sensitive to nab-paclitaxel, and identified Zinc Finger Protein 64 (ZFP64) as critical for nab-paclitaxel resistance in GC.	nab	185-188	ZFP64 zinc finger protein	Homo sapiens	138-160
34996504-3	2022	METHODS: We performed RNA sequencing (RNA-seq) on samples from patients who were resistant or sensitive to nab-paclitaxel, and identified Zinc Finger Protein 64 (ZFP64) as critical for nab-paclitaxel resistance in GC.	nab	185-188	ZFP64 zinc finger protein	Homo sapiens	162-167
34996504-6	2022	RESULTS: ZFP64 overexpression was linked with aggressive phenotypes, nab-paclitaxel resistance and served as an independent prognostic factor in GC.	nab	69-72	zinc finger protein 64	Mus musculus	9-14
34996504-8	2022	Importantly, compared to treatment with nab-paclitaxel alone, nab-paclitaxel plus GAL-1 blockade significantly enhanced the anti-tumor effect in mouse models, particularly in humanized mice.	nab	40-43	lectin, galactose binding, soluble 1	Mus musculus	82-87
34996504-8	2022	Importantly, compared to treatment with nab-paclitaxel alone, nab-paclitaxel plus GAL-1 blockade significantly enhanced the anti-tumor effect in mouse models, particularly in humanized mice.	nab	62-65	lectin, galactose binding, soluble 1	Mus musculus	82-87
35019820-2	2022	In vitro binding test of IL15 fusion protein to HSA and Nab-paclitaxel, as well as CTLL-2 cell stimulation assay were performed.	nab	56-59	interleukin 15	Mus musculus	25-29
35019820-5	2022	As a result, combination therapy of Nab-paclitaxel and IL-15 fusion protein effectively inhibits the tumor growth and produced a 78% reduction in tumor size for HCT116, as compared to vehicle group.	nab	36-39	interleukin 15	Mus musculus	55-60
35019820-8	2022	Furthermore, Nab-paclitaxel and IL-15 fusion protein showed a significant suppression of NF-kappaB-mediated immune suppressive markers and increased expression of CD8, Granzyme B, CD62L, CD49b, and CD86 without obvious organ toxicity.	nab	13-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	89-98
35019820-8	2022	Furthermore, Nab-paclitaxel and IL-15 fusion protein showed a significant suppression of NF-kappaB-mediated immune suppressive markers and increased expression of CD8, Granzyme B, CD62L, CD49b, and CD86 without obvious organ toxicity.	nab	13-16	granzyme B	Mus musculus	168-178
35019820-8	2022	Furthermore, Nab-paclitaxel and IL-15 fusion protein showed a significant suppression of NF-kappaB-mediated immune suppressive markers and increased expression of CD8, Granzyme B, CD62L, CD49b, and CD86 without obvious organ toxicity.	nab	13-16	selectin, lymphocyte	Mus musculus	180-185
35019820-8	2022	Furthermore, Nab-paclitaxel and IL-15 fusion protein showed a significant suppression of NF-kappaB-mediated immune suppressive markers and increased expression of CD8, Granzyme B, CD62L, CD49b, and CD86 without obvious organ toxicity.	nab	13-16	integrin alpha 2	Mus musculus	187-192
35019820-8	2022	Furthermore, Nab-paclitaxel and IL-15 fusion protein showed a significant suppression of NF-kappaB-mediated immune suppressive markers and increased expression of CD8, Granzyme B, CD62L, CD49b, and CD86 without obvious organ toxicity.	nab	13-16	CD86 antigen	Mus musculus	198-202
35019820-9	2022	In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU.	nab	38-41	T-associated maternal effect	Mus musculus	207-210
35019820-9	2022	In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU.	nab	38-41	interleukin 15	Mus musculus	342-347
35019820-9	2022	In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU.	nab	38-41	albumin	Mus musculus	355-368
35019820-9	2022	In conclusion, combination therapy of Nab-paclitaxel and IL-15 fusion protein can effectively stimulate the antitumor activity of immune effector cells, thereby inhibiting immunosuppressive cells within the TME of colorectal cancer, and the overall therapeutic effect has a significant advantage over monotherapy.AbbreviationsInterleukin 15, IL-15; Human serum albumin, HSA; Myeloid-derived suppressor cells, MDSC; Albumin binding domain, ABD; Tumor drainage lymph node, TDLN; Natural killer (NK); Tumor-draining lymph node (TDLN); Tumor infiltrating lymphocyte, TIL; Immunogenic cell death, ICD; Enhanced permeability retention, EPR; Liposomal doxorubicin, Doxil; 5-fluorouracil, 5-FU.	nab	38-41	toll-like receptor 1	Mus musculus	563-566
34996504-0	2022	Targeting ZFP64/GAL-1 axis promotes therapeutic effect of nab-paclitaxel and reverses immunosuppressive microenvironment in gastric cancer.	nab	58-61	zinc finger protein 64	Mus musculus	10-15
34996504-0	2022	Targeting ZFP64/GAL-1 axis promotes therapeutic effect of nab-paclitaxel and reverses immunosuppressive microenvironment in gastric cancer.	nab	58-61	lectin, galactose binding, soluble 1	Mus musculus	16-21
34996504-2	2022	Here, we aim to reveal the underlying mechanisms of nanoparticle albumin-bound paclitaxel (nab-paclitaxel) resistance in GC.	nab	91-94	albumin	Mus musculus	65-72
34996504-3	2022	METHODS: We performed RNA sequencing (RNA-seq) on samples from patients who were resistant or sensitive to nab-paclitaxel, and identified Zinc Finger Protein 64 (ZFP64) as critical for nab-paclitaxel resistance in GC.	nab	107-110	ZFP64 zinc finger protein	Homo sapiens	138-160
34996504-3	2022	METHODS: We performed RNA sequencing (RNA-seq) on samples from patients who were resistant or sensitive to nab-paclitaxel, and identified Zinc Finger Protein 64 (ZFP64) as critical for nab-paclitaxel resistance in GC.	nab	107-110	ZFP64 zinc finger protein	Homo sapiens	162-167
2920008-6	1989	NaB induction of p52 in KNRK cells occurred before cell spreading; other polar compounds, such as dimethyl sulphoxide, which did not induce KNRK cell spreading, similarly failed to elicit p52 production.	nab	0-3	nuclear factor kappa B subunit 2	Homo sapiens	17-20
2844835-6	1988	Increased cytoskeletal actin occurred within 24 hr of NaB exposure, correlating with the initial reorganization of actin-containing microfilaments detected microscopically, and reflected concomitant 3-fold increases in cellular alpha-actinin and fibronectin content.	nab	54-57	fibronectin 1	Rattus norvegicus	246-257
2844835-7	1988	In contrast, the amount of vimentin, tropomyosin, and tubulin in NaB-treated cells was significantly decreased.	nab	65-68	vimentin	Rattus norvegicus	27-35
3294239-4	1988	The potential for differentiation is not blocked by tamoxifen, indicating that the relationship to ER expression is likely secondary to the association of ER expression with a particular stage of secretory cell differentiation that is susceptible to NaB induction.	nab	250-253	estrogen receptor 1	Homo sapiens	155-157
2822731-3	1987	GFAP levels decreased by about 50% in the RF cell line, and S-100 protein levels decreased protein levels decreased by about 40% after treatment with 1 mM NaB for 48 h. In the C6 rat glioma cell line, isoproterenol with theophylline was found to increase S-100 levels by two-fold over basal levels.	nab	155-158	S100 calcium binding protein A1	Homo sapiens	255-260
2822731-4	1987	NaB was found to inhibit the induction of S-100 protein but exhibited no effect on the basal levels of the protein.	nab	0-3	S100 calcium binding protein A1	Homo sapiens	42-47
2822731-7	1987	This suggests that NaB may inhibit cells from expressing S-100 protein by attenuating cAMP levels.	nab	19-22	S100 calcium binding protein A1	Homo sapiens	57-62
3036718-2	1987	Although injection of the fumed silica Cab-o-sil 3 days before a threshold s.c. inoculum of L5178Y-F9 cells increased the tumor frequency in syngeneic DBA/2 mice, tumors recovered from silica-treated animals exhibited an augmented resistance to NAb and to in vivo NR.	nab	245-248	cardiac abnormality	Mus musculus	39-42
3668254-5	1987	GM3 lactone was detected in melanoma as 3H-labeled GM3 gangliosidol after melanoma cells were directly treated with NaB[3H]4.	nab	116-119	granulocyte macrophage antigen 3	Mus musculus	0-3
3668254-5	1987	GM3 lactone was detected in melanoma as 3H-labeled GM3 gangliosidol after melanoma cells were directly treated with NaB[3H]4.	nab	116-119	granulocyte macrophage antigen 3	Mus musculus	51-54
3036718-2	1987	Although injection of the fumed silica Cab-o-sil 3 days before a threshold s.c. inoculum of L5178Y-F9 cells increased the tumor frequency in syngeneic DBA/2 mice, tumors recovered from silica-treated animals exhibited an augmented resistance to NAb and to in vivo NR.	nab	245-248	Scl/Tal1 interrupting locus	Mus musculus	32-35
3036718-3	1987	Cab-o-sil increased in vivo NR and induced a biphasic modulation of anti-tumor NAb and NK activities.	nab	79-82	cardiac abnormality	Mus musculus	0-3
3036718-3	1987	Cab-o-sil increased in vivo NR and induced a biphasic modulation of anti-tumor NAb and NK activities.	nab	79-82	Scl/Tal1 interrupting locus	Mus musculus	6-9
6818950-1	1982	Cancer-associated galactosyltransferase acceptor (CAGA glycoprotein), a small glycoprotein purified from human malignant effusion that selectively kills transformed cells, was tritiated by reductive methylation in the presence of NaB(3)H(4).	nab	230-233	S100 calcium binding protein A8	Homo sapiens	50-54
3110272-9	1987	Conditioned media prepared from IL 2 receptor-positive marrow T cells in the presence of IL 2 also inhibited CFU-GM expression from marrow NAB-T cells (50% +/- 16).	nab	139-142	interleukin 2	Homo sapiens	32-36
3110272-9	1987	Conditioned media prepared from IL 2 receptor-positive marrow T cells in the presence of IL 2 also inhibited CFU-GM expression from marrow NAB-T cells (50% +/- 16).	nab	139-142	interleukin 2 receptor subunit beta	Homo sapiens	32-45
4042983-7	1985	Radioactive labeling of sialic acid by limited periodate oxidation and NaB[3H]4 reduction resulted in a higher specific activity for free alpha than for hCG alpha, suggesting that free alpha contains more sialic acid per immunoreactive molecule than does alpha dissociated from hCG.	nab	71-74	chromogranin A	Homo sapiens	153-162
6943381-3	1981	c) High NK cell activity was codominantly inherited and high serum NAb levels were recessive, which argues against the theory that the NK cell receptor is a passively acquired NAb.	nab	176-179	killer cell immunoglobulin like receptor, two Ig domains and long cytoplasmic tail 4	Homo sapiens	135-151
6158545-5	1980	J774 FcR was judged to be a glycoprotein based on the sensitivity of its isoelectric point to neuraminidase digestion, its labeling with galactose oxidase/NaB[3H4], and its binding to concanavalin A-Sepharose.	nab	155-158	Fc receptor	Mus musculus	5-8
20256-7	1977	This was shown for TRH, tetracosactide and a new beta2-adrenoceptor stimulant, NAB 365.	nab	79-82	beta-2 adrenergic receptor	Canis lupus familiaris	49-67
20487739-1	1980	The sugar chains of bovine rhodopsin released from opsin by hydrazinolysis were reduced with NaB((3)H)(4) and fractionated by paper chromatography.	nab	93-96	rhodopsin	Bos taurus	27-36
447724-1	1979	The sugar chains of bovine rhodopsin were released from the polypeptide moiety by hydrazinolysis and reduced with NaB[3H]4 after N-acetylation.	nab	114-117	rhodopsin	Bos taurus	27-36
549410-2	1979	Irradiation of ribosome-NAB-puromycin complexes leads to covalent attachment of the affinity label to proteins of the large ribosomal subunit, in particular to proteins L28/29, and, to a somewhat lower extent, to proteins L4, L6, L10 and L24.	nab	24-27	ribosomal protein L3	Rattus norvegicus	222-228
33905875-7	2021	Low and high doses of NaB significantly increased the content of tyrosine hydroxylase (TH) by 12.3% and 20.2%, while reduced alpha-synuclein activation by 159.4% and 132.7% in the substantia nigra pars compacta (SNpc), compared with PD groups.	nab	22-25	synuclein, alpha	Mus musculus	125-140
4359017-3	1973	Analyses of (3)H radioactivity in disc electrophoretic profiles of the CNBr peptides from bone collagens that had been treated with NaB(3)H indicated that a major site of intermolecular cross-linking in chicken bone collagen is located between the carboxy-terminal region of an alpha1 chain and a small CNBr peptide, probably situated near the amino-terminus of an alpha1 or alpha2 chain in an adjacent collagen molecule.	nab	132-135	collagen type III alpha 1 chain	Gallus gallus	95-103
4359017-3	1973	Analyses of (3)H radioactivity in disc electrophoretic profiles of the CNBr peptides from bone collagens that had been treated with NaB(3)H indicated that a major site of intermolecular cross-linking in chicken bone collagen is located between the carboxy-terminal region of an alpha1 chain and a small CNBr peptide, probably situated near the amino-terminus of an alpha1 or alpha2 chain in an adjacent collagen molecule.	nab	132-135	asparagine-linked glycosylation 12, alpha-1,6-mannosyltransferase homolog (S. cerevisiae)	Gallus gallus	365-381
4359017-3	1973	Analyses of (3)H radioactivity in disc electrophoretic profiles of the CNBr peptides from bone collagens that had been treated with NaB(3)H indicated that a major site of intermolecular cross-linking in chicken bone collagen is located between the carboxy-terminal region of an alpha1 chain and a small CNBr peptide, probably situated near the amino-terminus of an alpha1 or alpha2 chain in an adjacent collagen molecule.	nab	132-135	collagen type III alpha 1 chain	Gallus gallus	216-224
4359017-7	1973	A small cross-linked peptide was isolated from chicken bone collagen that had been reduced with NaB(3)H(4) and digested with bacterial collagenase.	nab	96-99	collagen type III alpha 1 chain	Gallus gallus	60-68
33785315-12	2021	Moreover, our results suggested that NaB suppressed the over-activation of microglia and the accumulation of Abeta in AD mice.	nab	37-40	amyloid beta (A4) precursor protein	Mus musculus	109-114
33636386-7	2021	Accordingly, NaB administration also markedly decreased huntingtin level in striatum and cortex.	nab	13-16	huntingtin	Mus musculus	56-66
33989817-7	2021	The stimulatory effects of NaB on Insig-1 activity are abolished in AMPKalpha1/alpha2 double knockout (AMPK-/-) mouse primary hepatocytes.	nab	27-30	insulin induced gene 1	Mus musculus	34-41
33989817-8	2021	Moreover, AMPK activation by NaB is mediated by LKB1 as evidenced by the observations showing NaB-mediated induction of phosphorylation of AMPK and its downstream target ACC is diminished in LKB1-/- mouse embryonic fibroblasts.	nab	29-32	serine/threonine kinase 11	Mus musculus	48-52
33989817-8	2021	Moreover, AMPK activation by NaB is mediated by LKB1 as evidenced by the observations showing NaB-mediated induction of phosphorylation of AMPK and its downstream target ACC is diminished in LKB1-/- mouse embryonic fibroblasts.	nab	29-32	serine/threonine kinase 11	Mus musculus	191-195
33989817-8	2021	Moreover, AMPK activation by NaB is mediated by LKB1 as evidenced by the observations showing NaB-mediated induction of phosphorylation of AMPK and its downstream target ACC is diminished in LKB1-/- mouse embryonic fibroblasts.	nab	94-97	serine/threonine kinase 11	Mus musculus	48-52
33989817-8	2021	Moreover, AMPK activation by NaB is mediated by LKB1 as evidenced by the observations showing NaB-mediated induction of phosphorylation of AMPK and its downstream target ACC is diminished in LKB1-/- mouse embryonic fibroblasts.	nab	94-97	serine/threonine kinase 11	Mus musculus	191-195
33958764-1	2021	Nanoparticulate albumin bound paclitaxel (nab-paclitaxel, nab-PTX) is among the most widely prescribed nanomedicines in clinical use, yet it remains unclear how nanoformulation affects nab-PTX behaviour in the tumour microenvironment.	nab	42-45	albumin	Mus musculus	16-23
33958764-1	2021	Nanoparticulate albumin bound paclitaxel (nab-paclitaxel, nab-PTX) is among the most widely prescribed nanomedicines in clinical use, yet it remains unclear how nanoformulation affects nab-PTX behaviour in the tumour microenvironment.	nab	58-61	albumin	Mus musculus	16-23
33958764-1	2021	Nanoparticulate albumin bound paclitaxel (nab-paclitaxel, nab-PTX) is among the most widely prescribed nanomedicines in clinical use, yet it remains unclear how nanoformulation affects nab-PTX behaviour in the tumour microenvironment.	nab	58-61	albumin	Mus musculus	16-23
33958764-3	2021	We found that nab-PTX uptake is profoundly and distinctly affected by cancer-cell autonomous RAS signalling, and RAS/RAF/MEK/ERK inhibition blocked its selective delivery and efficacy.	nab	14-17	midkine	Mus musculus	121-124
33958764-3	2021	We found that nab-PTX uptake is profoundly and distinctly affected by cancer-cell autonomous RAS signalling, and RAS/RAF/MEK/ERK inhibition blocked its selective delivery and efficacy.	nab	14-17	mitogen-activated protein kinase 1	Mus musculus	125-128
33923402-7	2021	CAGE analysis revealed 75 upregulated and 96 downregulated genes in the cells after 0.2 mM NaB stimulation for 3 h. Regarding GO term enrichment, the genes upregulated >4-fold participated predominantly in cell migration and proliferation.	nab	91-94	DEAD-box helicase 53	Homo sapiens	0-4
33958974-9	2021	The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice.	nab	15-18	interleukin 16	Mus musculus	9-14
33958974-9	2021	The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice.	nab	15-18	troponin T2, cardiac	Mus musculus	134-152
33958974-9	2021	The anti-IL-16 nAb significantly decreased serum levels of lactate dehydrogenase (LDH), myocardial-bound creatine kinase (CK-MB), and cardiac troponin T (cTnT) and elevated cardiac function in DOX-induced mice.	nab	15-18	troponin T2, cardiac	Mus musculus	154-158
33958974-10	2021	Treatment with the anti-IL-16 nAb also reduced p65 pathway activation, decreased M1 macrophage-related marker and cytokine expression, and protected against cardiomyocyte apoptosis in DOX-induced mice.	nab	30-33	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	47-50
33958974-11	2021	In cell studies, the anti-IL-16 nAb also reduced DOX-induced M1 macrophage differentiation and alleviated apoptosis in cardiomyocytes cocultured with macrophages.	nab	32-35	interleukin 16	Mus musculus	26-31
33764366-0	2021	CCL26 is upregulated by nab-paclitaxel in pancreatic cancer-associated fibroblasts and promotes PDAC invasiveness through activation of the PI3K/AKT/mTOR pathway.	nab	24-27	C-C motif chemokine ligand 26	Homo sapiens	0-5
33958974-12	2021	Conclusions: The anti-IL-16 nAb protects against DOX-induced cardiac injury by reducing cardiac inflammation, and IL-16 may be a promising target to prevent DOX-related cardiac injury.	nab	28-31	interleukin 16	Mus musculus	22-27
33764366-5	2021	In the present study, we aimed to determine the expression of CCL26 in the pancreatic cancer-associated fibroblasts (CAFs) after nab-paclitaxel treatment and to explore the role of CCL26 in the pancreatic adenocarcinoma (PDAC) invasion.	nab	129-132	C-C motif chemokine ligand 26	Homo sapiens	62-67
33764366-6	2021	Our results showed that nab-paclitaxel increased CCL26 mRNA and protein expression levels in a dose- and time-dependent manner.	nab	24-27	C-C motif chemokine ligand 26	Homo sapiens	49-54
33764366-11	2021	In summary, our results showed that nab-paclitaxel increased the expression of CCL26 in CAFs, and CCL26 enhanced the invasive potential of pancreatic cancer cells by activating the PI3K/AKT/mTOR axis.	nab	36-39	C-C motif chemokine ligand 26	Homo sapiens	79-84
33764366-11	2021	In summary, our results showed that nab-paclitaxel increased the expression of CCL26 in CAFs, and CCL26 enhanced the invasive potential of pancreatic cancer cells by activating the PI3K/AKT/mTOR axis.	nab	36-39	AKT serine/threonine kinase 1	Homo sapiens	186-189
33764366-11	2021	In summary, our results showed that nab-paclitaxel increased the expression of CCL26 in CAFs, and CCL26 enhanced the invasive potential of pancreatic cancer cells by activating the PI3K/AKT/mTOR axis.	nab	36-39	mechanistic target of rapamycin kinase	Homo sapiens	190-194
33649523-5	2021	The heterozygous genotype of CYP3A4*22 showed a trend of association with skin reactions in pts treated with paclitaxel and nab-paclitaxel (RR = 6.92; 95% CI 0.47, 99.8; p = 0.0766).	nab	124-127	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	29-35
33897442-12	2021	In parallel, NaB treatment could enhance the activation of autophagy, increase autophagic flux, decrease extracellular matrix degradation, and reduce apoptosis by restraining inflammation, ROS production, and cell cycle arrest in IL-1beta-treated chondrocytes.	nab	13-16	interleukin 1 alpha	Homo sapiens	230-238
33897442-14	2021	In conclusion, NaB could attenuate OA progression by restoring impaired autophagy and autophagic flux via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway, both in vitro and in vivo, implying that NaB could represent a novel therapeutic approach for OA.	nab	15-18	AKT serine/threonine kinase 1	Homo sapiens	161-164
33897442-14	2021	In conclusion, NaB could attenuate OA progression by restoring impaired autophagy and autophagic flux via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway, both in vitro and in vivo, implying that NaB could represent a novel therapeutic approach for OA.	nab	15-18	mechanistic target of rapamycin kinase	Homo sapiens	166-195
33897442-14	2021	In conclusion, NaB could attenuate OA progression by restoring impaired autophagy and autophagic flux via the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) pathway, both in vitro and in vivo, implying that NaB could represent a novel therapeutic approach for OA.	nab	15-18	mechanistic target of rapamycin kinase	Homo sapiens	197-201
33548860-3	2021	nab-paclitaxel is a nanoparticle albumin-bound formulation of paclitaxel that improves drug delivery into tumor compared to paclitaxel.	nab	0-3	albumin	Homo sapiens	33-40
33791699-2	2021	Here, we applied live bioluminescence imaging (BLI) to monitor the real-time effects of NAb treatment in prophylaxis and therapy of K18-hACE2 mice intranasally infected with SARS-CoV-2-nanoluciferase.	nab	88-91	keratin 18	Mus musculus	132-135
33791699-2	2021	Here, we applied live bioluminescence imaging (BLI) to monitor the real-time effects of NAb treatment in prophylaxis and therapy of K18-hACE2 mice intranasally infected with SARS-CoV-2-nanoluciferase.	nab	88-91	angiotensin converting enzyme 2	Homo sapiens	136-141
33683482-5	2021	Arm 1 patients received nab-paclitaxel and cisplatin, then cisplatin with radiation.	nab	24-27	kallikrein related peptidase 4	Homo sapiens	0-5
33683482-6	2021	Arm 2 patients received nab-paclitaxel, then cetuximab with radiation.	nab	24-27	Jupiter microtubule associated homolog 1	Homo sapiens	0-5
33732454-3	2021	The high pressure employed during the manufacture of nab-paclitaxel HSA (nab HSA) may influence its conformation and/or oligomerization, and ultimately its affinity for HSA.	nab	53-56	albumin	Homo sapiens	68-71
33732454-3	2021	The high pressure employed during the manufacture of nab-paclitaxel HSA (nab HSA) may influence its conformation and/or oligomerization, and ultimately its affinity for HSA.	nab	53-56	albumin	Homo sapiens	77-80
33732454-3	2021	The high pressure employed during the manufacture of nab-paclitaxel HSA (nab HSA) may influence its conformation and/or oligomerization, and ultimately its affinity for HSA.	nab	53-56	albumin	Homo sapiens	77-80
33732454-5	2021	In the present study, nab HSA was isolated from nab-paclitaxel by gel filtration, and the binding affinities (KDs) were determined by surface plasmon resonance.	nab	22-25	albumin	Homo sapiens	26-29
33732454-5	2021	In the present study, nab HSA was isolated from nab-paclitaxel by gel filtration, and the binding affinities (KDs) were determined by surface plasmon resonance.	nab	48-51	albumin	Homo sapiens	26-29
33732454-7	2021	Paclitaxel showed KDs of 8.93+-8.60 and 7.39+-5.81 microM for nab HSA and control HSA, respectively, whereas the corresponding KDs for docetaxel were 44.3+-9.50 and 55.9+-2.28 microM, respectively.	nab	62-65	albumin	Homo sapiens	66-69
33721354-15	2021	NaB attenuated NAFLD progression by regulating miR-150.	nab	0-3	microRNA 150	Mus musculus	47-54
33721354-17	2021	CONCLUSION: NaB mitigates HFD-induced NAFLD in mice by upregulating miR-150 expression to downregulate CXCR4.	nab	12-15	microRNA 150	Mus musculus	68-75
33721354-17	2021	CONCLUSION: NaB mitigates HFD-induced NAFLD in mice by upregulating miR-150 expression to downregulate CXCR4.	nab	12-15	chemokine (C-X-C motif) receptor 4	Mus musculus	103-108
33750427-14	2021	CONCLUSIONS: Our study shows high phosphorylation of several oncogenic receptor tyrosine kinases in PDAC cells and validated FAK inhibition as potential synergistic target with Nab-paclitaxel against this devastating disease.	nab	177-180	protein tyrosine kinase 2	Homo sapiens	125-128
33649523-6	2021	CYP2C8*3/*4 variant carriers showed a trend of association with overall AEs in pts treated with paclitaxel and nab-paclitaxel (RR = 1.28; 95% CI 0.96, 1.67; p = 0.0898).	nab	111-114	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	0-6
33649523-9	2021	Despite the population was heterogeneous, CYP3A4*22 and CYP2C8 SNPs may influence paclitaxel and nab-paclitaxel toxicity and ABCB1 c.3435 may affect taxanes effectiveness, even if any statistically significant was found.	nab	97-100	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	42-48
33649523-9	2021	Despite the population was heterogeneous, CYP3A4*22 and CYP2C8 SNPs may influence paclitaxel and nab-paclitaxel toxicity and ABCB1 c.3435 may affect taxanes effectiveness, even if any statistically significant was found.	nab	97-100	cytochrome P450 family 2 subfamily C member 8	Homo sapiens	56-62
33475895-7	2021	The scratch wound healing assay showed no effect of cell migration in the MS-275 (1.0 microM)-treated cells when compared with the controls at 24 h. Furthermore, MS-275, VPA, and NaB increased the mRNA expression levels of Bmp-2 and -4, Oc, and Runx2 followed by the mineralization of the cells.	nab	179-182	bone morphogenetic protein 2	Homo sapiens	223-235
33681555-6	2021	Relative to the controls, there were also significant fold change differences in palmitic and linoleic acid levels in the cell lysates, mitochondrial CPT1 activities, and mitochondrial medium-chain acyl-CoA dehydrogenase (MCAD) protein levels in the A549 cells subjected to the nab-paclitaxel and solvent-based paclitaxel formulations.	nab	278-281	acyl-CoA dehydrogenase medium chain	Homo sapiens	222-226
33541289-9	2021	Patients treated with nab-paclitaxel had better event-free survival (EFS; HR = 0.69, 95%CI: 0.57-0.85, P < 0.001) than with sb-taxanes.	nab	22-25	nuclear receptor subfamily 4 group A member 1	Homo sapiens	74-76
33475895-7	2021	The scratch wound healing assay showed no effect of cell migration in the MS-275 (1.0 microM)-treated cells when compared with the controls at 24 h. Furthermore, MS-275, VPA, and NaB increased the mRNA expression levels of Bmp-2 and -4, Oc, and Runx2 followed by the mineralization of the cells.	nab	179-182	bone gamma-carboxyglutamate protein	Homo sapiens	237-239
33475895-7	2021	The scratch wound healing assay showed no effect of cell migration in the MS-275 (1.0 microM)-treated cells when compared with the controls at 24 h. Furthermore, MS-275, VPA, and NaB increased the mRNA expression levels of Bmp-2 and -4, Oc, and Runx2 followed by the mineralization of the cells.	nab	179-182	RUNX family transcription factor 2	Homo sapiens	245-250
33479441-5	2021	Anti-TDP-43 NAb were found to be significantly increased in ALS patients compared to all the other groups (p < 0.001).	nab	12-15	TAR DNA binding protein	Homo sapiens	5-11
33479441-9	2021	For the first time, we report that serum anti-TDP-43 NAb are detectable in human serum of both healthy controls and patients affected by a variety of neurodegenerative disorders; furthermore, their levels are increased in ALS patients, representing a potentially interesting trait core marker of this disease.	nab	53-56	TAR DNA binding protein	Homo sapiens	46-52
32988260-2	2020	In March 2019, the combination of nab-paclitaxel and atezolizumab was approved by the US FDA for patients with PD-L1 positive metastatic triple-negative breast cancer based on positive results of the Impassion130 trial.	nab	34-37	CD274 molecule	Homo sapiens	111-116
33087331-2	2021	Previous studies demonstrate that caveolin-1 (Cav-1) expression is critical for nab-paclitaxel uptake into tumors and correlates with response.	nab	80-83	caveolin 1	Homo sapiens	34-44
33087331-2	2021	Previous studies demonstrate that caveolin-1 (Cav-1) expression is critical for nab-paclitaxel uptake into tumors and correlates with response.	nab	80-83	caveolin 1	Homo sapiens	46-51
33087331-3	2021	Gemcitabine increases nab-paclitaxel uptake by increasing Cav-1 expression.	nab	22-25	caveolin 1	Homo sapiens	58-63
33087331-4	2021	Thus, we hypothesized that pre-treatment with gemcitabine would further enhance the sensitivity of PDAC to nab-paclitaxel by increasing Cav-1 expression and nab-paclitaxel uptake.	nab	107-110	caveolin 1	Homo sapiens	136-141
33087331-8	2021	Cav-1 silencing reduced the uptake of albumin and therapeutic advantage observed when cells were pre-treated with gemcitabine prior to nab-paclitaxel.	nab	135-138	caveolin 1	Homo sapiens	0-5
33087331-8	2021	Cav-1 silencing reduced the uptake of albumin and therapeutic advantage observed when cells were pre-treated with gemcitabine prior to nab-paclitaxel.	nab	135-138	albumin	Homo sapiens	38-45
33475294-4	2021	Based on IMpassion130, the combination of atezolizumab and nab-paclitaxel is now considered a standard of care for the treatment of PD-L1-positive advanced TNBC.	nab	59-62	CD274 molecule	Homo sapiens	132-137
33506931-9	2021	The activities of NF-kappaB and JAK2/STAT3 signaling pathways were significantly increased in lung tissue after IR, whereas NaB inhibited the activity of NF-kappaB and JAK2/STAT3 signaling pathways.	nab	124-127	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	154-163
33506931-9	2021	The activities of NF-kappaB and JAK2/STAT3 signaling pathways were significantly increased in lung tissue after IR, whereas NaB inhibited the activity of NF-kappaB and JAK2/STAT3 signaling pathways.	nab	124-127	Janus kinase 2	Mus musculus	168-172
33506931-9	2021	The activities of NF-kappaB and JAK2/STAT3 signaling pathways were significantly increased in lung tissue after IR, whereas NaB inhibited the activity of NF-kappaB and JAK2/STAT3 signaling pathways.	nab	124-127	signal transducer and activator of transcription 3	Mus musculus	173-178
33506931-10	2021	CONCLUSIONS: NaB relieves LIRI by inhibiting NF-kappaB and JAK2/STAT3 signaling pathways to reduce inflammation and oxidative stress levels in lung tissue of mice after IR.	nab	13-16	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	45-54
33506931-10	2021	CONCLUSIONS: NaB relieves LIRI by inhibiting NF-kappaB and JAK2/STAT3 signaling pathways to reduce inflammation and oxidative stress levels in lung tissue of mice after IR.	nab	13-16	Janus kinase 2	Mus musculus	59-63
33506931-10	2021	CONCLUSIONS: NaB relieves LIRI by inhibiting NF-kappaB and JAK2/STAT3 signaling pathways to reduce inflammation and oxidative stress levels in lung tissue of mice after IR.	nab	13-16	signal transducer and activator of transcription 3	Mus musculus	64-69
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	nab	76-79	programmed cell death 1	Homo sapiens	159-177
33221685-1	2021	BACKGROUND: This study aimed to evaluate the effect of salvage therapy with nab-paclitaxel (nab-p) or temozolomide (TMZ) combined with antiangiogenic drugs in programmed death 1 (PD-1) inhibitor-resistant patients with unresectable metastatic melanoma.	nab	76-79	programmed cell death 1	Homo sapiens	179-183
33322698-8	2020	Therefore, our study suggested that CDKN2A-inactivated PDAC patients could benefit from the precision treatment with paclitaxel, whose albumin-stabilized nanoparticle formulation (nab-paclitaxel) has been approved for treating PDAC.	nab	180-183	cyclin dependent kinase inhibitor 2A	Homo sapiens	36-42
33152341-4	2021	NaB administration inhibited total HDAC activity and enhanced acetylation level of histones specifically in histone H4, accompanying the increase of transcription levels of immediate-early genes (IEGs) (c-fos and Arc) and neurotrophins (BDNF and NT-4) crucial for neuroplasticity in the motor cortex.	nab	0-3	LOC102641229	Mus musculus	108-118
33152341-4	2021	NaB administration inhibited total HDAC activity and enhanced acetylation level of histones specifically in histone H4, accompanying the increase of transcription levels of immediate-early genes (IEGs) (c-fos and Arc) and neurotrophins (BDNF and NT-4) crucial for neuroplasticity in the motor cortex.	nab	0-3	FBJ osteosarcoma oncogene	Mus musculus	203-208
33152341-4	2021	NaB administration inhibited total HDAC activity and enhanced acetylation level of histones specifically in histone H4, accompanying the increase of transcription levels of immediate-early genes (IEGs) (c-fos and Arc) and neurotrophins (BDNF and NT-4) crucial for neuroplasticity in the motor cortex.	nab	0-3	brain derived neurotrophic factor	Mus musculus	237-241
33152341-4	2021	NaB administration inhibited total HDAC activity and enhanced acetylation level of histones specifically in histone H4, accompanying the increase of transcription levels of immediate-early genes (IEGs) (c-fos and Arc) and neurotrophins (BDNF and NT-4) crucial for neuroplasticity in the motor cortex.	nab	0-3	neurotrophin 5	Mus musculus	246-250
32896048-0	2020	Bi-allelic mutations in EGR2 cause autosomal recessive demyelinating neuropathy by disrupting the EGR2-NAB complex.	nab	103-106	early growth response 2	Homo sapiens	24-28
32896048-0	2020	Bi-allelic mutations in EGR2 cause autosomal recessive demyelinating neuropathy by disrupting the EGR2-NAB complex.	nab	103-106	early growth response 2	Homo sapiens	98-102
33216087-3	2020	Accompanying the improved intestinal TJs, NaB not only relieved intestine inflammation of db/db mice and HG and LPS co-cultured Caco-2 cells but also restored intestinal Takeda G-protein-coupled (TGR5) expression, resulting in up-regulated serum GLP-1 levels.	nab	42-45	G protein-coupled bile acid receptor 1	Homo sapiens	196-200
33216087-3	2020	Accompanying the improved intestinal TJs, NaB not only relieved intestine inflammation of db/db mice and HG and LPS co-cultured Caco-2 cells but also restored intestinal Takeda G-protein-coupled (TGR5) expression, resulting in up-regulated serum GLP-1 levels.	nab	42-45	glucagon like peptide 1 receptor	Homo sapiens	246-251
33010913-9	2020	Acetylation of histone H3 protein, which promotes gene expression by affecting the structure of chromatin, was also upregulated by NaB in response to LPS stimulation.	nab	131-134	H3 clustered histone 14	Bos taurus	15-25
33010913-12	2020	The results showed that inhibitors of p38 MAPK, Erk, and JNK attenuated the NaB-induced upregulation of TNF and beta-defensin 5 (DEFB5) transcription, and that the inhibitor of Erk attenuated the NaB-induced upregulation of IL1B transcription during LPS challenge.	nab	76-79	interleukin 1 beta	Bos taurus	224-228
33010913-12	2020	The results showed that inhibitors of p38 MAPK, Erk, and JNK attenuated the NaB-induced upregulation of TNF and beta-defensin 5 (DEFB5) transcription, and that the inhibitor of Erk attenuated the NaB-induced upregulation of IL1B transcription during LPS challenge.	nab	196-199	beta-defensin 5	Bos taurus	129-134
33010913-13	2020	Enhanced transcription of CXCL8 by NaB was blocked by the inhibitor of Erk and p38 MAPK during LPS stimulation.	nab	35-38	C-X-C motif chemokine ligand 8	Bos taurus	26-31
33010913-14	2020	Overall, NaB boosted the LPS-induced innate immune response by promoting the expression of proinflammatory cytokines, chemokines, and beta-defensins, which was associated with enhanced MAPK signaling activation and histone H3 acetylation.	nab	9-12	H3 clustered histone 14	Bos taurus	215-225
33010913-10	2020	P38 mitogen-activated protein kinases (MAPK), JNK, and Erk 1 and 2 are key upstream regulators of the expression of proinflammatory cytokines, chemokines, and beta-defensins, and their activity was enhanced by NaB during LPS stimulation.	nab	210-213	mitogen-activated protein kinase 3	Bos taurus	55-66
33010913-12	2020	The results showed that inhibitors of p38 MAPK, Erk, and JNK attenuated the NaB-induced upregulation of TNF and beta-defensin 5 (DEFB5) transcription, and that the inhibitor of Erk attenuated the NaB-induced upregulation of IL1B transcription during LPS challenge.	nab	76-79	tumor necrosis factor	Bos taurus	104-107
33010913-12	2020	The results showed that inhibitors of p38 MAPK, Erk, and JNK attenuated the NaB-induced upregulation of TNF and beta-defensin 5 (DEFB5) transcription, and that the inhibitor of Erk attenuated the NaB-induced upregulation of IL1B transcription during LPS challenge.	nab	76-79	beta-defensin 5	Bos taurus	112-127
33010913-12	2020	The results showed that inhibitors of p38 MAPK, Erk, and JNK attenuated the NaB-induced upregulation of TNF and beta-defensin 5 (DEFB5) transcription, and that the inhibitor of Erk attenuated the NaB-induced upregulation of IL1B transcription during LPS challenge.	nab	76-79	beta-defensin 5	Bos taurus	129-134
32934716-3	2020	It was demonstrated that the HDAC inhibitor sodium butyrate (NaB) induced the differential expression of multidrug resistant ATP-binding cassette (ABC) transporters in lung cancer and colorectal cancer cells.	nab	61-64	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	125-145
33198652-1	2020	BACKGROUND: Nanoparticle albumin-bound paclitaxel (nab-PTX) has shown non-inferiority to paclitaxel (PTX) as second-line therapy for advanced gastric cancer (AGC) with fewer infusion-related reactions.	nab	51-54	albumin	Homo sapiens	25-32
32711612-1	2020	This study aims to compare the efficacy and side effects of albumin-binding paclitaxel plus carboplatin (NAB PC) and paclitaxel plus carboplatin (PC) in the first-line treatment of advanced non-small cell lung cancer (NSCLC).	nab	105-108	albumin	Homo sapiens	60-67
33283132-0	2020	Measuring Tumor Epichaperome Expression Using [124I] PU-H71 Positron Emission Tomography as a Biomarker of Response for PU-H71 Plus Nab-Paclitaxel in HER2-Negative Metastatic Breast Cancer.	nab	132-135	erb-b2 receptor tyrosine kinase 2	Homo sapiens	150-154
33336070-4	2020	Based on the results, several impressive drugs have been approved to benefit patients with TNBC, including the PARP inhibitors olaparib and talazoparib for germline BRCA mutation-associated breast cancer (gBRCAm-BC) and immunotherapy using the checkpoint inhibitor atezolizumab in combination with nab-paclitaxel for programmed cell death-ligand 1-positive (PD-L1+) advanced TNBC.	nab	298-301	poly(ADP-ribose) polymerase 1	Homo sapiens	111-115
33182800-6	2020	NaB inhibited or delayed the expression of D-type cyclin (CYCD3-1) and shoot-regeneration regulatory gene WUSCHEL (WUS) in cotyledon explants of tobacco and tomato.	nab	0-3	cyclin-D3-2-like	Nicotiana tabacum	58-65
33182800-6	2020	NaB inhibited or delayed the expression of D-type cyclin (CYCD3-1) and shoot-regeneration regulatory gene WUSCHEL (WUS) in cotyledon explants of tobacco and tomato.	nab	0-3	protein WUSCHEL-like	Nicotiana tabacum	106-113
33182800-6	2020	NaB inhibited or delayed the expression of D-type cyclin (CYCD3-1) and shoot-regeneration regulatory gene WUSCHEL (WUS) in cotyledon explants of tobacco and tomato.	nab	0-3	protein WUSCHEL-like	Nicotiana tabacum	106-109
33182800-7	2020	However, compared to that in control SIM, the expression of WUS was promoted more rapidly in tobacco calli cultured in NaB-containing SIM, but the expression of CYCD3-1 was inhibited.	nab	119-122	protein WUSCHEL-like	Nicotiana tabacum	60-63
33182800-8	2020	In conclusion, the effect of NaB on adventitious shoot formation and expression of CYCD3-1 and WUS genes depended on the plant species and whether the effects were tested on explants or protoplast-derived calli.	nab	29-32	cyclin-D3-2-like	Nicotiana tabacum	83-90
33182800-8	2020	In conclusion, the effect of NaB on adventitious shoot formation and expression of CYCD3-1 and WUS genes depended on the plant species and whether the effects were tested on explants or protoplast-derived calli.	nab	29-32	protein WUSCHEL-like	Nicotiana tabacum	95-98
33183015-0	2021	A heavily pre-treated adenocarcinoma patient with EGFR exon 20 insertion mutation responded to pembrolizumab plus nab-paclitaxel/bevacizumab: a case report.	nab	114-117	epidermal growth factor receptor	Homo sapiens	50-54
32934716-3	2020	It was demonstrated that the HDAC inhibitor sodium butyrate (NaB) induced the differential expression of multidrug resistant ATP-binding cassette (ABC) transporters in lung cancer and colorectal cancer cells.	nab	61-64	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	147-150
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily B member 1	Homo sapiens	58-82
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily B member 1	Homo sapiens	84-89
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily C member 10	Homo sapiens	92-98
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily C member 12	Homo sapiens	103-109
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily B member 1	Homo sapiens	144-166
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily B member 1	Homo sapiens	168-172
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily C member 10	Homo sapiens	175-216
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily C member 10	Homo sapiens	218-222
32934716-4	2020	Specifically, NaB increased the mRNA expression levels of ABC subfamily B member 1 (ABCB1), ABCC10 and ABCC12, and protein expression levels of multidrug resistance-1 (MDR1), multidrug resistance-associated protein 7 (MRP7) and MRP9.	nab	14-17	ATP binding cassette subfamily C member 12	Homo sapiens	228-232
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 1	Homo sapiens	49-54
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 2	Homo sapiens	56-61
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 3	Homo sapiens	66-71
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 1	Homo sapiens	99-103
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 2	Homo sapiens	105-109
32934716-5	2020	Moreover, NaB decreased the expression levels of ABCC1, ABCC2 and ABCC3 mRNAs, as well as those of MRP1, MRP2 and MRP3 proteins.	nab	10-13	ATP binding cassette subfamily C member 3	Homo sapiens	114-118
32934716-7	2020	NaB decreased the expression of HDAC4, but not HDAC1, HDAC2 or HDAC3.	nab	0-3	histone deacetylase 4	Homo sapiens	32-37
32934716-8	2020	In addition, NaB promoted histone H3 acetylation and methylation at lysine 9, as well as MDR1 acetylation, suggesting that acetylation and methylation may be involved in NaB-mediated ABC transporter expression.	nab	13-16	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	183-186
32934716-8	2020	In addition, NaB promoted histone H3 acetylation and methylation at lysine 9, as well as MDR1 acetylation, suggesting that acetylation and methylation may be involved in NaB-mediated ABC transporter expression.	nab	170-173	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	183-186
32755385-8	2020	In NHE8KO mice receiving sodium butyrate (NaB), 1mM NaB stimulated Muc2 expression without changing goblet cell theca, but 10mM NaB induced a significant reduction of goblet cell theca without altering Muc2 expression.	nab	52-55	mucin 2	Mus musculus	67-71
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	mechanistic target of rapamycin kinase	Bos taurus	105-136
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	mechanistic target of rapamycin kinase	Bos taurus	138-142
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	ribosomal protein S6 kinase B1	Bos taurus	148-157
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	ribosomal protein S6 kinase B1	Bos taurus	159-162
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	free fatty acid receptor 3	Bos taurus	264-293
32891612-8	2020	RESULTS: The results showed that NaB significantly promoted milk fat synthesis, promoted the activity of mechanistic target of rapamycin (mTOR) and S6 kinase (S6K), inhibited the activity of AMP-activated protein kinase (AMPK), and promoted the gene expression of G protein-coupled receptor 41 (GPR41).	nab	33-36	free fatty acid receptor 3	Bos taurus	295-300
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	sterol regulatory element binding transcription factor 1	Bos taurus	72-78
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	free fatty acid receptor 3	Bos taurus	87-92
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	mechanistic target of rapamycin kinase	Bos taurus	98-102
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	ribosomal protein S6 kinase B1	Bos taurus	103-106
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	free fatty acid receptor 3	Bos taurus	174-179
32891612-10	2020	These results indicated that NaB increased the nuclear translocation of SREBP1 via the GPR41/AMPK/mTOR/S6K signalling pathway, promoted the acetylation of mature SREBP1a via GPR41/AMPK/SIRT1, and then promoted milk synthesis.	nab	29-32	sirtuin 1	Bos taurus	185-190
32755385-8	2020	In NHE8KO mice receiving sodium butyrate (NaB), 1mM NaB stimulated Muc2 expression without changing goblet cell theca, but 10mM NaB induced a significant reduction of goblet cell theca without altering Muc2 expression.	nab	52-55	mucin 2	Mus musculus	67-71
32755385-9	2020	Furthermore, 5mM and 10mM NaB treated HT29-MTX cells displayed increased apoptosis, while 0.5mM NaB stimulated Muc2 gene expression.	nab	96-99	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	111-115
32172331-9	2020	In addition, NaB decreased T regulatory cells and increased natural killer T cells and T helper 17 cells, accordingly decreased IL-10 and increased IL-17 secretion in CLM mice liver.	nab	13-16	interleukin 10	Homo sapiens	128-133
32930844-8	2020	Simulation based on the developed PK/PD model showed a substantial impact of age and serum albumin level on the time course of neutrophil counts after nab-paclitaxel administration.	nab	151-154	albumin	Homo sapiens	91-98
32930844-10	2020	CONCLUSION: We have developed a novel PK/PD model for nab-paclitaxel in which age and serum albumin level were considered clinically important covariate factors.	nab	54-57	albumin	Homo sapiens	92-99
32768887-7	2020	On the other hand, NaB upregulated the expression of all the isoforms of the LAT transporter in vitro.	nab	19-22	linker for activation of T cells	Homo sapiens	77-80
32172331-9	2020	In addition, NaB decreased T regulatory cells and increased natural killer T cells and T helper 17 cells, accordingly decreased IL-10 and increased IL-17 secretion in CLM mice liver.	nab	13-16	interleukin 17A	Homo sapiens	148-153
32889602-7	2021	We also demonstrated that sodium benzoate (NaB), a metabolite of cinnamon, a widely used food additive and a FDA-approved drug for glycine encephalopathy, was also capable of reducing alpha-syn deposits in A53T mice.	nab	43-46	synuclein alpha	Homo sapiens	184-193
33117463-11	2020	Conclusions: Neoadjuvant chemotherapy using nab-PTX with trastuzumab every 3 weeks followed by FEC was suitably tolerated and associated with a high pCR rate of 55% for patients with HER2-positive breast cancer.	nab	44-47	erb-b2 receptor tyrosine kinase 2	Homo sapiens	183-187
32889602-11	2021	Accordingly, we observed upregulation and/or normalization of DJ-1 and Parkin in the nigra of A53T mice by treatment with cinnamon and NaB.	nab	135-138	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	62-66
32436244-0	2020	A multicenter phase II trial of nab-paclitaxel and capecitabine in HER-2 negative and triple- negative advanced breast cancer: Could be an old regimen a valid approach to a changing disease?	nab	32-35	erb-b2 receptor tyrosine kinase 2	Homo sapiens	67-72
32450725-3	2020	The results of the IMpassion130 trial have recently led to the approval of the combination of atezolizumab and nab-paclitaxel in the first-line treatment of patients with unresectable locally advanced or metastatic, PD-L1-positive TNBC.	nab	111-114	CD274 molecule	Homo sapiens	216-221
32555166-6	2020	We showed that NaB decreased the expression levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and Abeta accumulation induced by high cholesterol in SK-N-MC cells.	nab	15-18	beta-secretase 1	Homo sapiens	54-107
32556930-5	2020	In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1beta, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells.	nab	35-38	interleukin 1 alpha	Mus musculus	109-117
32556930-5	2020	In vitro study also confirmed that NaB could significantly exacerbate pro-inflammatory cytokines expression (IL-1beta, 4.11-fold, P < 0.01; IL-18, 3.42-fold, P < 0.01 and iNOS, 2.52-fold, P < 0.05) and NO production (1.55-fold, P < 0.001) in LPS-stimulated BV2 cells.	nab	35-38	interleukin 18	Mus musculus	140-145
32556930-6	2020	In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice.	nab	13-16	interleukin 6	Mus musculus	75-79
32556930-6	2020	In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice.	nab	13-16	interleukin 18	Mus musculus	102-107
32556930-6	2020	In addition, NaB upregulated the expression of pro-inflammatory cytokines (IL-6, 3.52-fold, P < 0.05; IL-18, 1.72-fold, P < 0.001) and NLRP3 (3.11-fold, P < 0.001) in the colon of PD mice.	nab	13-16	NLR family, pyrin domain containing 3	Mus musculus	135-140
32554208-1	2020	We investigated the involvement of klotho in the inhibition of oxidative stress by sodium butyrate (NaB) in human nucleus pulposus cells (NPCs).	nab	100-103	klotho	Homo sapiens	35-41
32554208-5	2020	NaB also reduced the TBHP-induced release of proteases that degrade the extracellular matrix, including matrix metalloproteinases 3 and 13, and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs 4).	nab	0-3	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	144-152
32554208-5	2020	NaB also reduced the TBHP-induced release of proteases that degrade the extracellular matrix, including matrix metalloproteinases 3 and 13, and ADAMTS-4 (a disintegrin and metalloproteinase with thrombospondin motifs 4).	nab	0-3	ADAM metallopeptidase with thrombospondin type 1 motif 4	Homo sapiens	154-218
32554208-6	2020	Intriguingly, NaB significantly reversed TBHP-induced klotho suppression.	nab	14-17	klotho	Homo sapiens	54-60
32554208-7	2020	However, the protective effects of NaB on NPCs were abolished by klotho-specific small interfering RNA (siRNA).	nab	35-38	klotho	Homo sapiens	65-71
32554208-11	2020	Therefore, NaB alleviates TBHP-induced oxidative stress in human NPCs by elevating PPARgamma-regulated klotho expression.	nab	11-14	peroxisome proliferator activated receptor gamma	Homo sapiens	83-92
32554208-11	2020	Therefore, NaB alleviates TBHP-induced oxidative stress in human NPCs by elevating PPARgamma-regulated klotho expression.	nab	11-14	klotho	Homo sapiens	103-109
32554208-12	2020	HDAC3 may be a critical HDAC subtype that mediates the regulation of PPARgamma activity by NaB under oxidative stress.	nab	91-94	histone deacetylase 3	Homo sapiens	0-5
32554208-12	2020	HDAC3 may be a critical HDAC subtype that mediates the regulation of PPARgamma activity by NaB under oxidative stress.	nab	91-94	peroxisome proliferator activated receptor gamma	Homo sapiens	69-78
32788915-4	2020	The aim of this study was to investigate the effect of sodium butyrate (NaB) as a histone deacetylase inhibitor (HDACi) on the expression of the HDAC8 gene in the colorectal cancer cell line, and the molecular docking of the LHX1 transcription factor with NaB.	nab	72-75	histone deacetylase 8	Homo sapiens	145-150
32788915-4	2020	The aim of this study was to investigate the effect of sodium butyrate (NaB) as a histone deacetylase inhibitor (HDACi) on the expression of the HDAC8 gene in the colorectal cancer cell line, and the molecular docking of the LHX1 transcription factor with NaB.	nab	72-75	LIM homeobox 1	Homo sapiens	225-229
32788915-8	2020	Molecular docking was also performed to investigate the interaction between NaB and LHX1.	nab	76-79	LIM homeobox 1	Homo sapiens	84-88
32788915-9	2020	Based on Real-time-PCR results, the concentration of 150 mM of NaB after 24 hours in HT-29 and HCT-116 cell lines caused a significant reduction in mRNA expression of HDAC8 (P<0.05).	nab	63-66	histone deacetylase 8	Homo sapiens	167-172
32788915-12	2020	Our results also showed that NaB bonded strongly to LHX1.	nab	29-32	LIM homeobox 1	Homo sapiens	52-56
32812944-6	2020	Results: Supplementation with NaB significantly reduced (p < 0.05) fatty acid synthase (Fas) gene expression and increased the expression of the carnitine palmitoyltransferase 1alpha (Cpt1a) gene, resulting in reduced triacylglycerol content in the livers of rats refed the NaB diet compared with controls at 24 h after the start of refeeding.	nab	30-33	fatty acid synthase	Rattus norvegicus	67-86
32812944-6	2020	Results: Supplementation with NaB significantly reduced (p < 0.05) fatty acid synthase (Fas) gene expression and increased the expression of the carnitine palmitoyltransferase 1alpha (Cpt1a) gene, resulting in reduced triacylglycerol content in the livers of rats refed the NaB diet compared with controls at 24 h after the start of refeeding.	nab	30-33	fatty acid synthase	Rattus norvegicus	88-91
32812944-6	2020	Results: Supplementation with NaB significantly reduced (p < 0.05) fatty acid synthase (Fas) gene expression and increased the expression of the carnitine palmitoyltransferase 1alpha (Cpt1a) gene, resulting in reduced triacylglycerol content in the livers of rats refed the NaB diet compared with controls at 24 h after the start of refeeding.	nab	30-33	carnitine palmitoyltransferase 1A	Rattus norvegicus	145-182
32812944-6	2020	Results: Supplementation with NaB significantly reduced (p < 0.05) fatty acid synthase (Fas) gene expression and increased the expression of the carnitine palmitoyltransferase 1alpha (Cpt1a) gene, resulting in reduced triacylglycerol content in the livers of rats refed the NaB diet compared with controls at 24 h after the start of refeeding.	nab	30-33	carnitine palmitoyltransferase 1A	Rattus norvegicus	184-189
32812944-9	2020	The acetylation levels of histone H4 around the Foxo3a gene tended to be increased (p = 0.055) by refeeding with the NaB diet.	nab	117-120	histone cluster 2, H4	Rattus norvegicus	26-36
32812944-9	2020	The acetylation levels of histone H4 around the Foxo3a gene tended to be increased (p = 0.055) by refeeding with the NaB diet.	nab	117-120	forkhead box O3	Rattus norvegicus	48-54
32635160-3	2020	Here we report that titers of the E06 NAb are selectively increased several-fold in Cd1d-deficient mice, whereas total IgM and IgM antibodies recognizing other oxidation specific epitopes such as in malondialdehyde-modified LDL (MDA-LDL) and OxLDL were not increased.	nab	38-41	CD1d1 antigen	Mus musculus	84-88
32635160-6	2020	The CD1d-mediated regulation of the E06 NAb generation is a novel mechanism that regulates the production of this specific oxidation epitope recognizing NAb.	nab	40-43	CD1d1 antigen	Mus musculus	4-8
32555166-13	2020	In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment.	nab	36-39	cytochrome b-245 beta chain	Homo sapiens	71-75
32555166-13	2020	In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment.	nab	36-39	superoxide dismutase 1	Homo sapiens	92-96
32555166-13	2020	In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment.	nab	36-39	H3 histone pseudogene 16	Homo sapiens	113-116
32555166-13	2020	In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment.	nab	36-39	NFE2 like bZIP transcription factor 2	Homo sapiens	117-121
32555166-13	2020	In conclusion, we demonstrated that NaB prevents excessive ROS through NOX2 suppression and SOD1 upregulation by p21/NRF2 pathway, which is critical for inhibiting BACE1-dependent amyloidogenesis in neuronal cells exposed to high cholesterol environment.	nab	36-39	beta-secretase 1	Homo sapiens	164-169
32555166-6	2020	We showed that NaB decreased the expression levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and Abeta accumulation induced by high cholesterol in SK-N-MC cells.	nab	15-18	beta-secretase 1	Homo sapiens	109-114
32555166-6	2020	We showed that NaB decreased the expression levels of beta-site amyloid precursor protein cleaving enzyme 1 (BACE1) and Abeta accumulation induced by high cholesterol in SK-N-MC cells.	nab	15-18	amyloid beta precursor protein	Homo sapiens	120-125
32555166-7	2020	We demonstrated that NaB was absorbed in cells through sodium-coupled monocarboxylate transporter 1 (SMCT1) and then inhibited high cholesterol-induced Abeta accumulation.	nab	21-24	solute carrier family 5 member 8	Homo sapiens	55-99
32555166-7	2020	We demonstrated that NaB was absorbed in cells through sodium-coupled monocarboxylate transporter 1 (SMCT1) and then inhibited high cholesterol-induced Abeta accumulation.	nab	21-24	solute carrier family 5 member 8	Homo sapiens	101-106
32555166-7	2020	We demonstrated that NaB was absorbed in cells through sodium-coupled monocarboxylate transporter 1 (SMCT1) and then inhibited high cholesterol-induced Abeta accumulation.	nab	21-24	amyloid beta precursor protein	Homo sapiens	152-157
32555166-9	2020	Meanwhile, NaB decreased NOX2 levels through a reduction of NF-kappaB activity, which ultimately inhibited Abeta accumulation caused by high cholesterol.	nab	11-14	cytochrome b-245 beta chain	Homo sapiens	25-29
32555166-9	2020	Meanwhile, NaB decreased NOX2 levels through a reduction of NF-kappaB activity, which ultimately inhibited Abeta accumulation caused by high cholesterol.	nab	11-14	nuclear factor kappa B subunit 1	Homo sapiens	60-69
32555166-9	2020	Meanwhile, NaB decreased NOX2 levels through a reduction of NF-kappaB activity, which ultimately inhibited Abeta accumulation caused by high cholesterol.	nab	11-14	amyloid beta precursor protein	Homo sapiens	107-112
32555166-10	2020	We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization.	nab	21-24	H3 histone pseudogene 16	Homo sapiens	60-63
32555166-10	2020	We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization.	nab	21-24	H3 histone pseudogene 16	Homo sapiens	104-107
32555166-10	2020	We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization.	nab	21-24	NFE2 like bZIP transcription factor 2	Homo sapiens	108-112
32555166-10	2020	We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization.	nab	21-24	NFE2 like bZIP transcription factor 2	Homo sapiens	114-157
32555166-10	2020	We demonstrated that NaB increased the expression levels of p21 under high cholesterol, contributing to p21/NRF2 (Nuclear factor erythroid 2-related factor 2) colocalization, which leads to NRF2 stabilization.	nab	21-24	NFE2 like bZIP transcription factor 2	Homo sapiens	190-194
32125042-4	2020	In addition, some DOX-treated mice received an injection of anti-IL-5-neutralizing antibody (nAb), and we found that treatment with a mouse anti-IL-5 nAb significantly upregulated the levels of myocardial injury markers, aggravated cardiac dysfunction, increased M1 macrophage (Mo1) and decreased M2 macrophage (Mo2) differentiation, and promoted apoptotic marker expression.	nab	93-96	interleukin 5	Mus musculus	65-69
32459091-6	2020	In conclusion, NaB promoted the Nrf2/GSK-3beta signaling pathway and mitochondrial function, and is a potential new therapeutic strategy for obesity and osteoporosis.	nab	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	32-36
32459091-6	2020	In conclusion, NaB promoted the Nrf2/GSK-3beta signaling pathway and mitochondrial function, and is a potential new therapeutic strategy for obesity and osteoporosis.	nab	15-18	glycogen synthase kinase 3 alpha	Rattus norvegicus	37-46
32518521-5	2020	Results: Dietary fiber and sodium butyrate (NaB) decreased CRC burden by decreasing IL-6 receptor gp130 and blocking IL-6/JAK2/STAT3 axis activation in vitro and in vivo.	nab	44-47	interleukin 6	Mus musculus	84-88
32518521-5	2020	Results: Dietary fiber and sodium butyrate (NaB) decreased CRC burden by decreasing IL-6 receptor gp130 and blocking IL-6/JAK2/STAT3 axis activation in vitro and in vivo.	nab	44-47	interleukin 6 signal transducer	Mus musculus	98-103
32518521-5	2020	Results: Dietary fiber and sodium butyrate (NaB) decreased CRC burden by decreasing IL-6 receptor gp130 and blocking IL-6/JAK2/STAT3 axis activation in vitro and in vivo.	nab	44-47	interleukin 6	Mus musculus	117-121
32518521-5	2020	Results: Dietary fiber and sodium butyrate (NaB) decreased CRC burden by decreasing IL-6 receptor gp130 and blocking IL-6/JAK2/STAT3 axis activation in vitro and in vivo.	nab	44-47	Janus kinase 2	Mus musculus	122-126
32518521-5	2020	Results: Dietary fiber and sodium butyrate (NaB) decreased CRC burden by decreasing IL-6 receptor gp130 and blocking IL-6/JAK2/STAT3 axis activation in vitro and in vivo.	nab	44-47	signal transducer and activator of transcription 3	Mus musculus	127-132
32518521-6	2020	Furthermore, NaB reduced the gp130 protein level by regulating its degradation rate via targeting TRAF5.	nab	13-16	interleukin 6 signal transducer	Mus musculus	29-34
32518521-6	2020	Furthermore, NaB reduced the gp130 protein level by regulating its degradation rate via targeting TRAF5.	nab	13-16	TNF receptor-associated factor 5	Mus musculus	98-103
32459091-4	2020	In particular, NaB promoted the activity of mitochondrial antioxidant enzymes and energy metabolism, preserved bone microstructure and calcium homeostasis, and activated bone metabolism, as shown by increased Nrf2/GSK-3beta signaling and the upregulation of PGC-1alpha and TFAM.	nab	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	209-213
32459091-4	2020	In particular, NaB promoted the activity of mitochondrial antioxidant enzymes and energy metabolism, preserved bone microstructure and calcium homeostasis, and activated bone metabolism, as shown by increased Nrf2/GSK-3beta signaling and the upregulation of PGC-1alpha and TFAM.	nab	15-18	glycogen synthase kinase 3 alpha	Rattus norvegicus	214-223
32459091-4	2020	In particular, NaB promoted the activity of mitochondrial antioxidant enzymes and energy metabolism, preserved bone microstructure and calcium homeostasis, and activated bone metabolism, as shown by increased Nrf2/GSK-3beta signaling and the upregulation of PGC-1alpha and TFAM.	nab	15-18	PPARG coactivator 1 alpha	Rattus norvegicus	258-268
32459091-4	2020	In particular, NaB promoted the activity of mitochondrial antioxidant enzymes and energy metabolism, preserved bone microstructure and calcium homeostasis, and activated bone metabolism, as shown by increased Nrf2/GSK-3beta signaling and the upregulation of PGC-1alpha and TFAM.	nab	15-18	transcription factor A, mitochondrial	Rattus norvegicus	273-277
32125042-4	2020	In addition, some DOX-treated mice received an injection of anti-IL-5-neutralizing antibody (nAb), and we found that treatment with a mouse anti-IL-5 nAb significantly upregulated the levels of myocardial injury markers, aggravated cardiac dysfunction, increased M1 macrophage (Mo1) and decreased M2 macrophage (Mo2) differentiation, and promoted apoptotic marker expression.	nab	93-96	interleukin 5	Mus musculus	145-149
32125042-5	2020	Furthermore, the effect of mouse IL-5 nAb on DOX-induced Mo differentiation and its role on mouse cardiomyocyte (MCM) cells apoptosis were detected in vitro, and the results exhibited that mouse IL-5 nAb promoted Mo1 differentiation but inhibited Mo2 differentiation in vitro and alleviated apoptosis in MCM cells.	nab	38-41	interleukin 5	Mus musculus	33-37
32125042-5	2020	Furthermore, the effect of mouse IL-5 nAb on DOX-induced Mo differentiation and its role on mouse cardiomyocyte (MCM) cells apoptosis were detected in vitro, and the results exhibited that mouse IL-5 nAb promoted Mo1 differentiation but inhibited Mo2 differentiation in vitro and alleviated apoptosis in MCM cells.	nab	38-41	interleukin 5	Mus musculus	195-199
32125042-5	2020	Furthermore, the effect of mouse IL-5 nAb on DOX-induced Mo differentiation and its role on mouse cardiomyocyte (MCM) cells apoptosis were detected in vitro, and the results exhibited that mouse IL-5 nAb promoted Mo1 differentiation but inhibited Mo2 differentiation in vitro and alleviated apoptosis in MCM cells.	nab	200-203	interleukin 5	Mus musculus	33-37
32125042-5	2020	Furthermore, the effect of mouse IL-5 nAb on DOX-induced Mo differentiation and its role on mouse cardiomyocyte (MCM) cells apoptosis were detected in vitro, and the results exhibited that mouse IL-5 nAb promoted Mo1 differentiation but inhibited Mo2 differentiation in vitro and alleviated apoptosis in MCM cells.	nab	200-203	interleukin 5	Mus musculus	195-199
32125042-6	2020	Our results found a mouse anti-IL-5 nAb-aggravated DOX-induced cardiac injury and dysfunction by alleviating the inflammatory response and myocardial cell apoptosis.	nab	36-39	interleukin 5	Mus musculus	31-35
32273207-0	2020	Effectiveness and Tolerability of Nab-paclitaxel in Younger versus Elderly Patients With Metastatic HR-positive/HER2-negative Breast Cancer: Results From the Noninterventional, Prospective Study NABUCCO.	nab	34-37	erb-b2 receptor tyrosine kinase 2	Homo sapiens	112-116
32547098-2	2020	However, the role of thioredoxin-1 (Trx-1) in NaB-induced anti-tumor effect has not been completely clarified.	nab	46-49	thioredoxin	Homo sapiens	21-34
32273207-9	2020	CONCLUSION: Treatment with nab-paclitaxel in first- or further-line of metastatic HR-positive/HER2-negative breast cancer resulted in similar effectiveness and safety, irrespective of age.	nab	27-30	erb-b2 receptor tyrosine kinase 2	Homo sapiens	94-98
32056089-6	2020	The HDAC inhibitor (HDACi) NaB reduced cell viability and expression of BMI1 and CD133 and increased acetylation in human MB cells.	nab	27-30	histone deacetylase 9	Homo sapiens	4-8
32056089-6	2020	The HDAC inhibitor (HDACi) NaB reduced cell viability and expression of BMI1 and CD133 and increased acetylation in human MB cells.	nab	27-30	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	72-76
32056089-6	2020	The HDAC inhibitor (HDACi) NaB reduced cell viability and expression of BMI1 and CD133 and increased acetylation in human MB cells.	nab	27-30	prominin 1	Homo sapiens	81-86
32056089-8	2020	MAPK/ERK inhibition reduced expression of the stemness markers, hindered MB neurosphere formation, and its antiproliferative effect was enhanced by combination with NaB.	nab	165-168	mitogen-activated protein kinase 1	Homo sapiens	5-8
32548230-2	2020	SPARC overexpression occurs in multiple tumors including pancreatic ductal adenocarcinoma (PDAC) and may predict favorable response to nab-paclitaxel.	nab	135-138	secreted protein acidic and cysteine rich	Homo sapiens	0-5
32547098-2	2020	However, the role of thioredoxin-1 (Trx-1) in NaB-induced anti-tumor effect has not been completely clarified.	nab	46-49	thioredoxin	Homo sapiens	36-41
32547098-9	2020	Results: NaB treatment significantly inhibited cell growth and decreased Trx-1 protein expression in CRC cells but not in normal colon epithelial cells.	nab	9-12	thioredoxin	Homo sapiens	73-78
32547098-12	2020	Moreover, downregulation of Trx-1 significantly enhanced NaB-induced inhibitory effects on cell growth and migration, whereas overexpression of Trx-1 attenuated NaB-induced inhibitory effects on growth and migration in CRC cells.	nab	57-60	thioredoxin	Homo sapiens	28-33
32547098-12	2020	Moreover, downregulation of Trx-1 significantly enhanced NaB-induced inhibitory effects on cell growth and migration, whereas overexpression of Trx-1 attenuated NaB-induced inhibitory effects on growth and migration in CRC cells.	nab	161-164	thioredoxin	Homo sapiens	144-149
32547098-13	2020	Conclusion: These findings indicate that the NaB-mediated anti-tumor effects on CRC cells are related to downregulation of Trx-1.	nab	45-48	thioredoxin	Homo sapiens	123-128
32377164-5	2020	The results showed that 2 mM NaB had a significant improvement effect on Abeta-induced N2a cell injury, by increasing cell viability and reducing ROS to reduce injury.	nab	29-32	amyloid beta (A4) precursor protein	Mus musculus	73-78
32408327-6	2020	Chemotherapy using nab-PTX plus CBDCA plus pembrolizumab may become one of the therapeutic choices for the recurrence after operation of an elderly person with squamous cell lung carcinoma and low PD-L1 expression.	nab	19-22	CD274 molecule	Homo sapiens	197-202
32534510-7	2020	NaB treatment of Mtb-stimulated splenocytes derived from arthritic rats resulted in significant increases in the gene expressions of Tregs-related cytokines (IL-10 and TGF-beta) and Foxp3 transcription factor, and significant decreases in the expression of Th1-related cytokines (TNF-alpha and IFN-gamma) and the T-bet transcription factor.	nab	0-3	interleukin 10	Rattus norvegicus	158-163
32534510-7	2020	NaB treatment of Mtb-stimulated splenocytes derived from arthritic rats resulted in significant increases in the gene expressions of Tregs-related cytokines (IL-10 and TGF-beta) and Foxp3 transcription factor, and significant decreases in the expression of Th1-related cytokines (TNF-alpha and IFN-gamma) and the T-bet transcription factor.	nab	0-3	transforming growth factor alpha	Rattus norvegicus	168-176
32534510-7	2020	NaB treatment of Mtb-stimulated splenocytes derived from arthritic rats resulted in significant increases in the gene expressions of Tregs-related cytokines (IL-10 and TGF-beta) and Foxp3 transcription factor, and significant decreases in the expression of Th1-related cytokines (TNF-alpha and IFN-gamma) and the T-bet transcription factor.	nab	0-3	forkhead box P3	Rattus norvegicus	182-187
32534510-7	2020	NaB treatment of Mtb-stimulated splenocytes derived from arthritic rats resulted in significant increases in the gene expressions of Tregs-related cytokines (IL-10 and TGF-beta) and Foxp3 transcription factor, and significant decreases in the expression of Th1-related cytokines (TNF-alpha and IFN-gamma) and the T-bet transcription factor.	nab	0-3	tumor necrosis factor	Rattus norvegicus	280-289
32534510-7	2020	NaB treatment of Mtb-stimulated splenocytes derived from arthritic rats resulted in significant increases in the gene expressions of Tregs-related cytokines (IL-10 and TGF-beta) and Foxp3 transcription factor, and significant decreases in the expression of Th1-related cytokines (TNF-alpha and IFN-gamma) and the T-bet transcription factor.	nab	0-3	interferon gamma	Rattus norvegicus	294-303
32426048-7	2020	Results: Our results demonstrated that atezolizumab plus nab-paclitaxel augmented versus nab-paclitaxel therapy cost $104,278 and $149,465 and yielded an additional 0.371 and 0.762 of quality-adjusted life year (QALY) in in all patients with unknown PD-L1 status and subpopulation with PD-L1-positive, respectively, which led to an ICER of $281,448 and $196,073 per QALY gained.	nab	57-60	CD274 molecule	Homo sapiens	250-255
32426048-7	2020	Results: Our results demonstrated that atezolizumab plus nab-paclitaxel augmented versus nab-paclitaxel therapy cost $104,278 and $149,465 and yielded an additional 0.371 and 0.762 of quality-adjusted life year (QALY) in in all patients with unknown PD-L1 status and subpopulation with PD-L1-positive, respectively, which led to an ICER of $281,448 and $196,073 per QALY gained.	nab	57-60	CD274 molecule	Homo sapiens	286-291
32426048-11	2020	Conclusion: The atezolizumab plus nab-paclitaxel treatment is likely to be a cost-effective option compared with chemotherapy based on nab-paclitaxel for the patients with PD-L1-positive advanced TNBC.	nab	34-37	CD274 molecule	Homo sapiens	172-177
32408327-0	2020	[A Case of Squamous Cell Lung Cancer in an Elderly Patient with Low PD-L1 Expression Effectively Treated with Nab-Paclitaxel(Nab-PTX)plus Carboplatin (CBDCA)plus Pembrolizumab for a Recurrence after Operation].	nab	110-113	CD274 molecule	Homo sapiens	68-73
32752588-1	2020	The aim of this study was to elucidate the neuronal protection effect of sodium butyrate (NaB) on neuronal apoptosis in rats with cerebral infarction (CI), and the involvement of the phosphatidilinositol 3-kinase/protein kinase B (PI3K/Akt) and extracellular-signal-regulated kinase 1/2 (ERK1/2) pathways.	nab	90-93	AKT serine/threonine kinase 1	Rattus norvegicus	236-239
32752588-1	2020	The aim of this study was to elucidate the neuronal protection effect of sodium butyrate (NaB) on neuronal apoptosis in rats with cerebral infarction (CI), and the involvement of the phosphatidilinositol 3-kinase/protein kinase B (PI3K/Akt) and extracellular-signal-regulated kinase 1/2 (ERK1/2) pathways.	nab	90-93	mitogen activated protein kinase 3	Rattus norvegicus	245-286
32752588-1	2020	The aim of this study was to elucidate the neuronal protection effect of sodium butyrate (NaB) on neuronal apoptosis in rats with cerebral infarction (CI), and the involvement of the phosphatidilinositol 3-kinase/protein kinase B (PI3K/Akt) and extracellular-signal-regulated kinase 1/2 (ERK1/2) pathways.	nab	90-93	mitogen activated protein kinase 3	Rattus norvegicus	288-294
32752588-9	2020	In addition, NaB treatment dose-dependently reduced apoptotic rate and Bax level, as well as enhanced Bcl-2 level.	nab	13-16	BCL2 associated X, apoptosis regulator	Rattus norvegicus	71-74
32752588-9	2020	In addition, NaB treatment dose-dependently reduced apoptotic rate and Bax level, as well as enhanced Bcl-2 level.	nab	13-16	BCL2, apoptosis regulator	Rattus norvegicus	102-107
32752588-10	2020	Protein levels of Akt and ERK1/2 were markedly upregulated in NaB-treated neurons.	nab	62-65	AKT serine/threonine kinase 1	Rattus norvegicus	18-21
32752588-10	2020	Protein levels of Akt and ERK1/2 were markedly upregulated in NaB-treated neurons.	nab	62-65	mitogen activated protein kinase 3	Rattus norvegicus	26-32
32752588-11	2020	NaB treatment alleviates neuronal apoptosis via the PI3K/Akt and ERK1/2 pathways in CI rats, thus protecting the deterioration of CI.	nab	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	57-60
32752588-11	2020	NaB treatment alleviates neuronal apoptosis via the PI3K/Akt and ERK1/2 pathways in CI rats, thus protecting the deterioration of CI.	nab	0-3	mitogen activated protein kinase 3	Rattus norvegicus	65-71
32109532-10	2020	Concomitantly, BDNF and TrkB expression, which was decreased by sevoflurane, was also restored by NaB.	nab	98-101	brain derived neurotrophic factor	Mus musculus	15-19
32109532-10	2020	Concomitantly, BDNF and TrkB expression, which was decreased by sevoflurane, was also restored by NaB.	nab	98-101	neurotrophic tyrosine kinase, receptor, type 2	Mus musculus	24-28
32377164-6	2020	In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF.	nab	48-51	tensin 2	Mus musculus	110-113
32377164-6	2020	In addition, by acting on the GPR109A receptor, NaB regulates the expression of AD-related genes such as APP, NEP, and BDNF.	nab	48-51	brain derived neurotrophic factor	Mus musculus	119-123
32377164-7	2020	Therefore, NaB protects N2a cells from Abeta-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.	nab	11-14	amyloid beta (A4) precursor protein	Mus musculus	39-44
32377164-7	2020	Therefore, NaB protects N2a cells from Abeta-induced cell damage through activating GPR109A, which provides an innovative idea for the treatment of AD.	nab	11-14	hydroxycarboxylic acid receptor 2	Mus musculus	84-91
32124940-1	2020	Our previous study demonstrated that intranasal administration of histone deacetylase inhibitor sodium butyrate (NaB) exhibits therapeutic effects on a mouse model of allergic rhinitis (AR).	nab	113-116	ferredoxin reductase	Mus musculus	186-188
32313566-0	2020	The AST/ALT (De Ritis) ratio predicts clinical outcome in patients with pancreatic cancer treated with first-line nab-paclitaxel and gemcitabine: post hoc analysis of an Austrian multicenter, noninterventional study.	nab	114-117	solute carrier family 17 member 5	Homo sapiens	4-11
32313566-3	2020	In the present study we investigated the AST/ALT ratio as a possible predictor of treatment response and disease outcome in patients with advanced PDAC treated with first-line gemcitabine/nab-paclitaxel.	nab	188-191	solute carrier family 17 member 5	Homo sapiens	41-44
32313566-10	2020	Conclusions: The pretreatment serum AST/ALT ratio predicts poor disease outcome and response rate in patients with advanced PDAC treated with gemcitabine/nab-paclitaxel and might represent a novel and inexpensive marker for individual risk assessment in the treatment of pancreatic cancer.	nab	154-157	solute carrier family 17 member 5	Homo sapiens	36-39
32124940-2	2020	However, whether NaB is effective on AR when administered orally and prophylactically, as well as its potential effects on gene expression, remained unknown.	nab	17-20	ferredoxin reductase	Mus musculus	37-39
32124940-8	2020	NaB exhibited a preventive effect in the murine AR model, diminished the increases in histone deacetylase 1 (HDAC1) and HDAC8 expression and increased OVA-induced acetylation of histone H3 at lysine 9.	nab	0-3	ferredoxin reductase	Mus musculus	48-50
32124940-8	2020	NaB exhibited a preventive effect in the murine AR model, diminished the increases in histone deacetylase 1 (HDAC1) and HDAC8 expression and increased OVA-induced acetylation of histone H3 at lysine 9.	nab	0-3	histone deacetylase 1	Mus musculus	86-107
32124940-8	2020	NaB exhibited a preventive effect in the murine AR model, diminished the increases in histone deacetylase 1 (HDAC1) and HDAC8 expression and increased OVA-induced acetylation of histone H3 at lysine 9.	nab	0-3	histone deacetylase 1	Mus musculus	109-114
32124940-8	2020	NaB exhibited a preventive effect in the murine AR model, diminished the increases in histone deacetylase 1 (HDAC1) and HDAC8 expression and increased OVA-induced acetylation of histone H3 at lysine 9.	nab	0-3	histone deacetylase 8	Mus musculus	120-125
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	ferredoxin reductase	Mus musculus	31-33
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	interleukin 2	Mus musculus	63-76
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	interleukin 2	Mus musculus	78-82
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	interferon gamma	Mus musculus	85-111
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	interleukin 4	Mus musculus	144-148
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	interleukin 5	Mus musculus	150-154
32124940-9	2020	In addition, NaB increased the AR-associated low expression of interleukin 2 (IL-2), interferon gamma and IL-17 and decreased the expression of IL-4, IL-5 and transforming growth factor beta1.	nab	13-16	transforming growth factor, beta 1	Mus musculus	159-191
32124940-12	2020	Thus, NaB may exhibit a preventive effect on AR.	nab	6-9	ferredoxin reductase	Mus musculus	45-47
32259780-2	2020	This report describes a patient with HER2-positive metastatic breast cancer with an exceptional response to trastuzumab and nab-paclitaxel who remains in complete remission several years after cessation of therapy.	nab	124-127	erb-b2 receptor tyrosine kinase 2	Homo sapiens	37-41
32129476-2	2020	Patients with metastatic or locally advanced TNBC with PD-L1 expression on immune cells occupying >=1% of tumor area demonstrated survival benefit with the addition of atezolizumab to nab-paclitaxel.	nab	184-187	CD274 molecule	Homo sapiens	55-60
31904405-2	2020	Sodium butyrate (NaB) has been reported to improve glucose homeostasis by modulation of the p38/ERK MAPK pathway.	nab	17-20	mitogen activated protein kinase 14	Rattus norvegicus	92-95
32265874-2	2020	It has been found that sodium butyrate (NaB), the inhibitor of histone deacetylase, can promote the expression of cathelicidin (LL37) and help the body to resist a variety of injuries.	nab	40-43	cathelicidin antimicrobial peptide	Homo sapiens	128-132
32265874-4	2020	We found an increased expression of LL37 in M. bovis infected THP-1 cells after NaB treatment.	nab	80-83	cathelicidin antimicrobial peptide	Homo sapiens	36-40
32265874-7	2020	Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1beta, TNF-alpha, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis.	nab	27-30	interleukin 1 alpha	Homo sapiens	91-99
32265874-7	2020	Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1beta, TNF-alpha, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis.	nab	27-30	tumor necrosis factor	Homo sapiens	101-110
32265874-7	2020	Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1beta, TNF-alpha, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis.	nab	27-30	interleukin 10	Homo sapiens	116-121
32265874-7	2020	Furthermore, we found that NaB treatment reduced the production of inflammatory cytokines (IL-1beta, TNF-alpha, and IL-10) and a key anti-apoptotic marker protein Bcl-2 in THP-1 cell infected with M. bovis.	nab	27-30	BCL2 apoptosis regulator	Homo sapiens	163-168
32265874-9	2020	The reduction of viable M. bovis bacilli indicates that NaB-induced inhibition of M. bovis infection mediated by upregulation of LL37 and inhibition of NF-kappaB signaling pathway.	nab	56-59	cathelicidin antimicrobial peptide	Homo sapiens	129-133
32521853-1	2020	PURPOSE: This study aimed to investigate the efficacy of albumin-bound paclitaxel (nab-paclitaxel) in the treatment of advanced refractory breast cancer (BC) and its effect on serum resistin.	nab	83-86	albumin	Homo sapiens	57-64
32521853-1	2020	PURPOSE: This study aimed to investigate the efficacy of albumin-bound paclitaxel (nab-paclitaxel) in the treatment of advanced refractory breast cancer (BC) and its effect on serum resistin.	nab	83-86	resistin	Homo sapiens	182-190
32521853-9	2020	CONCLUSION: The results indicated that nab-paclitaxel is very effective in treating advanced refractory BC and reduces the level of serum resistin.	nab	39-42	resistin	Homo sapiens	138-146
32218821-0	2020	The pathological complete response and secreted protein acidic and rich in cysteine expression in patients with breast cancer receiving neoadjuvant nab-paclitaxel chemotherapy.	nab	148-151	secreted protein acidic and cysteine rich	Homo sapiens	39-83
31119640-9	2020	Finally, expression levels of Hippo pathway kinases Lats2, MST1, and scaffold protein Sav1 were reduced in these cells, suggesting a possible link between Hippo pathway-dependent downregulation of PPARgamma and the NaB/F68 treatment.	nab	215-218	large tumor suppressor kinase 2	Homo sapiens	52-57
31119640-9	2020	Finally, expression levels of Hippo pathway kinases Lats2, MST1, and scaffold protein Sav1 were reduced in these cells, suggesting a possible link between Hippo pathway-dependent downregulation of PPARgamma and the NaB/F68 treatment.	nab	215-218	macrophage stimulating 1	Homo sapiens	59-63
31119640-9	2020	Finally, expression levels of Hippo pathway kinases Lats2, MST1, and scaffold protein Sav1 were reduced in these cells, suggesting a possible link between Hippo pathway-dependent downregulation of PPARgamma and the NaB/F68 treatment.	nab	215-218	salvador family WW domain containing protein 1	Homo sapiens	86-90
31119640-9	2020	Finally, expression levels of Hippo pathway kinases Lats2, MST1, and scaffold protein Sav1 were reduced in these cells, suggesting a possible link between Hippo pathway-dependent downregulation of PPARgamma and the NaB/F68 treatment.	nab	215-218	peroxisome proliferator activated receptor gamma	Homo sapiens	197-206
31562256-10	2020	In vivo, LY2090314 plus nab-paclitaxel significantly prolonged mice survival duration.Our study demonstrates a unique role for TAK1 in controlling YAP/TAZ in pancreatic cancer.	nab	24-27	mitogen-activated protein kinase kinase kinase 7	Mus musculus	127-131
31162838-9	2020	For nab-pac/gem, angiogenesis genes were negatively associated with pCR (ANGPTL4: p = 0.05; FGFR4: p = 0.02; VEGFA: p = 0.03).	nab	4-7	angiopoietin like 4	Homo sapiens	73-80
31162838-9	2020	For nab-pac/gem, angiogenesis genes were negatively associated with pCR (ANGPTL4: p = 0.05; FGFR4: p = 0.02; VEGFA: p = 0.03).	nab	4-7	fibroblast growth factor receptor 4	Homo sapiens	92-97
31162838-9	2020	For nab-pac/gem, angiogenesis genes were negatively associated with pCR (ANGPTL4: p = 0.05; FGFR4: p = 0.02; VEGFA: p = 0.03).	nab	4-7	vascular endothelial growth factor A	Homo sapiens	109-114
31836471-7	2020	Interestingly, we found that sodium butyrate (NaB) increases alpha-Synuclein mRNA expression, enhances Atg5-mediated autophagy (increased LC3B-II and decreased SQSTM1 (also known as p62) expression) in murine neuroendocrine STC-1 cells.	nab	46-49	synuclein, alpha	Mus musculus	61-76
31836471-7	2020	Interestingly, we found that sodium butyrate (NaB) increases alpha-Synuclein mRNA expression, enhances Atg5-mediated autophagy (increased LC3B-II and decreased SQSTM1 (also known as p62) expression) in murine neuroendocrine STC-1 cells.	nab	46-49	autophagy related 5	Mus musculus	103-107
31836471-7	2020	Interestingly, we found that sodium butyrate (NaB) increases alpha-Synuclein mRNA expression, enhances Atg5-mediated autophagy (increased LC3B-II and decreased SQSTM1 (also known as p62) expression) in murine neuroendocrine STC-1 cells.	nab	46-49	sequestosome 1	Mus musculus	160-166
31836471-7	2020	Interestingly, we found that sodium butyrate (NaB) increases alpha-Synuclein mRNA expression, enhances Atg5-mediated autophagy (increased LC3B-II and decreased SQSTM1 (also known as p62) expression) in murine neuroendocrine STC-1 cells.	nab	46-49	sequestosome 1	Mus musculus	182-185
31836471-9	2020	Moreover, the PI3K/Akt/mTOR pathway was significantly inhibited and cell apoptosis was activated by NaB.	nab	100-103	AKT serine/threonine kinase 1	Homo sapiens	19-22
31836471-9	2020	Moreover, the PI3K/Akt/mTOR pathway was significantly inhibited and cell apoptosis was activated by NaB.	nab	100-103	mechanistic target of rapamycin kinase	Homo sapiens	23-27
31836471-11	2020	Collectively, NaB causes alpha-Synuclein degradation by an Atg5-dependent and PI3K/Akt/mTOR-related autophagy pathway.	nab	14-17	synuclein alpha	Homo sapiens	25-40
31836471-11	2020	Collectively, NaB causes alpha-Synuclein degradation by an Atg5-dependent and PI3K/Akt/mTOR-related autophagy pathway.	nab	14-17	autophagy related 5	Homo sapiens	59-63
31836471-11	2020	Collectively, NaB causes alpha-Synuclein degradation by an Atg5-dependent and PI3K/Akt/mTOR-related autophagy pathway.	nab	14-17	AKT serine/threonine kinase 1	Homo sapiens	83-86
31836471-11	2020	Collectively, NaB causes alpha-Synuclein degradation by an Atg5-dependent and PI3K/Akt/mTOR-related autophagy pathway.	nab	14-17	mechanistic target of rapamycin kinase	Homo sapiens	87-91
32095126-5	2020	The patient responded to gemcitabine plus nab-paclitaxel in terms of elimination of tumor cells from the CSF and concurrent clinical improvement for 3 months.	nab	42-45	colony stimulating factor 2	Homo sapiens	105-108
31562256-10	2020	In vivo, LY2090314 plus nab-paclitaxel significantly prolonged mice survival duration.Our study demonstrates a unique role for TAK1 in controlling YAP/TAZ in pancreatic cancer.	nab	24-27	yes-associated protein 1	Mus musculus	147-150
31562256-10	2020	In vivo, LY2090314 plus nab-paclitaxel significantly prolonged mice survival duration.Our study demonstrates a unique role for TAK1 in controlling YAP/TAZ in pancreatic cancer.	nab	24-27	tafazzin, phospholipid-lysophospholipid transacylase	Mus musculus	151-154
31119595-4	2019	This study underlines the importance of sodium benzoate (NaB), a metabolite of commonly-used spice cinnamon, a food-additive and an FDA-approved drug against hyperammonemia, in stimulating GDNF in primary mouse and human astrocytes.	nab	57-60	glial cell line derived neurotrophic factor	Mus musculus	189-193
31856090-0	2020	ATM-Mutated Pancreatic Cancer: Clinical and Molecular Response to Gemcitabine/Nab-Paclitaxel After Genome-Based Therapy Resistance.	nab	78-81	ATM serine/threonine kinase	Homo sapiens	0-3
31612909-10	2019	In the PD-L1-positive subgroup, median PFS was 10.8 months (atezo + nab-P) versus 3.8 months (plac + nab-P; HR, 0.04; 95% CI, <0.01-0.35).	nab	68-71	CD274 molecule	Homo sapiens	7-12
31839159-6	2019	Combination of atezolizumab with nab-paclitaxel in a phase III study has recently seen success in terms of improved progression free and overall survival for the PD-L1 -positive population of metastatic TNBC in the first line/newly relapsed setting [3].	nab	33-36	CD274 molecule	Homo sapiens	162-167
31473434-8	2019	Effect of NaB on LDH release and PI positive cells was further enhanced by inhibiting caspase 1-GSDMD.	nab	10-13	caspase 1	Homo sapiens	86-95
31473434-8	2019	Effect of NaB on LDH release and PI positive cells was further enhanced by inhibiting caspase 1-GSDMD.	nab	10-13	gasdermin D	Homo sapiens	96-101
31473434-9	2019	In addition, high glucose-induced nuclear factor kappa-B (NF-kappaB)/NF-kappaB inhibitor alpha (IkappaB-alpha) signaling pathway was reversed by NaB or A-Y-C administration.	nab	145-148	nuclear factor kappa B subunit 1	Homo sapiens	34-56
31473434-9	2019	In addition, high glucose-induced nuclear factor kappa-B (NF-kappaB)/NF-kappaB inhibitor alpha (IkappaB-alpha) signaling pathway was reversed by NaB or A-Y-C administration.	nab	145-148	nuclear factor kappa B subunit 1	Homo sapiens	58-67
31473434-9	2019	In addition, high glucose-induced nuclear factor kappa-B (NF-kappaB)/NF-kappaB inhibitor alpha (IkappaB-alpha) signaling pathway was reversed by NaB or A-Y-C administration.	nab	145-148	NFKB inhibitor alpha	Homo sapiens	69-94
31473434-9	2019	In addition, high glucose-induced nuclear factor kappa-B (NF-kappaB)/NF-kappaB inhibitor alpha (IkappaB-alpha) signaling pathway was reversed by NaB or A-Y-C administration.	nab	145-148	NFKB inhibitor alpha	Homo sapiens	96-109
31473434-10	2019	In conclusion, NaB could ameliorate high-glucose induced GECs via caspase1-GSDMD canonical pyroptosis pathway; and NF-kappaB/IkappaB-alpha signaling pathway was involved in it.	nab	15-18	caspase 1	Homo sapiens	66-74
31473434-10	2019	In conclusion, NaB could ameliorate high-glucose induced GECs via caspase1-GSDMD canonical pyroptosis pathway; and NF-kappaB/IkappaB-alpha signaling pathway was involved in it.	nab	15-18	gasdermin D	Homo sapiens	75-80
31477168-2	2019	Dual HER2 blockade with ado-trastuzumab emtansine (T-DM1) and lapatinib plus nab-paclitaxel has shown efficacy in patients with metastatic HER2-positive breast cancer.	nab	77-80	erb-b2 receptor tyrosine kinase 2	Homo sapiens	5-9
31842957-14	2019	In addition to the recently approved combination of atezolizumab and nab-paclitaxel for PD-L1-positive mTNBC, new treatments resulting in durable clinical responses, prolonged survival, and manageable safety profile would greatly benefit patients with mTNBC.	nab	69-72	CD274 molecule	Homo sapiens	88-93
31806966-14	2019	In vivo, serum OPN, BGP, and ALP levels in the NAB group of rats were increased at both 2 and 4 weeks, indicating the repair and osteogenesis generation.	nab	47-50	secreted phosphoprotein 1	Rattus norvegicus	15-18
31806966-14	2019	In vivo, serum OPN, BGP, and ALP levels in the NAB group of rats were increased at both 2 and 4 weeks, indicating the repair and osteogenesis generation.	nab	47-50	bone gamma-carboxyglutamate protein	Rattus norvegicus	20-23
31806966-14	2019	In vivo, serum OPN, BGP, and ALP levels in the NAB group of rats were increased at both 2 and 4 weeks, indicating the repair and osteogenesis generation.	nab	47-50	alkaline phosphatase, placental	Homo sapiens	29-32
31119595-5	2019	Presence of cAMP response element (CRE) in the Gdnf gene promoter, recruitment of CREB to the Gdnf promoter by NaB and abrogation of NaB-mediated GDNF expression by siRNA knockdown of CREB suggest that NaB induces the transcription of Gdnf via CREB.	nab	111-114	glial cell line derived neurotrophic factor	Mus musculus	94-98
31119595-5	2019	Presence of cAMP response element (CRE) in the Gdnf gene promoter, recruitment of CREB to the Gdnf promoter by NaB and abrogation of NaB-mediated GDNF expression by siRNA knockdown of CREB suggest that NaB induces the transcription of Gdnf via CREB.	nab	111-114	glial cell line derived neurotrophic factor	Mus musculus	94-98
31119595-5	2019	Presence of cAMP response element (CRE) in the Gdnf gene promoter, recruitment of CREB to the Gdnf promoter by NaB and abrogation of NaB-mediated GDNF expression by siRNA knockdown of CREB suggest that NaB induces the transcription of Gdnf via CREB.	nab	133-136	glial cell line derived neurotrophic factor	Mus musculus	146-150
31119595-5	2019	Presence of cAMP response element (CRE) in the Gdnf gene promoter, recruitment of CREB to the Gdnf promoter by NaB and abrogation of NaB-mediated GDNF expression by siRNA knockdown of CREB suggest that NaB induces the transcription of Gdnf via CREB.	nab	133-136	glial cell line derived neurotrophic factor	Mus musculus	146-150
31119595-6	2019	Finally, oral administration of NaB and cinnamon itself increased the level of GDNF in vivo in the substantia nigra pars compacta (SNpc) of normal as well as MPTP-intoxicated mice.	nab	32-35	glial cell line derived neurotrophic factor	Mus musculus	79-83
31119595-7	2019	Accordingly, cinnamon and NaB treatment protected tyrosine hydroxylase positive neurons in the SNpc and fibers in the striatum, normalized striatal neurotransmitters, and improved locomotor activities in MPTP-intoxicated Gfapcre mice, but not GdnfDeltaastro mice lacking GDNF in astrocytes.	nab	26-29	glial cell line derived neurotrophic factor	Mus musculus	271-275
31119595-8	2019	These findings highlight the importance of astroglial GDNF in cinnamon- and NaB-mediated protection of the nigrostriatum in MPTP mouse model of PD and suggest possible therapeutic potential of cinnamon and NaB in PD patients.	nab	76-79	glial cell line derived neurotrophic factor	Mus musculus	54-58
31164413-0	2019	The Sustained Induction of c-MYC Drives Nab-Paclitaxel Resistance in Primary Pancreatic Ductal Carcinoma Cells.	nab	40-43	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	27-32
31146004-4	2019	Sodium butyrate (NaB) and trichostatin A (TSA) increase SERCA3 mRNA expression in AS-30D cells, whereas SERCA2b mRNA expression did not change.	nab	17-20	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Rattus norvegicus	56-62
31146004-6	2019	Besides, NaB treated cells increased Sp1 and Sp3 occupancy at ATP2A3 promoter; whereas TSA treated cells showed increased p300 levels at ATP2A3 promoter.	nab	9-12	Sp3 transcription factor	Homo sapiens	45-48
31204637-3	2019	Sodium butyrate (NaB) has been shown to alleviate oxidative stress and insulin resistance, yet how Nrf2 is involved in the action of NaB remains unclear.	nab	133-136	NFE2 like bZIP transcription factor 2	Rattus norvegicus	99-103
31204637-6	2019	Additionally, the insulin signalling pathway in the liver was activated by NaB, associated with significant activation of Nrf2, superoxide dismutase and glutathione.	nab	75-78	NFE2 like bZIP transcription factor 2	Rattus norvegicus	122-126
31204637-7	2019	Furthermore, hepatic up-regulation of Nrf2 in NaB-treated rats was associated with reduced protein content of histone deacetylase 1 and increased histone H3 acetyl K9 (H3K9Ac) modification on the Nrf2 promoter.	nab	46-49	NFE2 like bZIP transcription factor 2	Rattus norvegicus	38-42
31204637-7	2019	Furthermore, hepatic up-regulation of Nrf2 in NaB-treated rats was associated with reduced protein content of histone deacetylase 1 and increased histone H3 acetyl K9 (H3K9Ac) modification on the Nrf2 promoter.	nab	46-49	histone deacetylase 1	Rattus norvegicus	110-131
31204637-7	2019	Furthermore, hepatic up-regulation of Nrf2 in NaB-treated rats was associated with reduced protein content of histone deacetylase 1 and increased histone H3 acetyl K9 (H3K9Ac) modification on the Nrf2 promoter.	nab	46-49	NFE2 like bZIP transcription factor 2	Rattus norvegicus	196-200
31204637-8	2019	The actions of NaB were completely abolished when Nrf2 was knocked down in vitro.	nab	15-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	50-54
31204637-9	2019	Taken together, NaB acts as a histone deacetylase inhibitor to up-regulate Nrf2 expression with enhanced H3K9Ac modification on its promoter.	nab	16-19	NFE2 like bZIP transcription factor 2	Rattus norvegicus	75-79
31204637-10	2019	NaB-induced Nrf2 activation stimulates transcription of downstream antioxidant enzymes, thus contributing to the amelioration of high-fat diet-induced oxidative stress and insulin resistance.	nab	0-3	NFE2 like bZIP transcription factor 2	Rattus norvegicus	12-16
31146004-6	2019	Besides, NaB treated cells increased Sp1 and Sp3 occupancy at ATP2A3 promoter; whereas TSA treated cells showed increased p300 levels at ATP2A3 promoter.	nab	9-12	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	62-68
31146004-5	2019	NaB and TSA increase H3K9ac and H3K27ac in two ATP2A3 promoter regions.	nab	0-3	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	47-53
31427887-11	2019	In addition, anti-mouse IL-18-neutralizing monoclonal antibodies (anti-IL-18 nAb) inhibited angiotensin II-induced M1 macrophage differentiation and SMC apoptosis in vitro.	nab	77-80	interleukin 18	Homo sapiens	24-29
31427887-11	2019	In addition, anti-mouse IL-18-neutralizing monoclonal antibodies (anti-IL-18 nAb) inhibited angiotensin II-induced M1 macrophage differentiation and SMC apoptosis in vitro.	nab	77-80	interleukin 18	Homo sapiens	71-76
31427887-11	2019	In addition, anti-mouse IL-18-neutralizing monoclonal antibodies (anti-IL-18 nAb) inhibited angiotensin II-induced M1 macrophage differentiation and SMC apoptosis in vitro.	nab	77-80	angiotensinogen	Homo sapiens	92-106
31011879-7	2019	Western blotting results showed that combination of QCT and NaB increased apoptosis by decreasing anti-apoptotic Bcl-2 and increasing pro-apoptotic Bax, decreasing survivin, activating caspase-3, and degrading poly (ADP-ribose) polymerase (PARP).	nab	60-63	caspase 3	Homo sapiens	185-194
31250637-4	2019	In db/db mice, we found significant hypertrophy and steatosis in hepatic lobules accompanied by reduced glycogen storage, and expression of GPR43 was significantly decreased by 59.38 +- 3.33%; NaB administration significantly increased NaB receptor G-protein coupled receptor 43 (GPR43) level and increased glycogen storage in both mice and HepG2 cells.	nab	193-196	free fatty acid receptor 2	Mus musculus	140-145
31250637-5	2019	Glucose transporter 2 (GLUT2) and sodium-glucose cotransporter 1 (SGLT1) on cell membrane were upregulated by NaB.	nab	110-113	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	0-21
31250637-5	2019	Glucose transporter 2 (GLUT2) and sodium-glucose cotransporter 1 (SGLT1) on cell membrane were upregulated by NaB.	nab	110-113	solute carrier family 2 (facilitated glucose transporter), member 2	Mus musculus	23-28
31250637-5	2019	Glucose transporter 2 (GLUT2) and sodium-glucose cotransporter 1 (SGLT1) on cell membrane were upregulated by NaB.	nab	110-113	solute carrier family 5 (sodium/glucose cotransporter), member 1	Mus musculus	34-64
31250637-5	2019	Glucose transporter 2 (GLUT2) and sodium-glucose cotransporter 1 (SGLT1) on cell membrane were upregulated by NaB.	nab	110-113	solute carrier family 5 (sodium/glucose cotransporter), member 1	Mus musculus	66-71
31250637-6	2019	The activation of intracellular signaling Protein kinase B (PKB), also known as AKT, was inhibited while glycogen synthase kinase 3 (GSK3) was activated by NaB in both in vivo and in vitro studies.	nab	156-159	glycogen synthase kinase 3 beta	Mus musculus	105-131
31250637-6	2019	The activation of intracellular signaling Protein kinase B (PKB), also known as AKT, was inhibited while glycogen synthase kinase 3 (GSK3) was activated by NaB in both in vivo and in vitro studies.	nab	156-159	glycogen synthase kinase 3 beta	Mus musculus	133-137
32042863-6	2019	Biomarkers will allow clinicians to practice a precision medicine approach in ICBs (biomarker-based patient selection) such as treating triple-negative breast cancer patients that exhibit PD-L1 staining of tumor-infiltrating immune cells in >=1% of the tumor area with nanoparticle albumin-bound (nab)-paclitaxel plus anti-PD-L1 and treating patients of MSI-H or MMR deficient unresectable or metastatic solid tumors with pembrolizumab (anti-PD-1).	nab	297-300	CD274 molecule	Homo sapiens	188-193
30979740-9	2019	An increased response to nab-paclitaxel was observed only in PIK3CAwt breast cancer, with univariate significance for the complete cohort (P = 0.009) and the TNBC (P = 0.013) and multivariate significance in the HER2pos subcohort (test for interaction P = 0.0074).	nab	25-28	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	61-65
30979740-9	2019	An increased response to nab-paclitaxel was observed only in PIK3CAwt breast cancer, with univariate significance for the complete cohort (P = 0.009) and the TNBC (P = 0.013) and multivariate significance in the HER2pos subcohort (test for interaction P = 0.0074).	nab	25-28	erb-b2 receptor tyrosine kinase 2	Homo sapiens	212-216
31011879-7	2019	Western blotting results showed that combination of QCT and NaB increased apoptosis by decreasing anti-apoptotic Bcl-2 and increasing pro-apoptotic Bax, decreasing survivin, activating caspase-3, and degrading poly (ADP-ribose) polymerase (PARP).	nab	60-63	BCL2 apoptosis regulator	Homo sapiens	113-118
31011879-7	2019	Western blotting results showed that combination of QCT and NaB increased apoptosis by decreasing anti-apoptotic Bcl-2 and increasing pro-apoptotic Bax, decreasing survivin, activating caspase-3, and degrading poly (ADP-ribose) polymerase (PARP).	nab	60-63	BCL2 associated X, apoptosis regulator	Homo sapiens	148-151
31284554-4	2019	In this study, we found that NAB suppressed the LPS-induced inflammatory responses by restraining the expression of inducible nitric oxide synthase (iNOS) proteins and mRNA instead of cyclooxygenase-2 (COX-2) protein and mRNA in RAW264.7 cells, implying that NAB may have lower side effects compared with nonsteroidal anti-inflammatory drugs (NSAIDs).	nab	29-32	nitric oxide synthase 2, inducible	Mus musculus	116-147
31284554-4	2019	In this study, we found that NAB suppressed the LPS-induced inflammatory responses by restraining the expression of inducible nitric oxide synthase (iNOS) proteins and mRNA instead of cyclooxygenase-2 (COX-2) protein and mRNA in RAW264.7 cells, implying that NAB may have lower side effects compared with nonsteroidal anti-inflammatory drugs (NSAIDs).	nab	29-32	nitric oxide synthase 2, inducible	Mus musculus	149-153
31284554-4	2019	In this study, we found that NAB suppressed the LPS-induced inflammatory responses by restraining the expression of inducible nitric oxide synthase (iNOS) proteins and mRNA instead of cyclooxygenase-2 (COX-2) protein and mRNA in RAW264.7 cells, implying that NAB may have lower side effects compared with nonsteroidal anti-inflammatory drugs (NSAIDs).	nab	29-32	prostaglandin-endoperoxide synthase 2	Mus musculus	184-200
31284554-4	2019	In this study, we found that NAB suppressed the LPS-induced inflammatory responses by restraining the expression of inducible nitric oxide synthase (iNOS) proteins and mRNA instead of cyclooxygenase-2 (COX-2) protein and mRNA in RAW264.7 cells, implying that NAB may have lower side effects compared with nonsteroidal anti-inflammatory drugs (NSAIDs).	nab	29-32	prostaglandin-endoperoxide synthase 2	Mus musculus	202-207
31284554-5	2019	Besides, NAB upregulated the protein and mRNA expressions of heme oxygenase (HO)-1 when it exerted its anti-inflammatory effects.	nab	9-12	heme oxygenase 1	Mus musculus	61-82
31284554-6	2019	Also, NAB restrained the production of NO by increasing HO-1 expression in LPS-stimulated RAW264.7 cells.	nab	6-9	heme oxygenase 1	Mus musculus	56-60
31284554-7	2019	Thus, it is considered that the anti-inflammatory effect of NAB is associated with an induction of antioxidant protein HO-1, and thus NAB may be a potential HO-1 inducer for treating inflammatory diseases.	nab	60-63	heme oxygenase 1	Mus musculus	119-123
31284554-7	2019	Thus, it is considered that the anti-inflammatory effect of NAB is associated with an induction of antioxidant protein HO-1, and thus NAB may be a potential HO-1 inducer for treating inflammatory diseases.	nab	134-137	heme oxygenase 1	Mus musculus	157-161
31102323-3	2019	METHODS: Patients who failed oxaliplatin, irinotecan, and 5FU and whose archival tumors stained immunohistochemical (IHC) tumor positive for CK7 or MUC1 received nab-paclitaxel and gemcitabine therapy with or without cisplatin.	nab	162-165	keratin 7	Homo sapiens	141-144
31102323-3	2019	METHODS: Patients who failed oxaliplatin, irinotecan, and 5FU and whose archival tumors stained immunohistochemical (IHC) tumor positive for CK7 or MUC1 received nab-paclitaxel and gemcitabine therapy with or without cisplatin.	nab	162-165	mucin 1, cell surface associated	Homo sapiens	148-152
31296830-1	2019	The present study reports the outcomes of chemotherapy using nab-PTXplus RAM in 6 patients with metastatic gastric cancer as recommended in the JGCA guidelines for special conditions.	nab	61-64	CCDC26 long non-coding RNA	Homo sapiens	73-76
31011879-7	2019	Western blotting results showed that combination of QCT and NaB increased apoptosis by decreasing anti-apoptotic Bcl-2 and increasing pro-apoptotic Bax, decreasing survivin, activating caspase-3, and degrading poly (ADP-ribose) polymerase (PARP).	nab	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	210-238
31011879-7	2019	Western blotting results showed that combination of QCT and NaB increased apoptosis by decreasing anti-apoptotic Bcl-2 and increasing pro-apoptotic Bax, decreasing survivin, activating caspase-3, and degrading poly (ADP-ribose) polymerase (PARP).	nab	60-63	poly(ADP-ribose) polymerase 1	Homo sapiens	240-244
30965088-5	2019	By real-time PCR, we found that NaB induced significant decreases in zinc-dependent superoxide dismutase (sodC) and tip protein C (spaC) expression in CP from infected-RAW264.7 cells and in phospholipase D (pld) and spaC expression in CP from the spleens of infected mice.	nab	32-35	superoxide dismutase 1, soluble	Mus musculus	106-110
31002261-0	2019	Neonatal Fc Receptor (FcRn) Enhances Tissue Distribution and Prevents Excretion of nab-Paclitaxel.	nab	83-86	Fc fragment of IgG receptor and transporter	Mus musculus	0-20
31002261-0	2019	Neonatal Fc Receptor (FcRn) Enhances Tissue Distribution and Prevents Excretion of nab-Paclitaxel.	nab	83-86	Fc fragment of IgG receptor and transporter	Mus musculus	22-26
31002261-4	2019	This study aimed to investigate the effects of FcRn on nab-P elimination and distribution to targeted tissues.	nab	55-58	Fc fragment of IgG receptor and transporter	Mus musculus	47-51
30930221-4	2019	S. aureus pre-treated 2 h with 0.5 mM or 2 mM NaB showed a reduction in internalization into bMECs (~35% and ~55%; respectively), which coincided with a down-regulated expression of clumping factor B (ClfB).	nab	46-49	AT695_RS04065	Staphylococcus aureus	182-199
30930221-4	2019	S. aureus pre-treated 2 h with 0.5 mM or 2 mM NaB showed a reduction in internalization into bMECs (~35% and ~55%; respectively), which coincided with a down-regulated expression of clumping factor B (ClfB).	nab	46-49	AT695_RS04065	Staphylococcus aureus	201-205
30930221-6	2019	Moreover, the 2 mM NaB (24 h) pre-treatment induced bacterial internalization (~3-fold), which was related with an up-regulation of spa, clfB and sdrC genes.	nab	19-22	AT695_RS04065	Staphylococcus aureus	137-141
30965088-6	2019	NaB treatment significantly up-regulated cathelicidin-related antimicrobial peptide (cramp) expression in spleens of mice infected with CP.	nab	0-3	cathelicidin antimicrobial peptide	Mus musculus	41-83
30965088-6	2019	NaB treatment significantly up-regulated cathelicidin-related antimicrobial peptide (cramp) expression in spleens of mice infected with CP.	nab	0-3	cathelicidin antimicrobial peptide	Mus musculus	85-90
32743494-6	2019	We designed a competitive screening assay in which the presence of NAb in patients plasma prevents the binding of stable isotopically labeled (SIL) mAb infliximab to TNF-alpha ligand fixed on a 96-well plate.	nab	67-70	tumor necrosis factor	Homo sapiens	166-175
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	Parkinsonism associated deglycase	Rattus norvegicus	34-38
31231572-6	2019	For patients with PD-L1-positive tumours (PD-L1 expression on tumour-infiltrating immune cells &gt;=1%), we recommend first-line treatment with nab-paclitaxel and atezolizumab, when available.	nab	144-147	CD274 molecule	Homo sapiens	18-23
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	AKT serine/threonine kinase 1	Rattus norvegicus	42-45
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	Parkinsonism associated deglycase	Rattus norvegicus	152-156
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	AKT serine/threonine kinase 1	Rattus norvegicus	228-231
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	BCL2, apoptosis regulator	Rattus norvegicus	243-248
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	BCL2 associated X, apoptosis regulator	Rattus norvegicus	249-252
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	caspase 3	Rattus norvegicus	288-297
31114478-6	2019	The results showed that levels of DJ-1, p-Akt and p-IkappaB kinase (IKK) increased after ICH and peaked at 24 h. Besides, NaB significantly upregulated DJ-1 in both cytoplasm and mitochondria, and also increased the levels of p-Akt, p-IKK and Bcl-2/Bax ratio, but decreased the levels of caspase-3 and caspase-9.	nab	122-125	caspase 9	Rattus norvegicus	302-311
31114478-9	2019	Therefore, we concluded that NaB could attenuate secondary brain injury via inhibiting neuronal apoptosis and reducing mitochondria-mediated oxidative stress via DJ-1/Akt/IKK/NFkappaB pathway.	nab	29-32	Parkinsonism associated deglycase	Rattus norvegicus	162-166
31114478-9	2019	Therefore, we concluded that NaB could attenuate secondary brain injury via inhibiting neuronal apoptosis and reducing mitochondria-mediated oxidative stress via DJ-1/Akt/IKK/NFkappaB pathway.	nab	29-32	AKT serine/threonine kinase 1	Rattus norvegicus	167-170
30881589-0	2019	Alphalipoic Acid Prevents Oxidative Stress and Peripheral Neuropathy in Nab-Paclitaxel-Treated Rats through the Nrf2 Signalling Pathway.	nab	72-75	NFE2 like bZIP transcription factor 2	Rattus norvegicus	112-116
31164515-6	2019	After 4 courses of chemotherapy containinga combination of nab-PTX and GEM, the tumor reduced in size, but was still in contact with the portal vein and SMA on imaging.	nab	59-62	survival of motor neuron 1, telomeric	Homo sapiens	153-156
30952749-9	2019	CONCLUSION: Nab-paclitaxel plus trastuzumab followed by FEC in patients with HER2-positive operable breast cancer is considerably effective and well tolerated.	nab	12-15	erb-b2 receptor tyrosine kinase 2	Homo sapiens	77-81
30643929-15	2019	CONCLUSIONS: TUBB3 negative expression prior treatment and pCR may indicate a better prognosis for stage II and III ESCC patients after nab-paclitaxel plus cisplatin neoadjuvant chemotherapy following radical esophagectomy.	nab	136-139	tubulin beta 3 class III	Homo sapiens	13-18
30937307-8	2019	Among the identified factors, the MCM2-7 complex might be a target of NaB.	nab	70-73	minichromosome maintenance complex component 2	Homo sapiens	34-40
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	Parkinsonism associated deglycase	Rattus norvegicus	16-20
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	24-27
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	superoxide dismutase 2	Rattus norvegicus	33-37
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	BCL2, apoptosis regulator	Rattus norvegicus	109-114
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	BCL2 associated X, apoptosis regulator	Rattus norvegicus	115-118
30853891-8	2019	NaB upregulated DJ-1, p-Akt, and SOD2, decreased ROS, p-p38 MAPK/p38 MAPK ratio, and CC-3, and increased the Bcl-2/Bax ratio, which were reversed by DJ-1 siRNA.	nab	0-3	Parkinsonism associated deglycase	Rattus norvegicus	149-153
30853891-11	2019	Moreover, the level of oxDJ-1 increased after t-SCI, which was decreased by DJ-1 siRNA, NaB or the combination of them.	nab	88-91	Parkinsonism associated deglycase	Rattus norvegicus	25-29
30853891-13	2019	In conclusion, NaB increased DJ-1, and thus reduced ROS and ROS-induced neuronal apoptosis by promoting Akt phosphorylation in t-SCI rats.	nab	15-18	Parkinsonism associated deglycase	Rattus norvegicus	29-33
30853891-13	2019	In conclusion, NaB increased DJ-1, and thus reduced ROS and ROS-induced neuronal apoptosis by promoting Akt phosphorylation in t-SCI rats.	nab	15-18	AKT serine/threonine kinase 1	Rattus norvegicus	104-107
30881589-13	2019	Furthermore, alpha-LA could reverse the mRNA and protein expressions of Nrf2 (nuclear factor erythroid 2-related factor 2) and three Nrf2-responsive genes (HO-1, gamma-GCLC, and NQO1) altered by nab-PTX in the dorsal root ganglion (DRG) of rats.	nab	195-198	NFE2 like bZIP transcription factor 2	Rattus norvegicus	78-121
30881589-13	2019	Furthermore, alpha-LA could reverse the mRNA and protein expressions of Nrf2 (nuclear factor erythroid 2-related factor 2) and three Nrf2-responsive genes (HO-1, gamma-GCLC, and NQO1) altered by nab-PTX in the dorsal root ganglion (DRG) of rats.	nab	195-198	heme oxygenase 1	Rattus norvegicus	156-172
30487284-5	2019	Using highly NAb-sensitive hypervariable region 1 (HVR1)-deleted HCVcc, H77/JFH1DeltaHVR1 and J6(core-NS2)/JFH1DeltaHVR1, we previously reported a low barrier to developing AR5A NAb resistance substitutions.	nab	13-16	vasoactive intestinal peptide receptor 1	Homo sapiens	76-89
30487284-5	2019	Using highly NAb-sensitive hypervariable region 1 (HVR1)-deleted HCVcc, H77/JFH1DeltaHVR1 and J6(core-NS2)/JFH1DeltaHVR1, we previously reported a low barrier to developing AR5A NAb resistance substitutions.	nab	13-16	vasoactive intestinal peptide receptor 1	Homo sapiens	107-120
30840301-1	2019	OBJECTIVE: The aim of this study was to investigate whether sodium butyrate (NaB) attenuated cerebral ischemia-reperfusion injury (IRI) in mice by inhibiting JNK/STAT pathway, thereby exerting a neuroprotective role.	nab	77-80	mitogen-activated protein kinase 8	Mus musculus	158-161
30460489-0	2019	Metastatic or locally advanced breast cancer patients: towards an expert consensus on nab-paclitaxel treatment in HER2-negative tumours-the MACBETH project.	nab	86-89	erb-b2 receptor tyrosine kinase 2	Homo sapiens	114-118
30389433-4	2019	Co-administration of miR-1291 with gemcitabine plus nab-paclitaxel (Gem-nP) largely increased the levels of apoptosis, DNA damage and mitotic arrest in PC cells, compared to mono-drug treatment.	nab	52-55	microRNA 1291	Mus musculus	21-29
30840301-13	2019	Mice in the NaB treatment group showed significantly lower levels of IL-1beta, TNF-alpha and IL-8.	nab	12-15	interleukin 1 beta	Mus musculus	69-77
30840301-13	2019	Mice in the NaB treatment group showed significantly lower levels of IL-1beta, TNF-alpha and IL-8.	nab	12-15	tumor necrosis factor	Mus musculus	79-88
30840301-13	2019	Mice in the NaB treatment group showed significantly lower levels of IL-1beta, TNF-alpha and IL-8.	nab	12-15	chemokine (C-X-C motif) ligand 15	Mus musculus	93-97
30840301-15	2019	In addition, the protein expression levels of Jak2 and STAT3 were obviously upregulated in IRI mice, which were significantly downregulated after 10 mg/kg NaB treatment.	nab	155-158	Janus kinase 2	Mus musculus	46-50
30840301-15	2019	In addition, the protein expression levels of Jak2 and STAT3 were obviously upregulated in IRI mice, which were significantly downregulated after 10 mg/kg NaB treatment.	nab	155-158	signal transducer and activator of transcription 3	Mus musculus	55-60
30245304-7	2019	While IHC did not show any correlation between survival and the protein level of SERPINB7, RNA ISH revealed that expression of SERPINB7 was associated with a poor DFS (P = .01) and OS (P = .002) in the gem group but not in the gem/nab.	nab	231-234	serpin family B member 7	Homo sapiens	127-135
30362049-6	2019	NaB elevated the protein and mRNA expressions of LC3 in a dose-dependent manner.	nab	0-3	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	49-52
30362049-7	2019	NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC).	nab	0-3	serine/threonine kinase 11	Homo sapiens	87-102
30362049-7	2019	NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC).	nab	0-3	serine/threonine kinase 11	Homo sapiens	104-108
30362049-7	2019	NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC).	nab	0-3	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	111-139
30362049-7	2019	NaB treatment increased the formation of autolysosome and expression of phosphorylated liver kinase B1 (LKB1), AMP-activated protein kinase (AMPK), and acetyl-CoA carboxylase (ACC).	nab	0-3	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	141-145
30362049-8	2019	Treatment with compound C (an inhibitor of AMPK) and siRNA-mediated knockdown of AMPK and LKB1 significantly attenuated NaB-induced autophagy in CRC cells.	nab	120-123	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	81-85
30362049-8	2019	Treatment with compound C (an inhibitor of AMPK) and siRNA-mediated knockdown of AMPK and LKB1 significantly attenuated NaB-induced autophagy in CRC cells.	nab	120-123	serine/threonine kinase 11	Homo sapiens	90-94
30362049-9	2019	Collectively, these findings indicated that LKB1 and AMPK are critical for NaB-mediated autophagy and may act as the novel targets for colorectal cancer therapy in the future.	nab	75-78	serine/threonine kinase 11	Homo sapiens	44-48
30362049-9	2019	Collectively, these findings indicated that LKB1 and AMPK are critical for NaB-mediated autophagy and may act as the novel targets for colorectal cancer therapy in the future.	nab	75-78	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	53-57
30389744-2	2019	Here we report a case of Takotsubo cardiomyopathy associated with the use of dual anti-HER2 therapy in a 63-year-old woman who presented to the emergency department with an 8- to 10-hour history of progressive dyspnea after completing her third cycle of pertuzumab plus trastuzumab in addition to nab-paclitaxel chemotherapy.	nab	297-300	erb-b2 receptor tyrosine kinase 2	Homo sapiens	87-91
30629920-4	2019	V2 bNAb signature-guided mutations were introduced into Env 459C to create a trivalent vaccine, and immunization of guinea pigs with V2-SET vaccines resulted in increased breadth of NAb responses compared with Env 459C alone.	nab	4-7	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	56-59
30276569-9	2019	NaB did not affect hRFVT3 mRNA stability, rather it caused significant epigenetic changes (histone modifications) in the SLC52A3 gene where an increase in H3Ac and a reduction in H3K27me3 levels were observed in the NaB-treated Caco-2 cells compared to untreated controls.	nab	0-3	solute carrier family 52 member 3	Homo sapiens	121-128
30276569-9	2019	NaB did not affect hRFVT3 mRNA stability, rather it caused significant epigenetic changes (histone modifications) in the SLC52A3 gene where an increase in H3Ac and a reduction in H3K27me3 levels were observed in the NaB-treated Caco-2 cells compared to untreated controls.	nab	216-219	solute carrier family 52 member 3	Homo sapiens	121-128
30276569-10	2019	CONCLUSION: These findings demonstrate that NaB up-regulates intestinal RF uptake and that the effect appears to be mediated, at least in part, at the level of transcription of the SLC52A3 gene and may involve epigenetic mechanism(s).	nab	44-47	solute carrier family 52 member 3	Homo sapiens	181-188
30518684-8	2018	IL-6 neutralizing antibody (IL-6-Nab) combined with HMA fully eradicated OCSC, and the combination blocked IL-6/IL6-R/pSTAT3-mediated ALDH1A1 expression and eliminated OCSC in residual tumors that persisted in vivo after chemotherapy.	nab	33-36	interleukin 6	Homo sapiens	0-4
30518684-8	2018	IL-6 neutralizing antibody (IL-6-Nab) combined with HMA fully eradicated OCSC, and the combination blocked IL-6/IL6-R/pSTAT3-mediated ALDH1A1 expression and eliminated OCSC in residual tumors that persisted in vivo after chemotherapy.	nab	33-36	interleukin 6	Homo sapiens	28-32
30518684-8	2018	IL-6 neutralizing antibody (IL-6-Nab) combined with HMA fully eradicated OCSC, and the combination blocked IL-6/IL6-R/pSTAT3-mediated ALDH1A1 expression and eliminated OCSC in residual tumors that persisted in vivo after chemotherapy.	nab	33-36	interleukin 6	Homo sapiens	28-32
30518684-8	2018	IL-6 neutralizing antibody (IL-6-Nab) combined with HMA fully eradicated OCSC, and the combination blocked IL-6/IL6-R/pSTAT3-mediated ALDH1A1 expression and eliminated OCSC in residual tumors that persisted in vivo after chemotherapy.	nab	33-36	interleukin 6 receptor	Homo sapiens	112-117
30510243-4	2018	It is well-known that the gut metabolite sodium butyrate (NaB) could promote GLP-1 secretion from intestinal L cells.	nab	58-61	glucagon	Homo sapiens	77-82
30510243-7	2018	Similarly, in the NAFLD mouse model, mice fed with a high-fat diet showed reduced hepatic GLP-1R expression, which was reversed by NaB treatment and accompanied by markedly alleviated liver steatosis.	nab	131-134	glucagon-like peptide 1 receptor	Mus musculus	90-96
30510243-9	2018	Furthermore, NaB-enhanced GLP-1R expression in HepG2 cells by inhibiting histone deacetylase-2 independent of GPR43/GPR109a.	nab	13-16	glucagon like peptide 1 receptor	Homo sapiens	26-32
30510243-9	2018	Furthermore, NaB-enhanced GLP-1R expression in HepG2 cells by inhibiting histone deacetylase-2 independent of GPR43/GPR109a.	nab	13-16	histone deacetylase 2	Homo sapiens	73-94
30510243-9	2018	Furthermore, NaB-enhanced GLP-1R expression in HepG2 cells by inhibiting histone deacetylase-2 independent of GPR43/GPR109a.	nab	13-16	free fatty acid receptor 2	Homo sapiens	110-115
30510243-10	2018	These results indicate that NaB is able to prevent the progression of NAFL to NASH via promoting hepatic GLP-1R expression.	nab	28-31	glucagon like peptide 1 receptor	Homo sapiens	105-111
30510243-11	2018	NaB is a GLP-1 sensitizer and represents a potential therapeutic adjuvant to prevent NAFL progression to NASH.	nab	0-3	glucagon	Homo sapiens	9-14
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	190-194
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	activating transcription factor 4	Homo sapiens	296-300
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	DNA damage inducible transcript 3	Homo sapiens	306-355
30342372-6	2018	Further research showed NaB down-regulated the expression of endoplasmic reticulum stress (ERS) related proteins, including phosphorylated type I transmembrane ER-resident protein kinase (p-PERK), phosphorylated eukaryotic initiation factor 2alpha (p-eIF2alpha), activating transcription factor (ATF4) and CCAAT/enhancer-binding protein homologous protein (CHOP).	nab	24-27	DNA damage inducible transcript 3	Homo sapiens	357-361
30342372-7	2018	Consequently, NaB mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of ERS.	nab	14-17	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	58-62
30342372-7	2018	Consequently, NaB mitigates type 2 diabetes by inhibiting PERK-CHOP pathway of ERS.	nab	14-17	DNA damage inducible transcript 3	Homo sapiens	63-67
30382080-7	2018	F6 was a GP120-specific nAb and recognized the linear epitope.	nab	24-27	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	9-14
30145846-8	2018	The combined treatment with NaB + Nico resulted in increased BDNF level and higher PI3K, APE1, and the downstream NF-kappaB activation, which were blocked by pretreatment with their respective inhibitors.	nab	28-31	brain derived neurotrophic factor	Mus musculus	61-65
30145846-8	2018	The combined treatment with NaB + Nico resulted in increased BDNF level and higher PI3K, APE1, and the downstream NF-kappaB activation, which were blocked by pretreatment with their respective inhibitors.	nab	28-31	apurinic/apyrimidinic endonuclease 1	Mus musculus	89-93
30145846-8	2018	The combined treatment with NaB + Nico resulted in increased BDNF level and higher PI3K, APE1, and the downstream NF-kappaB activation, which were blocked by pretreatment with their respective inhibitors.	nab	28-31	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	114-123
30345906-11	2018	CONCLUSIONS: Atezolizumab plus nab-paclitaxel prolonged progression-free survival among patients with metastatic triple-negative breast cancer in both the intention-to-treat population and the PD-L1-positive subgroup.	nab	31-34	CD274 molecule	Homo sapiens	193-198
30319614-8	2018	SR-BI has received the most attention and it appears that HVR1 is involved in a multimodal HCV/SR-BI interaction involving high-density-lipoprotein associated ApoCI, which may prime the virus for later entry events by exposing conserved NAb epitopes, like those in the CD81 binding site.	nab	237-240	scavenger receptor class B member 1	Homo sapiens	95-100
29703690-0	2018	Quality-Adjusted Survival With nab-Paclitaxel Versus Standard Paclitaxel in Metastatic Breast Cancer: A Q-TWiST Analysis.	nab	31-34	twist family bHLH transcription factor 1	Homo sapiens	106-111
30259565-2	2018	We found that NaB significantly increased the activities of antioxidant enzymes, including superoxide dismutase, glutathione peroxidase, catalase, peroxidase, and total antioxidant capacity and decreased the reactive oxygen species production in LPS-induced MAC-T cells.	nab	14-17	catalase	Bos taurus	137-145
30259565-4	2018	The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB.	nab	153-156	caspase 3	Bos taurus	35-44
30259565-4	2018	The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB.	nab	153-156	caspase 9	Bos taurus	46-55
30259565-4	2018	The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB.	nab	153-156	BCL2 associated X, apoptosis regulator	Bos taurus	61-64
30259565-4	2018	The messenger RNA (mRNA) levels of caspase-3, caspase-9, and Bax decreased, while the Bcl-2 mRNA level increased in LPS-induced MAC-T cells treated with NaB.	nab	153-156	BCL2 apoptosis regulator	Bos taurus	86-91
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Bos taurus	52-77
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	AKT serine/threonine kinase 1	Bos taurus	97-100
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	AKT serine/threonine kinase 1	Bos taurus	104-107
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	BCL2 associated X, apoptosis regulator	Bos taurus	150-153
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	caspase 3	Bos taurus	155-164
30259565-5	2018	Our results showed that NaB treatment increased the phosphoinositide 3-kinase (PI3K) and phospho-AKT (P-AKT) protein levels, whereas it decreased the Bax, caspase-3, and caspase-9 protein levels in LPS-induced MAC-T cells.	nab	24-27	caspase 9	Bos taurus	170-179
30259565-6	2018	However, the increase in PI3K and P-AKT protein levels and the decrease in Bax, caspase-3, and caspase-9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor).	nab	131-134	BCL2 associated X, apoptosis regulator	Homo sapiens	75-78
30259565-6	2018	However, the increase in PI3K and P-AKT protein levels and the decrease in Bax, caspase-3, and caspase-9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor).	nab	131-134	caspase 3	Homo sapiens	80-89
30259565-6	2018	However, the increase in PI3K and P-AKT protein levels and the decrease in Bax, caspase-3, and caspase-9 protein levels induced by NaB treatment were reversed when the cells were pretreated with LY294002 (PI3K inhibitor).	nab	131-134	caspase 9	Homo sapiens	95-104
30259565-8	2018	In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells.	nab	13-16	caspase 3	Bos taurus	51-60
30259565-8	2018	In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells.	nab	13-16	caspase 9	Bos taurus	62-71
30259565-8	2018	In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells.	nab	13-16	BCL2 associated X, apoptosis regulator	Bos taurus	77-80
30259565-8	2018	In addition, NaB decreased apoptosis by inhibiting caspase-3, caspase-9, and Bax protein levels, and this action was mainly achieved via activation of the PI3K/AKT signaling pathways in LPS-induced MAC-T cells.	nab	13-16	AKT serine/threonine kinase 1	Bos taurus	160-163
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	superoxide dismutase [Cu-Zn]	Capra hircus	170-174
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	superoxide dismutase [Mn], mitochondrial	Capra hircus	176-180
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	extracellular superoxide dismutase [Cu-Zn]	Capra hircus	182-186
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	glutathione peroxidase 1	Capra hircus	188-192
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	catalase	Capra hircus	197-200
30200953-3	2018	RESULTS: When added to the HG diet, NaB increased the mean ruminal pH and reduced the levels of ruminal, portal and hepatic LPS; Additionally, we observed an increase in SOD1, SOD2, SOD3, GPX1 and CAT mRNA expression, increased levels of TSOD and CAT enzyme activity as well as increased total antioxidant capacity (T-AOC) and decreased malondialdehyde (MDA) in both the liver and plasma, while GPx activity increased in the liver of goats fed the HG + NaB diet.	nab	36-39	catalase	Capra hircus	247-250
29960044-7	2018	Until further in vivo evidence is established, clinicians should consider the current in vitro data demonstrating NAB cross-reactivity between pegIFNbeta-1a and rIFNbeta when discussing new treatment options with MS patients.	nab	114-117	interferon beta 1	Rattus norvegicus	161-169
29397557-6	2018	NaB-induced effects included suppression of cell proliferation accompanied by reduced transcriptional expression of the EWS-FLI1 fusion oncogene, decreased expression of key survival and pluripotency-associated genes, and re-expression of the differentiation neuronal marker betaIII-tubulin.	nab	0-3	EWS RNA binding protein 1	Homo sapiens	120-123
29397557-6	2018	NaB-induced effects included suppression of cell proliferation accompanied by reduced transcriptional expression of the EWS-FLI1 fusion oncogene, decreased expression of key survival and pluripotency-associated genes, and re-expression of the differentiation neuronal marker betaIII-tubulin.	nab	0-3	Fli-1 proto-oncogene, ETS transcription factor	Homo sapiens	124-128
29397557-3	2018	Here, we investigated whether the potent HDAC inhibitor, sodium butyrate (NaB), has the ability to reprogram EWS cells towards a more differentiated state and affect their growth and survival.	nab	74-77	EWS RNA binding protein 1	Homo sapiens	109-112
29397557-4	2018	Exposure of two EWS cell lines to NaB resulted in rapid and potent inhibition of HDAC activity (1 h, IC50 1.5 mM) and a significant arrest of cell cycle progression (72 h, IC50 0.68-0.76 mM), marked by G0/G1 accumulation.	nab	34-37	EWS RNA binding protein 1	Homo sapiens	16-19
29397557-7	2018	Finally, NaB reduced c-MYC levels and impaired survival in putative EWS cancer stem cells.	nab	9-12	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	21-26
29397557-7	2018	Finally, NaB reduced c-MYC levels and impaired survival in putative EWS cancer stem cells.	nab	9-12	EWS RNA binding protein 1	Homo sapiens	68-71
30140713-4	2018	After the re-administration in two NAb-negative dogs with AAV8 vectors carrying human factor VIII (hFVIII), along with the proteasome inhibitor bortezomib, we observed a phenotypic improvement in both dogs that persisted in one dog.	nab	35-38	coagulation factor VIII	Homo sapiens	99-105
29964168-3	2018	Sodium butyrate (NaB) is an inhibitor of histone deacetylase (HDAC) and an activator of NRF2.	nab	17-20	nuclear factor, erythroid derived 2, like 2	Mus musculus	88-92
29964168-6	2018	Additionally, the mechanism by which NaB activates NRF2 was unclear.	nab	37-40	nuclear factor, erythroid derived 2, like 2	Mus musculus	51-55
29964168-11	2018	NaB inhibited HDAC activity, and increased occupancy of the transcription factor aryl hydrocarbon receptor and the co-activator P300 at the Nrf2 gene promoter.	nab	0-3	aryl-hydrocarbon receptor	Mus musculus	81-106
29964168-11	2018	NaB inhibited HDAC activity, and increased occupancy of the transcription factor aryl hydrocarbon receptor and the co-activator P300 at the Nrf2 gene promoter.	nab	0-3	E1A binding protein p300	Mus musculus	128-132
29964168-11	2018	NaB inhibited HDAC activity, and increased occupancy of the transcription factor aryl hydrocarbon receptor and the co-activator P300 at the Nrf2 gene promoter.	nab	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	140-144
29964168-12	2018	Further, the P300 inhibitor C646 completely abolished NaB"s efficacies.	nab	54-57	E1A binding protein p300	Mus musculus	13-17
29964168-13	2018	Thus, NRF2 is required for both self-defense and NaB"s protection against diabetes-induced aortic endothelial dysfunction.	nab	49-52	nuclear factor, erythroid derived 2, like 2	Mus musculus	6-10
29964168-14	2018	Other findings suggest that P300 mediates the transcriptional activation of Nrf2 by NaB.	nab	84-87	E1A binding protein p300	Mus musculus	28-32
29964168-14	2018	Other findings suggest that P300 mediates the transcriptional activation of Nrf2 by NaB.	nab	84-87	nuclear factor, erythroid derived 2, like 2	Mus musculus	76-80
30075754-6	2018	The histone deacetylase-inhibitor (HDAC) sodium butyrate (NaB) and the methylation-inhibitor 5-azacytidine (5-AZA), as epigenetic modifiers, induced CEA-expression in HCT116 and WiDr cells.	nab	58-61	CEA cell adhesion molecule 3	Homo sapiens	149-152
30075754-8	2018	The cytolytic function of anti-CEA-CAR NK-92MI cells was increased from 22.99 +- 2.04% of lysis background to 69.20 +- 11.92% after NaB treatment, and 69.70 +- 9.93% after 5-AZA treatment, at a 10:1 E/T ratio in HCT116 cells.	nab	132-135	CEA cell adhesion molecule 3	Homo sapiens	31-34
29941022-15	2018	Knockdown of TSG-6 by NAb or by siRNA in EXO abrogated the therapeutic effects of EXO, suggesting TSG-6 as an important therapeutic molecule.	nab	22-25	tumor necrosis factor alpha induced protein 6	Mus musculus	13-18
29902349-0	2018	Nab-paclitaxel interrupts cancer-stromal interaction through C-X-C motif chemokine 10-mediated interleukin-6 downregulation in vitro.	nab	0-3	C-X-C motif chemokine ligand 10	Homo sapiens	61-85
29902349-0	2018	Nab-paclitaxel interrupts cancer-stromal interaction through C-X-C motif chemokine 10-mediated interleukin-6 downregulation in vitro.	nab	0-3	interleukin 6	Homo sapiens	95-108
29902349-11	2018	Moreover, nab-PTX increased CXCL10 expression of cancer cells which blocked CAF IL-6 expression and secretion.	nab	10-13	C-X-C motif chemokine ligand 10	Homo sapiens	28-34
29902349-11	2018	Moreover, nab-PTX increased CXCL10 expression of cancer cells which blocked CAF IL-6 expression and secretion.	nab	10-13	lysine acetyltransferase 2B	Homo sapiens	76-79
29902349-11	2018	Moreover, nab-PTX increased CXCL10 expression of cancer cells which blocked CAF IL-6 expression and secretion.	nab	10-13	interleukin 6	Homo sapiens	80-84
29902349-12	2018	Nab-PTX treatment could increase CXCL10 expression of cancer cells which blocks CAF cancer cell migration and invasion-promoting effect by inhibiting IL-6 expression.	nab	0-3	C-X-C motif chemokine ligand 10	Homo sapiens	33-39
29902349-12	2018	Nab-PTX treatment could increase CXCL10 expression of cancer cells which blocks CAF cancer cell migration and invasion-promoting effect by inhibiting IL-6 expression.	nab	0-3	interleukin 6	Homo sapiens	150-154
30008892-6	2018	Treatment of KATO III and NCI-N87 human gastric cancer cells with sodium butyrate (NaB) or Trichostatin A (TSA) induced Per1 and Per2 mRNA expression in a dose-dependent manner.	nab	83-86	period circadian regulator 2	Homo sapiens	129-133
30008892-9	2018	It was also observed that binding of Sp1 and Sp3 to the Per1 promoter decreased following NaB treatment, whereas Sp1 binding increased at the Per2 promoter of NaB- and TSA-treated cells.	nab	90-93	Sp3 transcription factor	Homo sapiens	45-48
30008892-9	2018	It was also observed that binding of Sp1 and Sp3 to the Per1 promoter decreased following NaB treatment, whereas Sp1 binding increased at the Per2 promoter of NaB- and TSA-treated cells.	nab	159-162	period circadian regulator 2	Homo sapiens	142-146
29961332-2	2018	Sodium butyrate (NaB) has been shown to alleviate NAFLD, yet whether and how PPARalpha is involved in the action of NaB remains elusive.	nab	116-119	peroxisome proliferator activated receptor alpha	Rattus norvegicus	77-86
29961332-3	2018	In this study, NaB administration alleviated high-fat-diet-induced NAFLD in adult rats, with a decrease of hepatic triglyceride content from 108.18 +- 5.77 to 81.34 +- 7.94 mug/mg ( p &lt; 0.05), which was associated with a significant activation of PPARalpha.	nab	15-18	peroxisome proliferator activated receptor alpha	Rattus norvegicus	250-259
30087850-0	2018	nab-Paclitaxel-Based Therapy in Underserved Patient Populations: The ABOUND.PS2 Study in Patients With NSCLC and a Performance Status of 2.	nab	0-3	taste 2 receptor member 64 pseudogene	Homo sapiens	76-79
29961332-5	2018	NaB-induced PPARalpha upregulation coincided with a reduced protein content of histone deacetylase 1 and promoted histone H3 acetyl K9 (H3K9Ac) modification on the promoter of PPARalpha, whereas NaB-induced suppression of inflammation was linked to significantly increased PPARalpha binding with p-p65.	nab	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	12-21
29961332-5	2018	NaB-induced PPARalpha upregulation coincided with a reduced protein content of histone deacetylase 1 and promoted histone H3 acetyl K9 (H3K9Ac) modification on the promoter of PPARalpha, whereas NaB-induced suppression of inflammation was linked to significantly increased PPARalpha binding with p-p65.	nab	0-3	histone deacetylase 1	Rattus norvegicus	79-100
29961332-5	2018	NaB-induced PPARalpha upregulation coincided with a reduced protein content of histone deacetylase 1 and promoted histone H3 acetyl K9 (H3K9Ac) modification on the promoter of PPARalpha, whereas NaB-induced suppression of inflammation was linked to significantly increased PPARalpha binding with p-p65.	nab	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	176-185
29961332-5	2018	NaB-induced PPARalpha upregulation coincided with a reduced protein content of histone deacetylase 1 and promoted histone H3 acetyl K9 (H3K9Ac) modification on the promoter of PPARalpha, whereas NaB-induced suppression of inflammation was linked to significantly increased PPARalpha binding with p-p65.	nab	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	176-185
29961332-6	2018	NaB acts as a histone deacetylase inhibitor to upregulate PPARalpha expression with enhanced H3K9Ac modification on it promoter.	nab	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	58-67
29961332-7	2018	NaB-induced PPARalpha activation stimulates fatty acid beta oxidation and inhibits NF-kappaB-mediated inflammation pathways via protein-protein interaction, thus contributing to amelioration of high-fat-diet-induced NAFLD in adult rats.	nab	0-3	peroxisome proliferator activated receptor alpha	Rattus norvegicus	12-21
29867447-6	2018	We also observed that tau hyperphosphorylation and inflammation related protein glial fibrillary acidic protein (GFAP) level were decreased in cDKO mice by NaB.	nab	156-159	glial fibrillary acidic protein	Mus musculus	80-111
29898396-6	2018	These studies therefore provide important guideposts for design of immunogens that prime and mature nAb responses to the Env V2-apex.	nab	100-103	endogenous retrovirus group K member 20	Homo sapiens	121-124
29898396-6	2018	These studies therefore provide important guideposts for design of immunogens that prime and mature nAb responses to the Env V2-apex.	nab	100-103	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	128-132
29867447-6	2018	We also observed that tau hyperphosphorylation and inflammation related protein glial fibrillary acidic protein (GFAP) level were decreased in cDKO mice by NaB.	nab	156-159	glial fibrillary acidic protein	Mus musculus	113-117
29327055-4	2018	Objective: To determine whether nab-paclitaxel improves the outcomes of early and locally advanced human epidermal growth factor receptor 2 (ERBB2/HER2)-negative breast cancer compared with paclitaxel when delivered in a neoadjuvant setting.	nab	32-35	erb-b2 receptor tyrosine kinase 2	Homo sapiens	105-139
29504299-11	2018	CONCLUSIONS: These results further support that persistent NAb positivity is associated with disease activity in MS patients treated with IFN-beta.	nab	59-62	interferon beta 1	Homo sapiens	138-146
29052293-2	2018	Sodium butyrate (NaB) could induce colonic hypersensitivity via peripheral up-regulation of NGF in animals.	nab	17-20	nerve growth factor	Rattus norvegicus	92-95
29052293-14	2018	An improved NGF expression level was observed in NaB-treated rats.	nab	49-52	nerve growth factor	Rattus norvegicus	12-15
29052293-15	2018	Meanwhile, a 2.1-fold increase in co-expression of GFAP and NGF was also determined in rats received NaB enemas.	nab	101-104	glial fibrillary acidic protein	Rattus norvegicus	51-55
29052293-15	2018	Meanwhile, a 2.1-fold increase in co-expression of GFAP and NGF was also determined in rats received NaB enemas.	nab	101-104	nerve growth factor	Rattus norvegicus	60-63
29052293-16	2018	In cultured cells, both NaB and TSA treatment could cause obvious NGF expression.	nab	24-27	nerve growth factor	Homo sapiens	66-69
27787294-9	2018	After controlling for comorbidity, receipt of neoadjuvant therapy, and nodal involvement, a longer survival was associated with undergoing combination gemcitabine and nab-paclitaxel [time ratio (TR) = 1.26, 95% CI: 1.02-1.57, P = 0.035) or capecitabine and radiation (TR = 1.25, 95% CI: 1.04-1.51, P = 0.018).	nab	167-170	nodal growth differentiation factor	Homo sapiens	71-76
29489437-2	2018	We previously reported a genotype 1a HCV virus like particle (VLP) vaccine that produced HCV specific NAb and T cell responses that were substantially enhanced by Toll-like receptor 2 (TLR2) agonists.	nab	102-105	toll like receptor 2	Homo sapiens	163-183
29489437-2	2018	We previously reported a genotype 1a HCV virus like particle (VLP) vaccine that produced HCV specific NAb and T cell responses that were substantially enhanced by Toll-like receptor 2 (TLR2) agonists.	nab	102-105	toll like receptor 2	Homo sapiens	185-189
29565269-0	2018	Food Additive Sodium Benzoate (NaB) Activates NFkappaB and Induces Apoptosis in HCT116 Cells.	nab	31-34	nuclear factor kappa B subunit 1	Homo sapiens	46-54
29565269-6	2018	NaB (6.25 mM-50 mM) treatment inhibited cell viability by inducing apoptosis, which was evident with increased Annexin V-PE staining and caspase-3 activity.	nab	0-3	annexin A5	Homo sapiens	111-120
29565269-6	2018	NaB (6.25 mM-50 mM) treatment inhibited cell viability by inducing apoptosis, which was evident with increased Annexin V-PE staining and caspase-3 activity.	nab	0-3	caspase 3	Homo sapiens	137-146
29565269-7	2018	NFkappaB activation accompanied the induction of apoptosis in NaB treated cells.	nab	62-65	nuclear factor kappa B subunit 1	Homo sapiens	0-8
29565269-12	2018	Overall, these results suggest that NaB induces apoptosis and activates NFkappaB in HCT116 colon cancer cells.	nab	36-39	nuclear factor kappa B subunit 1	Homo sapiens	72-80
29327055-4	2018	Objective: To determine whether nab-paclitaxel improves the outcomes of early and locally advanced human epidermal growth factor receptor 2 (ERBB2/HER2)-negative breast cancer compared with paclitaxel when delivered in a neoadjuvant setting.	nab	32-35	erb-b2 receptor tyrosine kinase 2	Homo sapiens	141-146
29328489-11	2018	In conclusion, trastuzumab/nab-paclitaxel could mediate targeted therapy and enhance antitumor efficacy, which could represent a novel therapeutic agent for HER2-positive GC.	nab	27-30	erb-b2 receptor tyrosine kinase 2	Homo sapiens	157-161
29418071-11	2018	CONCLUSION: NaB inhibits CRC cell migration by enhancing miR-200c expression-mediated downregulation of Bmi-1.	nab	12-15	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	104-109
29418071-6	2018	NaB reciprocally increased miR-200s but reduced expression of their target genes (Bmi-1, Zeb1, EZH2).	nab	0-3	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	82-87
29418071-6	2018	NaB reciprocally increased miR-200s but reduced expression of their target genes (Bmi-1, Zeb1, EZH2).	nab	0-3	zinc finger E-box binding homeobox 1	Homo sapiens	89-93
29418071-6	2018	NaB reciprocally increased miR-200s but reduced expression of their target genes (Bmi-1, Zeb1, EZH2).	nab	0-3	enhancer of zeste 2 polycomb repressive complex 2 subunit	Homo sapiens	95-99
29418071-7	2018	Cells transfected with miR-200c shRNA displayed a significant blockade of NaB-induced anti-invasive activity.	nab	74-77	microRNA 200c	Homo sapiens	23-31
29418071-8	2018	Upregulation of Bmi-1 expression partially reversed the effect of NaB.	nab	66-69	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	16-21
29418071-9	2018	In addition to inhibition of tumor growth in vivo, qRT-PCR results showed that NaB increased miR-200c/200b/492 expression in the tumor tissues.	nab	79-82	microRNA 200c	Homo sapiens	93-101
29418071-10	2018	Immunohistochemistry and Western blotting results demonstrated that NaB decreased Bmi-1 expression in vivo.	nab	68-71	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	82-87
29418071-11	2018	CONCLUSION: NaB inhibits CRC cell migration by enhancing miR-200c expression-mediated downregulation of Bmi-1.	nab	12-15	microRNA 200c	Homo sapiens	57-65
29876485-2	2018	Following treatment of the HDAC inhibitors, such as MS-275, NaB, TSA, or VPA, the phenotypes of NI-hADSCs exhibit neuron-like features and the neurofilament-L (NFL)-positive cells were increased.	nab	60-63	neurofilament light chain	Homo sapiens	143-158
29876485-2	2018	Following treatment of the HDAC inhibitors, such as MS-275, NaB, TSA, or VPA, the phenotypes of NI-hADSCs exhibit neuron-like features and the neurofilament-L (NFL)-positive cells were increased.	nab	60-63	neurofilament light chain	Homo sapiens	160-163
29474444-4	2018	One autologous NAb epitope on the BG505 Env trimer is known to involve residues lining a hole in the glycan shield that is blocked by adding a glycan at either residue 241 or 289.	nab	15-18	endogenous retrovirus group K member 20	Homo sapiens	40-43
29474444-11	2018	In macaques, NAb responses induced by BG505 SOSIP trimers are more often directed at the C3/465 epitope than the 241/289-glycan hole.	nab	13-16	complement C3	Homo sapiens	89-95
29222332-3	2018	Ideally, Env immunogens should present broadly neutralizing antibody epitopes but limit the presentation of immunodominant non-NAb epitopes that might induce off-target and potentially interfering responses.	nab	127-130	endogenous retrovirus group K member 20	Homo sapiens	9-12
29043770-4	2018	Here, we present a series of GluN2C/2D-selective negative allosteric modulators built around a N-aryl benzamide (NAB) core.	nab	113-116	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	29-35
29043770-5	2018	The prototypical compound, NAB-14, is &gt;800-fold selective for recombinant GluN2C/GluN2D over GluN2A/GluN2B in Xenopus oocytes and has an IC50 value of 580 nM at recombinant GluN2D-containing receptors expressed in mammalian cells.	nab	27-30	glutamate ionotropic receptor NMDA type subunit 2C	Rattus norvegicus	77-83
29043770-5	2018	The prototypical compound, NAB-14, is &gt;800-fold selective for recombinant GluN2C/GluN2D over GluN2A/GluN2B in Xenopus oocytes and has an IC50 value of 580 nM at recombinant GluN2D-containing receptors expressed in mammalian cells.	nab	27-30	glutamate ionotropic receptor NMDA type subunit 2D	Rattus norvegicus	84-90
29043770-5	2018	The prototypical compound, NAB-14, is &gt;800-fold selective for recombinant GluN2C/GluN2D over GluN2A/GluN2B in Xenopus oocytes and has an IC50 value of 580 nM at recombinant GluN2D-containing receptors expressed in mammalian cells.	nab	27-30	glutamate ionotropic receptor NMDA type subunit 2A	Rattus norvegicus	96-102
29043770-5	2018	The prototypical compound, NAB-14, is &gt;800-fold selective for recombinant GluN2C/GluN2D over GluN2A/GluN2B in Xenopus oocytes and has an IC50 value of 580 nM at recombinant GluN2D-containing receptors expressed in mammalian cells.	nab	27-30	glutamate ionotropic receptor NMDA type subunit 2D	Rattus norvegicus	176-182
29043770-7	2018	Site-directed mutagenesis suggests that structural determinants for NAB-14 inhibition reside in the GluN2D M1 transmembrane helix.	nab	68-71	glutamate ionotropic receptor NMDA type subunit 2D	Rattus norvegicus	100-106
31435511-8	2018	Indeed, short-term treatment with NaB results in FoxO activation, which takes place through nuclear translocation, and accompanied by accumulation of such ROS scavengers as MnSOD and SOD2.	nab	34-37	superoxide dismutase 2, mitochondrial	Mus musculus	173-178
31435511-8	2018	Indeed, short-term treatment with NaB results in FoxO activation, which takes place through nuclear translocation, and accompanied by accumulation of such ROS scavengers as MnSOD and SOD2.	nab	34-37	superoxide dismutase 2, mitochondrial	Mus musculus	183-187
29222332-4	2018	The V3 loop in gp120 is such a non-NAb epitope that can effectively elicit non-NAbs when animals are immunized with SOSIP.664 trimers.	nab	35-38	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	15-20
29030220-3	2018	The effects of DNA methyltransferase inhibitor 5-aza-dC or/and histone deacetylase inhibitor (HDACi, sodium butyrate, NaB) on the DNA methylation status and mRNA expression levels of hDAT were examined.	nab	118-121	solute carrier family 6 member 3	Homo sapiens	183-187
29375555-12	2017	This SNP is located in TLR1A, which suggests a fundamental role of TLR1A on regulation of IgM levels (i.e., KLH-binding IgM NAb, and total IgM concentration), or B cells biology, or both.	nab	124-127	toll-like receptor 1 family member A	Gallus gallus	23-28
29375555-12	2017	This SNP is located in TLR1A, which suggests a fundamental role of TLR1A on regulation of IgM levels (i.e., KLH-binding IgM NAb, and total IgM concentration), or B cells biology, or both.	nab	124-127	toll-like receptor 1 family member A	Gallus gallus	67-72
30150888-1	2018	Aim of the study: This study aimed to assess the efficacy of anthracycline-based (AB) and non-anthracycline-based (nAB) adjuvant therapies in the human epidermal growth factor receptor 2 (HER2)-positive non-metastatic BC (nMBC) patients.	nab	115-118	erb-b2 receptor tyrosine kinase 2	Homo sapiens	188-192
29453918-9	2018	RESULTS: TSA, VPA, and NaB inhibited the expression of Pdx1 and Mafa genes and their products.	nab	23-26	pancreatic and duodenal homeobox 1	Mus musculus	55-59
29453918-9	2018	RESULTS: TSA, VPA, and NaB inhibited the expression of Pdx1 and Mafa genes and their products.	nab	23-26	v-maf musculoaponeurotic fibrosarcoma oncogene family, protein A (avian)	Mus musculus	64-68
28610743-10	2018	VPA and NaB also attenuated the Mn-induced decrease in GLT-1 and GLAST mRNA and protein levels in the cerebral cortical and cerebellar regions of mice.	nab	8-11	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	55-60
28610743-10	2018	VPA and NaB also attenuated the Mn-induced decrease in GLT-1 and GLAST mRNA and protein levels in the cerebral cortical and cerebellar regions of mice.	nab	8-11	solute carrier family 1 (glial high affinity glutamate transporter), member 3	Mus musculus	65-70
28610743-12	2018	VPA and NaB pretreatment in mice enhancing astrocytic glutamate transporter GLT-1 expression as well as locomotor activities.	nab	8-11	solute carrier family 1 (glial high affinity glutamate transporter), member 2	Mus musculus	76-81
28857504-6	2018	A history of nicotine exposure significantly decreased H3K14 acetylation at the brain-derived neurotrophic factor (BDNF) exon IV promoter, and this effect was abolished with NaB treatment.	nab	174-177	brain-derived neurotrophic factor	Rattus norvegicus	80-113
28857504-6	2018	A history of nicotine exposure significantly decreased H3K14 acetylation at the brain-derived neurotrophic factor (BDNF) exon IV promoter, and this effect was abolished with NaB treatment.	nab	174-177	brain-derived neurotrophic factor	Rattus norvegicus	115-119
28857504-8	2018	Quantitative PCR-identified changes in several genes associated with NaB treatment that were independent of nicotine exposure; however, an interaction of nicotine history and NaB treatment was detected only in the expression of BDNF IV and BDNF IX.	nab	175-178	brain-derived neurotrophic factor	Rattus norvegicus	228-232
28857504-8	2018	Quantitative PCR-identified changes in several genes associated with NaB treatment that were independent of nicotine exposure; however, an interaction of nicotine history and NaB treatment was detected only in the expression of BDNF IV and BDNF IX.	nab	175-178	brain-derived neurotrophic factor	Rattus norvegicus	240-244
28857504-9	2018	Together these results suggest that nicotine self-administration leads to a number of epigenetic changes at both the BDNF and Cdk-5 promoters, and that these changes may contribute to the enhanced extinction of nicotine-seeking by NaB.	nab	231-234	brain-derived neurotrophic factor	Rattus norvegicus	117-121
28857504-9	2018	Together these results suggest that nicotine self-administration leads to a number of epigenetic changes at both the BDNF and Cdk-5 promoters, and that these changes may contribute to the enhanced extinction of nicotine-seeking by NaB.	nab	231-234	cyclin-dependent kinase 5	Rattus norvegicus	126-131
30150888-1	2018	Aim of the study: This study aimed to assess the efficacy of anthracycline-based (AB) and non-anthracycline-based (nAB) adjuvant therapies in the human epidermal growth factor receptor 2 (HER2)-positive non-metastatic BC (nMBC) patients.	nab	115-118	erb-b2 receptor tyrosine kinase 2	Homo sapiens	152-186
29030220-5	2018	5-aza-dC and NaB decreased hypermethylation,while increase hDAT expression in SH-SY-5Y cells and recovered hDAT mRNA expression in HEK293 cells.	nab	13-16	solute carrier family 6 member 3	Homo sapiens	59-63
29030220-5	2018	5-aza-dC and NaB decreased hypermethylation,while increase hDAT expression in SH-SY-5Y cells and recovered hDAT mRNA expression in HEK293 cells.	nab	13-16	solute carrier family 6 member 3	Homo sapiens	107-111
29030220-7	2018	hDAT silencing was reversed by the introduction of DNA hypomethylation via 5-aza-dC or/and NaB.	nab	91-94	solute carrier family 6 member 3	Homo sapiens	0-4
28991639-12	2017	Unexpectedly, NaB in combination with HA suppressed the phosphorylation of Chk2 on threonine 68 and Chk1 on serine 345 in A2780 cells and downregulated p21WAF1/Cip1 in both tested cell lines.	nab	14-17	checkpoint kinase 2	Homo sapiens	75-79
29162799-4	2017	We here employ computational and structure-guided design to develop improved native-like trimers that reduce exposure of non-nAb epitopes in the V3-loop and trimer base, minimize both CD4 reactivity and CD4-induced non-nAb epitope exposure, and increase thermal stability while maintaining bnAb antigenicity.	nab	125-128	CD4 molecule	Homo sapiens	184-187
29162799-4	2017	We here employ computational and structure-guided design to develop improved native-like trimers that reduce exposure of non-nAb epitopes in the V3-loop and trimer base, minimize both CD4 reactivity and CD4-induced non-nAb epitope exposure, and increase thermal stability while maintaining bnAb antigenicity.	nab	125-128	CD4 molecule	Homo sapiens	203-206
29162799-4	2017	We here employ computational and structure-guided design to develop improved native-like trimers that reduce exposure of non-nAb epitopes in the V3-loop and trimer base, minimize both CD4 reactivity and CD4-induced non-nAb epitope exposure, and increase thermal stability while maintaining bnAb antigenicity.	nab	219-222	CD4 molecule	Homo sapiens	203-206
29435178-0	2018	Inhibition of the MEK/ERK pathway augments nab-paclitaxel-based chemotherapy effects in preclinical models of pancreatic cancer.	nab	43-46	mitogen-activated protein kinase kinase 7	Homo sapiens	18-21
29435178-0	2018	Inhibition of the MEK/ERK pathway augments nab-paclitaxel-based chemotherapy effects in preclinical models of pancreatic cancer.	nab	43-46	mitogen-activated protein kinase 1	Homo sapiens	22-25
29435178-9	2018	These findings suggest that the effects of nab-paclitaxel-based chemotherapy can be enhanced through specific inhibition of MEK1/2 kinase activity, and supports the clinical application of trametinib in combination with standard nab-paclitaxel-based chemotherapy in PDAC patients.	nab	43-46	mitogen-activated protein kinase kinase 1	Homo sapiens	124-130
29285378-14	2017	Thus, neoadjuvant therapy with FEC followed by nab-PTX for operable HER2-negative breast cancer was found to be a safe and effective option.	nab	47-50	erb-b2 receptor tyrosine kinase 2	Homo sapiens	68-72
28991639-12	2017	Unexpectedly, NaB in combination with HA suppressed the phosphorylation of Chk2 on threonine 68 and Chk1 on serine 345 in A2780 cells and downregulated p21WAF1/Cip1 in both tested cell lines.	nab	14-17	checkpoint kinase 1	Homo sapiens	100-104
28991639-12	2017	Unexpectedly, NaB in combination with HA suppressed the phosphorylation of Chk2 on threonine 68 and Chk1 on serine 345 in A2780 cells and downregulated p21WAF1/Cip1 in both tested cell lines.	nab	14-17	cyclin dependent kinase inhibitor 1A	Homo sapiens	160-164
29348852-8	2017	Knockdown of FBXW7 in vitro enhanced cell proliferation, and migration, and invasion abilities and promoted gemcitabine and nab-paclitaxel chemoresistance in pancreatic cancer cells.	nab	124-127	F-box and WD repeat domain containing 7	Homo sapiens	13-18
28923854-7	2017	Cav-1 protein levels correlated positively with nab-paclitaxel sensitivity.	nab	48-51	caveolin 1	Homo sapiens	0-5
29101359-6	2017	We furthermore show the complementary binding region on all three monoclonal antibodies to be the CDR H3 loop of the Fab region, and show that they all have nano to micromolar affinity for HSA Peptide 40 and nab-paclitaxel nanoparticles.	nab	208-211	FA complementation group B	Homo sapiens	117-120
28923854-8	2017	RNAi-mediated attenuation of Cav-1 expression reduced uptake of albumin and nab-paclitaxel in cancer cells and rendered them resistant to nab-paclitaxel-induced apoptosis.	nab	76-79	caveolin 1	Homo sapiens	29-34
28923854-9	2017	Conversely, Cav-1 overexpression enhanced sensitivity to nab-paclitaxel.	nab	57-60	caveolin 1	Homo sapiens	12-17
28923854-10	2017	Selection for cellular resistance to nab-paclitaxel in cell culture correlated with a loss of Cav-1 expression.	nab	37-40	caveolin 1	Homo sapiens	94-99
28923854-11	2017	In mouse xenograft models, cancer cells, where Cav-1 was attenuated, exhibited resistance to the antitumor effects of nab-paclitaxel therapy.	nab	118-121	caveolin 1, caveolae protein	Mus musculus	47-52
28923854-12	2017	Overall, our findings suggest Cav-1 as a predictive biomarker for the response to nab-paclitaxel and other albumin-based cancer therapeutic drugs.	nab	82-85	caveolin 1	Homo sapiens	30-35
28684304-7	2017	Mechanistically, the NaB-mediated inhibition of Th17 cell differentiation may occur via inhibition of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/interleukin-6 receptor pathway.	nab	21-24	nuclear factor, erythroid derived 2, like 2	Mus musculus	106-149
28701571-2	2017	We evaluated nab-Paclitaxel efficacy as neoadjuvant treatment for early estrogen receptor-positive (ER+), human epidermal growth factor receptor 2-negative (HER2-) disease.	nab	13-16	erb-b2 receptor tyrosine kinase 2	Homo sapiens	112-146
28684304-7	2017	Mechanistically, the NaB-mediated inhibition of Th17 cell differentiation may occur via inhibition of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/interleukin-6 receptor pathway.	nab	21-24	nuclear factor, erythroid derived 2, like 2	Mus musculus	151-155
28684304-7	2017	Mechanistically, the NaB-mediated inhibition of Th17 cell differentiation may occur via inhibition of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/interleukin-6 receptor pathway.	nab	21-24	heme oxygenase 1	Mus musculus	157-173
28684304-7	2017	Mechanistically, the NaB-mediated inhibition of Th17 cell differentiation may occur via inhibition of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1)/interleukin-6 receptor pathway.	nab	21-24	heme oxygenase 1	Mus musculus	175-179
28684304-8	2017	Moreover, the NaB-mediated inhibition on Th17 cell differentiation and uveitis were abrogated when an HO-1 inhibitor, SnPP, was used.	nab	14-17	heme oxygenase 1	Mus musculus	102-106
28684304-9	2017	These findings suggest that NaB inverts the differentiation of Th17 cells toward Treg cells and attenuates experimental autoimmune uveitis by modulating the Nrf2/HO-1 pathway.	nab	28-31	nuclear factor, erythroid derived 2, like 2	Mus musculus	157-161
28684304-9	2017	These findings suggest that NaB inverts the differentiation of Th17 cells toward Treg cells and attenuates experimental autoimmune uveitis by modulating the Nrf2/HO-1 pathway.	nab	28-31	heme oxygenase 1	Mus musculus	162-166
28687352-8	2017	In conclusion, we found that nAb-PTX treatment of gem-resistant PDAC can be enhanced by (1) gem through up-regulation of caveolin-1 and (2) MSV through increasing accumulation of nAb-PTX in the tumor.	nab	29-32	caveolin 1	Homo sapiens	121-131
28991675-9	2017	Moreover, NaB treatment prevented the MPTP-induced dopaminergic degeneration and decreased expression level of TH in the striatum.	nab	10-13	tyrosine hydroxylase	Mus musculus	111-113
28991675-10	2017	NaB treatment attenuated the PD-associated disruption of BBB by upregulation of Occludin and zonula occludens (ZO)-1.	nab	0-3	occludin	Mus musculus	80-88
28991675-10	2017	NaB treatment attenuated the PD-associated disruption of BBB by upregulation of Occludin and zonula occludens (ZO)-1.	nab	0-3	tight junction protein 1	Mus musculus	93-116
28991675-11	2017	In addition, NaB resulted in increased level of Bcl-2 and decreased level of Bax.	nab	13-16	B cell leukemia/lymphoma 2	Mus musculus	48-53
28991675-11	2017	In addition, NaB resulted in increased level of Bcl-2 and decreased level of Bax.	nab	13-16	BCL2-associated X protein	Mus musculus	77-80
28991675-12	2017	Particularly, NaB-treated mice with PD exhibited increased colonic GLP-1 level as well as upregulation of brain GLP-1R expression compared with PD group.	nab	14-17	glucagon	Mus musculus	67-72
28991675-12	2017	Particularly, NaB-treated mice with PD exhibited increased colonic GLP-1 level as well as upregulation of brain GLP-1R expression compared with PD group.	nab	14-17	glucagon-like peptide 1 receptor	Mus musculus	112-118
28991675-13	2017	Our findings suggest that NaB has potential as a novel therapeutic for treatment of PD, and its mechanism was associated with stimulating colonic GLP-1secretion.	nab	26-29	glucagon	Mus musculus	146-151
29036920-8	2017	The in vitro results indicated that the pattern gel showed angiogenic and osteogenic responses with good ALP activity and enhanced HIF-1alpha, and Runx2 levels in the presence of DMOG and NaB in MC3T3 cells.	nab	188-191	hypoxia inducible factor 1 subunit alpha	Homo sapiens	131-141
29036920-8	2017	The in vitro results indicated that the pattern gel showed angiogenic and osteogenic responses with good ALP activity and enhanced HIF-1alpha, and Runx2 levels in the presence of DMOG and NaB in MC3T3 cells.	nab	188-191	RUNX family transcription factor 2	Homo sapiens	147-152
28581516-4	2017	Although the drug targeting inactivation of tumor suppressors by DNA methylation had little effect, the inhibition of Mek, a K-Ras effector, in combination with the standard of care (chemotherapy consisting of gemcitabine/Nab-paclitaxel), reduced the growth of three out of five PC-PDXs and impaired metastasis.	nab	222-225	mitogen-activated protein kinase kinase 7	Homo sapiens	118-121
28581516-9	2017	Together with the gemcitabine/Nab-paclitaxel backbone, Mek inhibition could be effective in treatment of PC.	nab	30-33	mitogen-activated protein kinase kinase 7	Homo sapiens	55-58
28651144-4	2017	S-nitrosated human serum albumin dimer (SNO-HSA Dimer) shown promising activity previously was evaluated for the synergistic effect when used as a pretreatment agent in nab-PTX therapy against various tumor models.	nab	169-172	snubnose	Mus musculus	40-43
28651144-5	2017	In the high vascular permeability C26 murine colon cancer subcutaneous inoculation model, SNO-HSA Dimer enhanced tumor selectivity of nab-PTX, and attenuated myelosuppression.	nab	134-137	snubnose	Mus musculus	90-93
28651144-6	2017	SNO-HSA Dimer also augmented the tumor growth inhibition of nab-PTX in low vascular permeability B16 murine melanoma subcutaneous inoculation model.	nab	60-63	snubnose	Mus musculus	0-3
28539451-8	2017	The additional introduction of the E64K ground-state stabilizing substitution markedly reduced or ablated soluble CD4 (sCD4) induction of non-NAb epitopes in V3 and/or associated with the coreceptor binding site.	nab	142-145	CD4 molecule	Homo sapiens	114-117
31305693-0	2017	Erratum: Marked response to nab-paclitaxel in EGFR mutated lung neuroendocrine carcinoma: A case report: Erratum.	nab	28-31	epidermal growth factor receptor	Homo sapiens	46-50
28631095-7	2017	Transfected neuroblastoma cells stably expressed DCN, with in vivo and in vitro studies demonstrating rAAV-DCN sensitized the anticancer effect of nab-paclitaxel.	nab	147-150	decorin	Homo sapiens	49-52
28631095-7	2017	Transfected neuroblastoma cells stably expressed DCN, with in vivo and in vitro studies demonstrating rAAV-DCN sensitized the anticancer effect of nab-paclitaxel.	nab	147-150	decorin	Homo sapiens	107-110
28631095-10	2017	The systemic administration of rAAV-DCN up-regulates DCN in neuroblastoma and accelerates the intratumoral uptake of nab-paclitaxel by inhibiting stabilin-1 mediated SPARC degradation.	nab	117-120	decorin	Homo sapiens	36-39
28631095-10	2017	The systemic administration of rAAV-DCN up-regulates DCN in neuroblastoma and accelerates the intratumoral uptake of nab-paclitaxel by inhibiting stabilin-1 mediated SPARC degradation.	nab	117-120	stabilin 1	Mus musculus	146-156
28596114-5	2017	Secondary liver transduction with the same dose of AAV1-human factor IX (hFIX) in the presence of high levels of anti-AAV5ch NAB proved to be successful because expression/activity of both reporter transgenes was observed.	nab	125-128	coagulation factor IX	Homo sapiens	73-77
28541630-1	2017	OBJECTIVE: To report on the incidence of nab-paclitaxel hypersensitivity reactions (HSRs) in patients with prior taxane HSR.	nab	41-44	HSR	Homo sapiens	84-87
28574840-6	2017	Treatment on 4910 and 5310 xenograft cell lines with sodium butyrate (NaB) significantly decreased HEY1 expression with a concomitant increase in DNMT1 expression, confirming that promoter methylation may regulate HEY1 expression in GBM.	nab	70-73	hes related family bHLH transcription factor with YRPW motif 1	Homo sapiens	99-103
28574840-6	2017	Treatment on 4910 and 5310 xenograft cell lines with sodium butyrate (NaB) significantly decreased HEY1 expression with a concomitant increase in DNMT1 expression, confirming that promoter methylation may regulate HEY1 expression in GBM.	nab	70-73	DNA methyltransferase 1	Homo sapiens	146-151
28574840-6	2017	Treatment on 4910 and 5310 xenograft cell lines with sodium butyrate (NaB) significantly decreased HEY1 expression with a concomitant increase in DNMT1 expression, confirming that promoter methylation may regulate HEY1 expression in GBM.	nab	70-73	hes related family bHLH transcription factor with YRPW motif 1	Homo sapiens	214-218
28599410-8	2017	Cabozantinib and crizotinib sensitized tumor cells to nab-paclitaxel and paclitaxel in the same dose-dependent manner in cell lines overexpressing ABCB1, without altering the downstream signaling of tyrosine kinases.	nab	54-57	ATP binding cassette subfamily B member 1	Homo sapiens	147-152
28599410-9	2017	These results suggest that the overexpression of ABCB1 confers resistance to nab-paclitaxel in urothelial cancer cells.	nab	77-80	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
28256066-0	2017	Randomized phase II study of nab-paclitaxel as first-line chemotherapy in patients with HER2-negative metastatic breast cancer.	nab	29-32	erb-b2 receptor tyrosine kinase 2	Homo sapiens	88-92
28108630-5	2017	The macropinocytic uptake of nab-paclitaxel induced macrophage immunostimulatory (M1) cytokine expression and synergized with IFNgamma to promote inducible nitric oxide synthase expression in a TLR4-dependent manner.	nab	29-32	interferon gamma	Homo sapiens	126-134
28538405-0	2017	Marked response to nab-paclitaxel in EGFR mutated lung neuroendocrine carcinoma: A case report.	nab	19-22	epidermal growth factor receptor	Homo sapiens	37-41
28413662-3	2017	Based on these results, a phase I study of combination therapy with nab-paclitaxel, carboplatin and trastuzumab was planned, in order to estimate its efficacy and safety for HER2-overexpressing locally advanced breast cancer.	nab	68-71	erb-b2 receptor tyrosine kinase 2	Homo sapiens	174-178
27635089-8	2017	In all three tumor xenograft models, changes in human serum mesothelin correlated with response to therapy and were undetectable in mice with complete tumor regression with RG7787 and nab-paclitaxel.Conclusions: RG7787 plus nab-paclitaxel is very active against primary human mesothelioma cells in vitro as well as in vivo, with serum mesothelin levels correlating with tumor response.	nab	184-187	mesothelin	Mus musculus	60-70
27635089-8	2017	In all three tumor xenograft models, changes in human serum mesothelin correlated with response to therapy and were undetectable in mice with complete tumor regression with RG7787 and nab-paclitaxel.Conclusions: RG7787 plus nab-paclitaxel is very active against primary human mesothelioma cells in vitro as well as in vivo, with serum mesothelin levels correlating with tumor response.	nab	224-227	mesothelin	Mus musculus	60-70
28273882-7	2017	Treatment with NLRP3 inhibitors using NaB and HBA preserved corneal clarity and decreased NLRP3, caspase-1, and IL-1beta mRNA transcripts, as well as NLRP3 protein expression on post-injury compared to BSS-treated corneas.	nab	38-41	NLR family, pyrin domain containing 3	Mus musculus	15-20
28273882-7	2017	Treatment with NLRP3 inhibitors using NaB and HBA preserved corneal clarity and decreased NLRP3, caspase-1, and IL-1beta mRNA transcripts, as well as NLRP3 protein expression on post-injury compared to BSS-treated corneas.	nab	38-41	NLR family, pyrin domain containing 3	Mus musculus	90-95
28273882-7	2017	Treatment with NLRP3 inhibitors using NaB and HBA preserved corneal clarity and decreased NLRP3, caspase-1, and IL-1beta mRNA transcripts, as well as NLRP3 protein expression on post-injury compared to BSS-treated corneas.	nab	38-41	caspase 1	Mus musculus	97-106
28273882-7	2017	Treatment with NLRP3 inhibitors using NaB and HBA preserved corneal clarity and decreased NLRP3, caspase-1, and IL-1beta mRNA transcripts, as well as NLRP3 protein expression on post-injury compared to BSS-treated corneas.	nab	38-41	interleukin 1 beta	Mus musculus	112-120
28273882-7	2017	Treatment with NLRP3 inhibitors using NaB and HBA preserved corneal clarity and decreased NLRP3, caspase-1, and IL-1beta mRNA transcripts, as well as NLRP3 protein expression on post-injury compared to BSS-treated corneas.	nab	38-41	NLR family, pyrin domain containing 3	Mus musculus	90-95
27831502-7	2017	In HER2+/HR+ tumors, the pCR rate was 52.9% (49.7% Pac, 56.4% nab-Pac).	nab	62-65	erb-b2 receptor tyrosine kinase 2	Homo sapiens	3-7
28279830-2	2017	In new immunizations, we attempted to improve nAb responses by removing the N362 glycan that also lines the CD4bs.	nab	46-49	CD4 molecule	Homo sapiens	108-111
28460447-9	2017	Furthermore, NaB could still promote pBD3 and pEP2C expression and inhibit IL-6 production in the presence of the toll-like receptor 2 (TLR2) ligand peptidoglycan.	nab	13-16	interleukin 6	Sus scrofa	75-79
28460447-9	2017	Furthermore, NaB could still promote pBD3 and pEP2C expression and inhibit IL-6 production in the presence of the toll-like receptor 2 (TLR2) ligand peptidoglycan.	nab	13-16	toll like receptor 2	Sus scrofa	114-134
28460447-9	2017	Furthermore, NaB could still promote pBD3 and pEP2C expression and inhibit IL-6 production in the presence of the toll-like receptor 2 (TLR2) ligand peptidoglycan.	nab	13-16	toll like receptor 2	Sus scrofa	136-140
28108630-5	2017	The macropinocytic uptake of nab-paclitaxel induced macrophage immunostimulatory (M1) cytokine expression and synergized with IFNgamma to promote inducible nitric oxide synthase expression in a TLR4-dependent manner.	nab	29-32	toll like receptor 4	Homo sapiens	194-198
28057758-11	2017	The binding of histone H3 to the promoter region of miR-497 was inhibited by TSA and NaB, whereas that of claudin-2 was not.	nab	85-88	microRNA 497	Homo sapiens	52-59
28057758-3	2017	We found that azacitidine (AZA), a DNA methylation inhibitor, and trichostatin A (TSA) and sodium butyrate (NaB), histone deacetylase (HDAC) inhibitors, decrease claudin-2 levels.	nab	108-111	claudin 2	Homo sapiens	162-171
28057758-13	2017	Cell proliferation was additively decreased by AZA, TSA, and NaB, which was partially rescued by ectopic expression of claudin-2.	nab	61-64	claudin 2	Homo sapiens	119-128
27980102-6	2017	Therapeutic potential of CCL2-CCR2 axis blockade was determined by treating KO mice with a CCL2-neutralizing antibody (nAb).	nab	119-122	chemokine (C-C motif) ligand 2	Mus musculus	25-29
28293479-0	2017	MxA mRNA decrease preceding NAb detection in IFNbeta-treated MS patients.	nab	28-31	MX dynamin like GTPase 1	Homo sapiens	0-3
28293479-3	2017	AIMS: The aim of this study was to analyze the kinetics of MxA mRNA expression during long-term IFNbeta treatment and assess its relationship to NAb production.	nab	145-148	MX dynamin like GTPase 1	Homo sapiens	59-62
27980102-6	2017	Therapeutic potential of CCL2-CCR2 axis blockade was determined by treating KO mice with a CCL2-neutralizing antibody (nAb).	nab	119-122	chemokine (C-C motif) ligand 2	Mus musculus	91-95
27980102-8	2017	Furthermore, treatment of tumor-bearing KO mice with CCL2 nAb for 8 weeks significantly reduced liver damage, hepatocellular carcinoma incidence, and tumor burden.	nab	58-61	chemokine (C-C motif) ligand 2	Mus musculus	53-57
27980102-10	2017	In addition, CCL2 nAb enhanced hepatic NK-cell cytotoxicity and IFNgamma production, which is likely to contribute to the inhibition of tumorigenesis.	nab	18-21	C-C motif chemokine ligand 2	Homo sapiens	13-17
27980102-10	2017	In addition, CCL2 nAb enhanced hepatic NK-cell cytotoxicity and IFNgamma production, which is likely to contribute to the inhibition of tumorigenesis.	nab	18-21	interferon gamma	Homo sapiens	64-72
28420840-0	2017	Successful Long-term Management with a Single Administration of Tri-weekly Nab-paclitaxel in a Patient with Advanced Gastric Cancer with Peritoneal Dissemination.	nab	75-78	tRNA-Ile (anticodon AAT) 9-1	Homo sapiens	64-67
28081207-9	2017	In NAb negative patients, clinical status was correlated to MxA mRNA values.	nab	3-6	MX dynamin like GTPase 1	Homo sapiens	60-63
28041878-5	2017	Conversion with inhibitors of histone deacetylases (HDACi), NaB, TSA, or VPA, further increased Rex1 expression, while decreasing expression of exogenous genes.	nab	60-63	RNA exonuclease 1 homolog	Homo sapiens	96-100
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	myeloid differentiation primary response gene 88	Mus musculus	44-49
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	mast cell protease 1	Mus musculus	82-87
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	tumor necrosis factor	Mus musculus	89-98
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	interleukin 1 complex	Mus musculus	100-104
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	interleukin 2	Mus musculus	106-110
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	interleukin 6	Mus musculus	112-116
28104981-7	2017	Endotoxin-associated genes such as TLR4 and Myd88, pro-inflammation genes such as MCP-1, TNF-alpha, IL-1, IL-2, IL-6 and IFN-gamma in liver or epididymal fat were obviously downregulated after NaB intervention.	nab	193-196	interferon gamma	Mus musculus	121-130
28104981-8	2017	Liver inflammation and fat accumulation were ameliorated, the levels of TG and cholesterol in liver were decreased after NaB intervention, NAS score was significantly decreased, metabolic indices such as FBG and HOMA-IR and liver function indicators ALT and AST were improved compared with HF group.	nab	121-124	glutamic pyruvic transaminase, soluble	Mus musculus	250-253
28104981-8	2017	Liver inflammation and fat accumulation were ameliorated, the levels of TG and cholesterol in liver were decreased after NaB intervention, NAS score was significantly decreased, metabolic indices such as FBG and HOMA-IR and liver function indicators ALT and AST were improved compared with HF group.	nab	121-124	transmembrane protease, serine 11d	Mus musculus	258-261
27799462-4	2017	Sodium butyrate (NaB) is a known activator of NRF2.	nab	17-20	nuclear factor, erythroid derived 2, like 2	Mus musculus	46-50
27799462-8	2017	NaB inhibited histone deacetylase (HDAC) activity and elevated the expression of Nrf2 and its downstream targets heme oxygenase 1 and NAD(P)H dehydrogenase quinone 1.	nab	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	81-85
27799462-8	2017	NaB inhibited histone deacetylase (HDAC) activity and elevated the expression of Nrf2 and its downstream targets heme oxygenase 1 and NAD(P)H dehydrogenase quinone 1.	nab	0-3	heme oxygenase 1	Mus musculus	113-165
27799462-9	2017	Notably, deletion of the Nrf2 gene completely abolished NaB activation of NRF2 signaling and protection against diabetes-induced renal injury.	nab	56-59	nuclear factor, erythroid derived 2, like 2	Mus musculus	25-29
27799462-9	2017	Notably, deletion of the Nrf2 gene completely abolished NaB activation of NRF2 signaling and protection against diabetes-induced renal injury.	nab	56-59	nuclear factor, erythroid derived 2, like 2	Mus musculus	74-78
27799462-12	2017	Therefore, the present study indicates, for the first time, that NRF2 plays a key role in NaB protection against DN.	nab	90-93	nuclear factor, erythroid derived 2, like 2	Mus musculus	65-69
27799462-13	2017	Other findings suggest that NaB may activate Nrf2 at the transcriptional level, possibly by the inhibition of HDAC activity.	nab	28-31	nuclear factor, erythroid derived 2, like 2	Mus musculus	45-49
28399090-12	2017	An analysis of nAB profiles to pain regulators showed that they were correlated with higher and high indices, with the predominance of nAB to beta-endorphin, orphanin and histamine in both groups.	nab	15-18	proopiomelanocortin	Homo sapiens	142-156
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	interleukin 22	Mus musculus	5-10
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	signal transducer and activator of transcription 3	Mus musculus	143-148
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	mitogen-activated protein kinase 1	Mus musculus	153-156
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	interleukin 17A	Mus musculus	215-220
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	interleukin 6	Mus musculus	222-226
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	interleukin 1 beta	Mus musculus	228-236
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	interferon gamma	Mus musculus	238-247
29358851-8	2017	Anti-IL-22 nAb significantly alleviated the severity of hypertrophy, prevented systolic and diastolic abnormalities, reduced cardiac fibrosis, STAT3 and ERK phosphorylation, and downregulated the mRNA expression of IL-17, IL-6, IL-1beta, IFN-gamma, and TNF-alpha.	nab	11-14	tumor necrosis factor	Mus musculus	253-262
29358851-9	2017	In addition, IL-22 nAb attenuated angiotensin II-induced hypertrophy in H9C2 cells.	nab	19-22	interleukin 22	Rattus norvegicus	13-18
29358851-9	2017	In addition, IL-22 nAb attenuated angiotensin II-induced hypertrophy in H9C2 cells.	nab	19-22	angiotensinogen	Rattus norvegicus	34-48
27905989-9	2016	At the early acute phase (2 days post stroke), NaB treatment decreased brain lipid peroxides, and reduced serum levels of GFAP, a surrogate marker of blood-brain barrier (BBB) permeability.	nab	47-50	glial fibrillary acidic protein	Rattus norvegicus	122-126
27941965-9	2016	In HIV-infected participants, each 10% increase in CD4/CD8 ratio predicted a mean 21% higher post-baseline YFV Nab titer (p = 0.024).	nab	111-114	CD4 molecule	Homo sapiens	51-54
27941965-9	2016	In HIV-infected participants, each 10% increase in CD4/CD8 ratio predicted a mean 21% higher post-baseline YFV Nab titer (p = 0.024).	nab	111-114	CD8a molecule	Homo sapiens	55-58
27919976-0	2016	Phase I Study of Triweekly Nab-Paclitaxel Combined with S-1 in Patients with HER2-negative Metastatic Breast Cancer.	nab	27-30	erb-b2 receptor tyrosine kinase 2	Homo sapiens	77-81
27342118-3	2016	NaB induced the activation of CREB in hippocampal neurons via protein kinase A (PKA), which was responsible for the upregulation of plasticity-related molecules.	nab	0-3	cAMP responsive element binding protein 1	Mus musculus	30-34
27342118-5	2016	However, oral treatment of cinnamon and NaB increased spatial memory consolidation-induced activation of CREB and expression of plasticity-related molecules in the hippocampus of poor-learning mice and converted poor learners into good learners.	nab	40-43	cAMP responsive element binding protein 1	Mus musculus	105-109
27905989-10	2016	NaB also reduced expression of the inflammatory cytokine IL-1beta in circulation and IL-18 in the ischemic hemisphere.	nab	0-3	interleukin 1 beta	Rattus norvegicus	57-65
27905989-10	2016	NaB also reduced expression of the inflammatory cytokine IL-1beta in circulation and IL-18 in the ischemic hemisphere.	nab	0-3	interleukin 18	Rattus norvegicus	85-90
27905989-11	2016	At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor.	nab	46-49	interleukin 1 beta	Rattus norvegicus	104-112
27905989-11	2016	At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor.	nab	46-49	interleukin 17A	Rattus norvegicus	114-120
27905989-11	2016	At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor.	nab	46-49	interleukin 18	Rattus norvegicus	126-131
27905989-11	2016	At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor.	nab	46-49	interleukin 1 beta	Rattus norvegicus	248-256
27905989-11	2016	At the late acute phase (5 days post stroke), NaB treatment further suppressed MCAo-induced increase of IL-1beta, IL-17A, and IL-18 in brain lysates (cortex and striatum) from the ischemic hemisphere, and decreased ischemia-induced upregulation of IL-1beta and IL-18 in circulation, indicating a potent anti-inflammatory effect of the HDAC inhibitor.	nab	46-49	interleukin 18	Rattus norvegicus	261-266
27905989-12	2016	Moreover, NaB treatment also increased expression of IGF-1, a known neuroprotectant, in peripheral tissue including serum, liver, and spleen at the late acute phase.	nab	10-13	insulin-like growth factor 1	Rattus norvegicus	53-58
27905989-14	2016	Additionally, these data also show that in addition to its well-known anti-inflammatory actions, NaB may exert a biphasic effect after stroke, operating initially to reduce BBB permeability and oxidative stress in the brain, and later, elevating IGF-1 expression in peripheral tissues.	nab	97-100	insulin-like growth factor 1	Rattus norvegicus	246-251
27615158-7	2016	Treatment of FRDA iPSCs with two compounds, sodium butyrate (NaB) and Parnate, led to an increase in FXN expression and correction of repressive marks at the FXN locus, which persisted for several passages.	nab	61-64	frataxin	Homo sapiens	101-104
27615158-7	2016	Treatment of FRDA iPSCs with two compounds, sodium butyrate (NaB) and Parnate, led to an increase in FXN expression and correction of repressive marks at the FXN locus, which persisted for several passages.	nab	61-64	frataxin	Homo sapiens	158-161
27920708-6	2016	CONCLUSION: A multidisciplinary approach to local control and attenuated doses of nab-paclitaxel and trastuzumab suggest a durable response to HER-2-positive breast cancer with cutaneous metastasis.	nab	82-85	erb-b2 receptor tyrosine kinase 2	Homo sapiens	143-148
27880897-5	2016	Unexpectedly, nAb development best correlated with booster immunization GC B cell magnitude and Tfh characteristics of the Env-specific CD4 T cells.	nab	14-17	endogenous retrovirus group V member 2 Env polyprotein	Macaca mulatta	123-126
27735862-5	2016	Upon the activation of AMPK, NaB promoted the reassembly of tight junctions (TJs) based on reducing the phosphorylation of myosin II regulatory light chain (MLC2) at Ser19 and increasing phosphorylation of protein kinase C beta2 (PKCbeta2) at Ser660.	nab	29-32	myosin light chain 2	Homo sapiens	157-161
27914464-4	2016	Cell lines sensitive to IFN-beta activity also quantifying NAb level are applied because direct measurement of IFN-beta antiviral activity is complicated.	nab	59-62	interferon beta 1	Homo sapiens	111-119
27914464-5	2016	This study was aimed at standardization and validation of a reporter cell system for measuring anti-human IFN-beta NAb titers, and evaluation data were obtained with samples from 33 patients with multiple sclerosis.	nab	115-118	interferon beta 1	Homo sapiens	106-114
27822069-2	2016	Secreted protein acidic and rich in cysteine (SPARC) binds to albumin, suggesting that SPARC plays an important role in tumor uptake of nab-paclitaxel.	nab	136-139	secreted protein acidic and cysteine rich	Homo sapiens	0-44
27822069-2	2016	Secreted protein acidic and rich in cysteine (SPARC) binds to albumin, suggesting that SPARC plays an important role in tumor uptake of nab-paclitaxel.	nab	136-139	secreted protein acidic and cysteine rich	Homo sapiens	46-51
27822069-2	2016	Secreted protein acidic and rich in cysteine (SPARC) binds to albumin, suggesting that SPARC plays an important role in tumor uptake of nab-paclitaxel.	nab	136-139	secreted protein acidic and cysteine rich	Homo sapiens	87-92
27822069-9	2016	Furthermore, patients with high stromal SPARC reactivity in biopsy specimens such as transbronchial lung biopsy or surgical specimens tended to respond better to nab-paclitaxel.	nab	162-165	secreted protein acidic and cysteine rich	Homo sapiens	40-45
27822069-11	2016	SPARC may be a useful predictive marker for selecting patients likely to respond favorably to nab-paclitaxel treatment.	nab	94-97	secreted protein acidic and cysteine rich	Homo sapiens	0-5
27981013-0	2016	PLGA-PNIPAM Microspheres Loaded with the Gastrointestinal Nutrient NaB Ameliorate Cardiac Dysfunction by Activating Sirt3 in Acute Myocardial Infarction.	nab	67-70	sirtuin 3	Rattus norvegicus	116-121
27981013-5	2016	Here, this study shows that PP-N can significantly ameliorate cardiac dysfunction in AMI, and NaB can specially bind to Sirt3 structure, activating its deacetylation ability and inhibiting the generation of reactive oxygen species, autophagy, and angiogenesis promotion.	nab	94-97	sirtuin 3	Rattus norvegicus	120-125
27605008-7	2016	Furthermore, we demonstrated that blocking of TGF-beta by neutralizing Abs abrogated NaB-mediated protection of Tregs and experimental allergic encephalomyelitis.	nab	85-88	transforming growth factor beta 1	Homo sapiens	46-54
27605008-8	2016	These studies identify a new function of NaB in upregulating TGF-beta via activation of STAT6, which may be beneficial in MS patients.	nab	41-44	transforming growth factor beta 1	Homo sapiens	61-69
27605008-8	2016	These studies identify a new function of NaB in upregulating TGF-beta via activation of STAT6, which may be beneficial in MS patients.	nab	41-44	signal transducer and activator of transcription 6	Homo sapiens	88-93
27930644-5	2016	In combination with nab-paclitaxel, confirmed response rates were 46% in a PD-L1-unselected population in the first-line metastatic triple-negative breast cancer setting.	nab	20-23	CD274 molecule	Homo sapiens	75-80
27605008-4	2016	Because TGF-beta is an important inducer of Tregs, we examined the effect of NaB on the status of TGF-beta.	nab	77-80	transforming growth factor beta 1	Homo sapiens	98-106
27605008-5	2016	In this study, we demonstrated that NaB induced the expression of TGF-beta mRNA and protein in normal as well as proteolipid protein-primed splenocytes.	nab	36-39	transforming growth factor beta 1	Homo sapiens	66-74
27735862-6	2016	Inhibiting (protein kinase C beta) PKCbeta blocked the reassembly of TJs induced by NaB in the barrier monolayer model.	nab	84-87	protein kinase C beta	Homo sapiens	12-33
27735862-6	2016	Inhibiting (protein kinase C beta) PKCbeta blocked the reassembly of TJs induced by NaB in the barrier monolayer model.	nab	84-87	protein kinase C beta	Homo sapiens	35-42
27735862-7	2016	These results indicated that NaB could activate the calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) pathway to mediate AMPK phosphorylating, which then inhibited the phosphorylation of MLC2 and promoted the phosphorylation of PKCbeta2, respectively, so that the downstream molecules of AMPK coordinately contributed to the reassembly of TJs in the Caco-2 barrier model.	nab	29-32	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	109-118
27735862-7	2016	These results indicated that NaB could activate the calcium/calmodulin-dependent protein kinase kinase beta (CaMKKbeta) pathway to mediate AMPK phosphorylating, which then inhibited the phosphorylation of MLC2 and promoted the phosphorylation of PKCbeta2, respectively, so that the downstream molecules of AMPK coordinately contributed to the reassembly of TJs in the Caco-2 barrier model.	nab	29-32	myosin light chain 2	Homo sapiens	205-209
27307148-10	2016	Treatment with NaB not only restored the histone acetylation of the GLT-1 and mGLuR1/5 promoter regions and glutamate excitatory neurotoxicity in hippocampal neurons, but also improved cognitive impairment in vivo.	nab	15-18	solute carrier family 1 member 2	Rattus norvegicus	68-73
27611715-2	2016	Sodium benzoate (NaB) deviates the cytokine profile to Th2 (or IL-4 producing) cells in EAE and thus might be effective in the treatment of MS.	nab	17-20	interleukin 4	Homo sapiens	63-67
27611715-3	2016	Therefore, in this study the effect of different concentrations of NaB on the percentage and mRNA levels of IL-4 and interferon gamma (IFN-gamma)-producing peripheral blood mononuclear cells (PBMCs) of 20 Relapsing-remitting multiple sclerosis (RR-MS) patients and eight healthy controls was evaluated in the presence of mitogen (phytohemagglutinin, PHA) or specific antigen (myelin basic protein, MBP).	nab	67-70	interleukin 4	Homo sapiens	108-112
27611715-3	2016	Therefore, in this study the effect of different concentrations of NaB on the percentage and mRNA levels of IL-4 and interferon gamma (IFN-gamma)-producing peripheral blood mononuclear cells (PBMCs) of 20 Relapsing-remitting multiple sclerosis (RR-MS) patients and eight healthy controls was evaluated in the presence of mitogen (phytohemagglutinin, PHA) or specific antigen (myelin basic protein, MBP).	nab	67-70	interferon gamma	Homo sapiens	117-144
27611715-4	2016	Our results showed that in the patient"s group the percentage of CD4(+)IL-4(+) cells was significantly increased in the presence of all concentrations of NaB when PBMCs were stimulated by MBP (p = 0.001) or PHA (p &lt; 0.03).	nab	154-157	CD4 molecule	Homo sapiens	65-68
27611715-4	2016	Our results showed that in the patient"s group the percentage of CD4(+)IL-4(+) cells was significantly increased in the presence of all concentrations of NaB when PBMCs were stimulated by MBP (p = 0.001) or PHA (p &lt; 0.03).	nab	154-157	interleukin 4	Homo sapiens	71-75
27611715-4	2016	Our results showed that in the patient"s group the percentage of CD4(+)IL-4(+) cells was significantly increased in the presence of all concentrations of NaB when PBMCs were stimulated by MBP (p = 0.001) or PHA (p &lt; 0.03).	nab	154-157	myelin basic protein	Homo sapiens	188-191
27611715-6	2016	Moreover, in the patient"s group the percentage of CD4(+)IFN-gamma(+) cells was decreased significantly when the PBMCs were stimulated by PHA and NaB (p &lt; 0.004) or by MBP and 1000 microg/ml of NaB (p &lt; 0.03).	nab	146-149	CD4 molecule	Homo sapiens	51-54
27611715-6	2016	Moreover, in the patient"s group the percentage of CD4(+)IFN-gamma(+) cells was decreased significantly when the PBMCs were stimulated by PHA and NaB (p &lt; 0.004) or by MBP and 1000 microg/ml of NaB (p &lt; 0.03).	nab	146-149	interferon gamma	Homo sapiens	57-66
27611715-6	2016	Moreover, in the patient"s group the percentage of CD4(+)IFN-gamma(+) cells was decreased significantly when the PBMCs were stimulated by PHA and NaB (p &lt; 0.004) or by MBP and 1000 microg/ml of NaB (p &lt; 0.03).	nab	197-200	CD4 molecule	Homo sapiens	51-54
27611715-6	2016	Moreover, in the patient"s group the percentage of CD4(+)IFN-gamma(+) cells was decreased significantly when the PBMCs were stimulated by PHA and NaB (p &lt; 0.004) or by MBP and 1000 microg/ml of NaB (p &lt; 0.03).	nab	197-200	interferon gamma	Homo sapiens	57-66
27611715-7	2016	The effect of NaB on IL-4 and IFN-gamma production was also documented at the mRNA levels.	nab	14-17	interleukin 4	Homo sapiens	21-25
27611715-7	2016	The effect of NaB on IL-4 and IFN-gamma production was also documented at the mRNA levels.	nab	14-17	interferon gamma	Homo sapiens	30-39
27611715-8	2016	In conclusion, our data suggest that NaB is able to induce IL-4 production by human PBMCs and therefore might be a useful candidate for conjunctive therapy in RR-MS.	nab	37-40	interleukin 4	Homo sapiens	59-63
26331238-6	2016	Results show a marked induction of SERCA3a and pan-SERCA3 mRNA expression in human MCF-7 and MDA-MB-231 cells treated with sodium butyrate (NaB) or trichostatin A (TSA); whereas SERCA2b mRNA expression did not change significantly.	nab	140-143	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	35-41
26331238-7	2016	ChIP assays show that NaB or TSA treatment of MDA-MB-231 cells increases H3K9 acetylation on ATP2A3 promoter.	nab	22-25	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	93-99
26331238-8	2016	NaB also decreases H3K9 trimethylation; suggesting that these modifications stimulate ATP2A3 gene expression, through a chromatin remodeling mechanism.	nab	0-3	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	86-92
27307148-10	2016	Treatment with NaB not only restored the histone acetylation of the GLT-1 and mGLuR1/5 promoter regions and glutamate excitatory neurotoxicity in hippocampal neurons, but also improved cognitive impairment in vivo.	nab	15-18	glutamate metabotropic receptor 1	Rattus norvegicus	78-84
26868208-9	2016	CONCLUSIONS: NAb-producing B-1b B cells are increased in Id3(Bcell KO) mice and attenuate adipose tissue inflammation and glucose intolerance in diet-induced obese mice.	nab	13-16	inhibitor of DNA binding 3	Mus musculus	57-69
26876786-3	2016	Further, SAHA and NaB decrease the phosphorylation, protein and mRNA levels of mutant p53 (mtp53) in TNBC cells.	nab	18-21	tumor protein p53	Homo sapiens	86-89
26876786-7	2016	The luciferase assay and ChIP analysis reveal that both SAHA and NaB can reduce the binding of transcription factor Yin Yang 1 (YY1) with the -102 to -96 position of human p53 promoter.	nab	65-68	YY1 transcription factor	Homo sapiens	116-126
26876786-7	2016	The luciferase assay and ChIP analysis reveal that both SAHA and NaB can reduce the binding of transcription factor Yin Yang 1 (YY1) with the -102 to -96 position of human p53 promoter.	nab	65-68	YY1 transcription factor	Homo sapiens	128-131
26876786-7	2016	The luciferase assay and ChIP analysis reveal that both SAHA and NaB can reduce the binding of transcription factor Yin Yang 1 (YY1) with the -102 to -96 position of human p53 promoter.	nab	65-68	tumor protein p53	Homo sapiens	172-175
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	histone deacetylase 8	Homo sapiens	53-58
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	YY1 transcription factor	Homo sapiens	63-66
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	YY1 transcription factor	Homo sapiens	112-115
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	YY1 transcription factor	Homo sapiens	112-115
26876786-9	2016	Further, SAHA and NaB can inhibit the association of HDAC8 and YY1, increase acetylation of residues 170-200 of YY1, then decrease its transcription activities, and finally suppress YY1 induced p53 transcription.	nab	18-21	tumor protein p53	Homo sapiens	194-197
26975664-8	2016	We suggest that DWME integration of BMP signaling maintains nab expression in proliferating margin descendants that have divided away from Notch-Delta boundary signaling.	nab	60-63	decapentaplegic	Drosophila melanogaster	36-39
27171333-6	2016	Upon identification of an ERBB2 gene amplification within the NCT MASTER (Molecularly Aided Stratification for Tumor Eradication Research) exome sequencing program with resulting overexpression of HER2 in the tumors cells, the patient received a targeted therapy with the HER2 antibodies pertuzumab and trastuzumab in combination with nab-paclitaxel, which led to a durable remission for more than one year.	nab	335-338	erb-b2 receptor tyrosine kinase 2	Homo sapiens	26-31
27025446-8	2016	In addition, the combination of NaB and RC-3095 increased hippocampal levels of the brain-derived neurotrophic factor (BDNF).	nab	32-35	brain-derived neurotrophic factor	Rattus norvegicus	84-117
27025446-8	2016	In addition, the combination of NaB and RC-3095 increased hippocampal levels of the brain-derived neurotrophic factor (BDNF).	nab	32-35	brain-derived neurotrophic factor	Rattus norvegicus	119-123
26957230-6	2016	However, NaB treatment significantly ameliorated behavioral deficits of the CUMS-induced mice, increased 5-HT concentration, increased BDNF expression, and up-regulated Occludin and zonula occludens-1(ZO-1) protein levels in the hippocampus, which demonstrated that NaB could partially restore CUMS-induced blood-brain barrier (BBB) impairments.	nab	9-12	brain derived neurotrophic factor	Mus musculus	135-139
26957230-6	2016	However, NaB treatment significantly ameliorated behavioral deficits of the CUMS-induced mice, increased 5-HT concentration, increased BDNF expression, and up-regulated Occludin and zonula occludens-1(ZO-1) protein levels in the hippocampus, which demonstrated that NaB could partially restore CUMS-induced blood-brain barrier (BBB) impairments.	nab	9-12	occludin	Mus musculus	169-177
26957230-6	2016	However, NaB treatment significantly ameliorated behavioral deficits of the CUMS-induced mice, increased 5-HT concentration, increased BDNF expression, and up-regulated Occludin and zonula occludens-1(ZO-1) protein levels in the hippocampus, which demonstrated that NaB could partially restore CUMS-induced blood-brain barrier (BBB) impairments.	nab	9-12	tight junction protein 1	Mus musculus	182-205
26957230-8	2016	In conclusion, these results demonstrated that NaB significantly improved depression-like behaviors in CUMS-induced mice and its antidepressant actions might be related with, at least in part, the increasing brain 5-HT concentration and BDNF expression and restoring BBB impairments.	nab	47-50	brain derived neurotrophic factor	Mus musculus	237-241
26671829-7	2016	Interestingly, the VH gene of this weak NAb belongs to the IGHV5-51 lineage, with a somatic mutation rate of 7.99 %.	nab	40-43	immunoglobulin heavy variable 5-51	Homo sapiens	59-67
27478804-3	2016	We used histone deacetylase (HDAC) inhibitor, NaB and DNA demethylating agent, 5-azacytidine (5-AZA) to induce CEA expression in HT29/219 and SW742 colorectal cancer cell lines.	nab	46-49	CEA cell adhesion molecule 3	Homo sapiens	111-114
27478804-6	2016	Treatment of HT29/219 cell line with NaB and 5-AZA increased CEA expression by 29% and 31%, respectively.	nab	37-40	CEA cell adhesion molecule 3	Homo sapiens	61-64
27478804-8	2016	Treatment of SW742 cells with NaB or 5-AZA increased neither CEA expression nor the IC50 value for 5-FU.	nab	30-33	CEA cell adhesion molecule 3	Homo sapiens	61-64
26464112-3	2016	More importantly, the impairing effect of TrkB antagonism on consolidation was completely prevented by the histone deacetylase (HDAC) inhibitor sodium butyrate (NaB).	nab	161-164	neurotrophic receptor tyrosine kinase 2	Rattus norvegicus	42-46
26832793-0	2016	SPARC-Independent Delivery of Nab-Paclitaxel without Depleting Tumor Stroma in Patient-Derived Pancreatic Cancer Xenografts.	nab	30-33	secreted protein acidic and cysteine rich	Homo sapiens	0-5
26832793-1	2016	The study goal was to examine the relationship between nab-paclitaxel delivery and SPARC (secreted protein acidic and rich in cysteine) expression in pancreatic tumor xenografts and to determine the antistromal effect of nab-paclitaxel, which may affect tumor vascular perfusion.	nab	55-58	secreted protein acidic and cysteine rich	Homo sapiens	83-88
26832793-1	2016	The study goal was to examine the relationship between nab-paclitaxel delivery and SPARC (secreted protein acidic and rich in cysteine) expression in pancreatic tumor xenografts and to determine the antistromal effect of nab-paclitaxel, which may affect tumor vascular perfusion.	nab	55-58	secreted protein acidic and cysteine rich	Homo sapiens	90-134
27031114-3	2016	Beta 2 Glycoprotein I (beta2GPI) is a plasma protein that binds to neoepitopes on damaged cells including anionic phospholipids through its highly conserved Domain V. Domain I of beta2GPI binds circulating IgM NAbs and may provide a link between the innate immune system, IgM NAb binding and cardiac IRI.	nab	210-213	apolipoprotein H	Mus musculus	0-21
27031114-3	2016	Beta 2 Glycoprotein I (beta2GPI) is a plasma protein that binds to neoepitopes on damaged cells including anionic phospholipids through its highly conserved Domain V. Domain I of beta2GPI binds circulating IgM NAbs and may provide a link between the innate immune system, IgM NAb binding and cardiac IRI.	nab	210-213	apolipoprotein H	Mus musculus	23-31
27031114-3	2016	Beta 2 Glycoprotein I (beta2GPI) is a plasma protein that binds to neoepitopes on damaged cells including anionic phospholipids through its highly conserved Domain V. Domain I of beta2GPI binds circulating IgM NAbs and may provide a link between the innate immune system, IgM NAb binding and cardiac IRI.	nab	210-213	apolipoprotein H	Mus musculus	179-187
26526555-2	2016	METHODS: TRAIL (0.2, 0.4, 1.0%)- and Dox-loaded HSA nanoparticles (TRAIL/Dox HSA NPs) were prepared by using the nab(TM) technology.	nab	113-116	albumin	Homo sapiens	48-51
26526555-2	2016	METHODS: TRAIL (0.2, 0.4, 1.0%)- and Dox-loaded HSA nanoparticles (TRAIL/Dox HSA NPs) were prepared by using the nab(TM) technology.	nab	113-116	TNF superfamily member 10	Homo sapiens	67-72
26123189-3	2015	Tumor-associated stromal caveolin-1 (Cav-1) expression was correlated with improved response rate and survival in NSCLC patients who received nab-paclitaxel in this phase II trial.	nab	142-145	caveolin 1	Homo sapiens	25-35
26673577-3	2015	nab-paclitaxel-based regimens (with gemcitabine or carboplatin+-bevacizumab) also demonstrated efficacy and safety in first-line phase II trials of human epidermal growth factor receptor 2-negative metastatic breast cancer.	nab	0-3	erb-b2 receptor tyrosine kinase 2	Homo sapiens	154-188
26471700-5	2015	The results showed that the TLR2 membrane abundance (MA) and mRNA expression were induced by 0.5mM NaB ~1.6-fold and ~1.7-fold, respectively.	nab	99-102	toll like receptor 2	Bos taurus	28-32
26471700-6	2015	Additionally, 0.5mM NaB induced p38 phosphorylation, but not JNK1/2 or ERK1/2 phosphorylation in bMECs, which reached the baseline when the bMECs were S. aureus-challenged.	nab	20-23	mitogen-activated protein kinase 14	Bos taurus	32-35
26471700-12	2015	In conclusion, our results suggest that 0.5mM NaB activates bMECs via TLR2/p38, which leads to improved antimicrobial defense before/after pathogen invasion, and NaB may exert anti-inflammatory effects during infection.	nab	46-49	toll like receptor 2	Bos taurus	70-74
26471700-12	2015	In conclusion, our results suggest that 0.5mM NaB activates bMECs via TLR2/p38, which leads to improved antimicrobial defense before/after pathogen invasion, and NaB may exert anti-inflammatory effects during infection.	nab	46-49	mitogen-activated protein kinase 14	Bos taurus	75-78
26869204-3	2016	Native-like Env trimers can induce autologous NAb responses against resistant (Tier-2) viruses in several animal models.	nab	46-49	endogenous retrovirus group K member 20	Homo sapiens	12-15
26869204-4	2016	Here we review recent studies aimed at addressing the challenge of driving the strong but narrowly focused NAb responses to Env trimers towards ones with much greater breadth.	nab	107-110	endogenous retrovirus group K member 20	Homo sapiens	124-127
27067684-3	2016	We retrospectively investigated prognostic factors related to time to treatment failure(TTF)in 11 patients with unresectable or recurrent gastric cancer treated with nab- PTX in our hospital.	nab	166-169	ras homolog family member H	Homo sapiens	88-91
27067684-6	2016	PNI could contribute to adequate patient selection and the improvement of nab-PTX therapy efficacy ingastric cancer.	nab	74-77	serpin family E member 2	Homo sapiens	0-3
26857796-9	2016	Another weaker DAAO inhibitor NaB (400 mg/kg), and NaB plus D-serine also significantly reduced PCP-induced locomotor activity, but without affecting plasma or brain D-serine level, arguing against a DAAO-mediated effect.	nab	30-33	D-amino acid oxidase	Mus musculus	15-19
26857796-10	2016	However, NaB reduced plasma L-serine and based on reports that NaB also elevates various plasma metabolites, for example aminoisobutyric acid (AIB), a potential effect via the System A amino acid carrier may be involved in the regulation of synaptic glycine level to modulate NMDAR function needs to be investigated.	nab	9-12	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	276-281
26857796-10	2016	However, NaB reduced plasma L-serine and based on reports that NaB also elevates various plasma metabolites, for example aminoisobutyric acid (AIB), a potential effect via the System A amino acid carrier may be involved in the regulation of synaptic glycine level to modulate NMDAR function needs to be investigated.	nab	63-66	glutamate receptor, ionotropic, NMDA1 (zeta 1)	Mus musculus	276-281
26123189-3	2015	Tumor-associated stromal caveolin-1 (Cav-1) expression was correlated with improved response rate and survival in NSCLC patients who received nab-paclitaxel in this phase II trial.	nab	142-145	caveolin 1	Homo sapiens	37-42
26399250-8	2015	The activation of cAMP response element binding (CREB) protein by NaB, the recruitment of CREB and CREB-binding protein to the CNTF promoter by NaB and the abrogation of NaB-induced expression of CNTF in astrocytes by siRNA knockdown of CREB suggest that NaB increases the expression of CNTF via the activation of CREB.	nab	144-147	ciliary neurotrophic factor	Mus musculus	127-131
26318839-3	2015	We have developed an ELISA for detecting neutralizing capacity of anti-C1-inh positive plasma samples that can be used to study changes in NAb repertoire in patient plasma over the course of disease.	nab	139-142	serpin family G member 1	Homo sapiens	71-77
26399250-4	2015	Here, we delineate that NaB is also capable of increasing the mRNA and protein expression of CNTF in primary mouse astrocytes and oligodendrocytes and primary human astrocytes.	nab	24-27	ciliary neurotrophic factor	Mus musculus	93-97
26399250-8	2015	The activation of cAMP response element binding (CREB) protein by NaB, the recruitment of CREB and CREB-binding protein to the CNTF promoter by NaB and the abrogation of NaB-induced expression of CNTF in astrocytes by siRNA knockdown of CREB suggest that NaB increases the expression of CNTF via the activation of CREB.	nab	144-147	ciliary neurotrophic factor	Mus musculus	127-131
26399250-5	2015	Accordingly, oral administration of NaB and cinnamon led to the upregulation of astroglial and oligodendroglial CNTF in vivo in mouse brain.	nab	36-39	ciliary neurotrophic factor	Mus musculus	112-116
26386664-7	2015	ACM (30%)+VEGF NAb (15 mug/ml) decreased the expressions of cyclin D1 and increased cell death compared with ACM (30%).	nab	15-18	vascular endothelial growth factor A	Rattus norvegicus	10-14
26399250-7	2015	While investigating underlying mechanisms, we observed that NaB induced the activation of protein kinase A (PKA) and H-89, an inhibitor of PKA, abrogated NaB-induced expression of CNTF.	nab	60-63	ciliary neurotrophic factor	Mus musculus	180-184
26399250-7	2015	While investigating underlying mechanisms, we observed that NaB induced the activation of protein kinase A (PKA) and H-89, an inhibitor of PKA, abrogated NaB-induced expression of CNTF.	nab	154-157	ciliary neurotrophic factor	Mus musculus	180-184
26399250-8	2015	The activation of cAMP response element binding (CREB) protein by NaB, the recruitment of CREB and CREB-binding protein to the CNTF promoter by NaB and the abrogation of NaB-induced expression of CNTF in astrocytes by siRNA knockdown of CREB suggest that NaB increases the expression of CNTF via the activation of CREB.	nab	144-147	ciliary neurotrophic factor	Mus musculus	127-131
26589781-8	2015	ELISA showed CTSs do not have anti-Gal nAb, and flow cytometry indicated CTSs have anti-non-Gal IgM and IgG nAb in serum.	nab	108-111	cathepsin S	Rattus norvegicus	73-77
26589781-11	2015	CTSs are valuable small animals to study mechanisms and strategies to avoid non-Gal nAb-mediated xenograft rejection.	nab	84-87	cathepsin S	Rattus norvegicus	0-4
26386664-7	2015	ACM (30%)+VEGF NAb (15 mug/ml) decreased the expressions of cyclin D1 and increased cell death compared with ACM (30%).	nab	15-18	cyclin D1	Rattus norvegicus	60-69
26261312-4	2015	Here we determined serum nAb titers against breakthrough transmitted/founder (T/F) SIVsmE660-derived envelope glycoprotein (Env) variants from 14 RMs immunized with SIVmac239-based DNA-prime/modified vaccinia virus Ankara-boost vaccine regimens that included GM-CSF or CD40L adjuvants and conferred significant but incomplete protection against repeated low-dose intrarectal challenge.	nab	25-28	endogenous retrovirus group V member 2 Env polyprotein	Macaca mulatta	101-122
26261312-4	2015	Here we determined serum nAb titers against breakthrough transmitted/founder (T/F) SIVsmE660-derived envelope glycoprotein (Env) variants from 14 RMs immunized with SIVmac239-based DNA-prime/modified vaccinia virus Ankara-boost vaccine regimens that included GM-CSF or CD40L adjuvants and conferred significant but incomplete protection against repeated low-dose intrarectal challenge.	nab	25-28	endogenous retrovirus group V member 2 Env polyprotein	Macaca mulatta	124-127
26070258-8	2015	CONCLUSIONS: Thus, the mutation BRAF G469A in MM might be related to a weak effectiveness of therapy with BRAF inhibitors and a promising therapeutic approach may be with nab-paclitaxel.	nab	171-174	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	32-36
26234821-8	2015	Gene expression analysis showed that NaB inhibited cytokines and immunological markers including CD68, Interferon-gamma and Mcp in adipose tissues in db/db mice.	nab	37-40	CD68 antigen	Mus musculus	97-101
26234821-8	2015	Gene expression analysis showed that NaB inhibited cytokines and immunological markers including CD68, Interferon-gamma and Mcp in adipose tissues in db/db mice.	nab	37-40	interferon gamma	Mus musculus	103-119
26234821-8	2015	Gene expression analysis showed that NaB inhibited cytokines and immunological markers including CD68, Interferon-gamma and Mcp in adipose tissues in db/db mice.	nab	37-40	CD46 antigen, complement regulatory protein	Mus musculus	124-127
26234821-9	2015	Moreover, NaB inhibited cytokine releasing in 3T3-L1 adipocytes treated with TNF-alpha.	nab	10-13	tumor necrosis factor	Mus musculus	77-86
26234821-10	2015	Further analysis of inflammation pathway showed that NLRP3 was activated in db/db mice, which was efficiently inhibited by NaB treatment.	nab	123-126	NLR family, pyrin domain containing 3	Mus musculus	53-58
25947567-12	2015	SPARC resulted up-regulated in both cell lines treated with bevacizumab+nab-paclitaxel.	nab	72-75	secreted protein acidic and cysteine rich	Homo sapiens	0-5
25510910-9	2015	Glucose-6-phosphate dehydrogenase activity was shown to be differentially modulated by NaB in the cell lines investigated: the enzyme was inhibited in MCF-7 cells, whereas in T-47D and MDA-MB-231 cells, G6PDH was activated.	nab	87-90	glucose-6-phosphate dehydrogenase	Homo sapiens	0-33
25982413-11	2015	On the other hand, Aza-2 and NaB inhibit DNMT1 and HDAC2 respectively, up-regulate BDNF and Arc expression and recover memory consolidation.	nab	29-32	DNA methyltransferase 1	Homo sapiens	41-46
25982413-11	2015	On the other hand, Aza-2 and NaB inhibit DNMT1 and HDAC2 respectively, up-regulate BDNF and Arc expression and recover memory consolidation.	nab	29-32	histone deacetylase 2	Homo sapiens	51-56
25982413-11	2015	On the other hand, Aza-2 and NaB inhibit DNMT1 and HDAC2 respectively, up-regulate BDNF and Arc expression and recover memory consolidation.	nab	29-32	brain derived neurotrophic factor	Homo sapiens	83-87
25579459-9	2015	The present study evaluated the activity and safety of nab-PTX as a neoadjuvant treatment of HER2(+) breast cancer.	nab	55-58	erb-b2 receptor tyrosine kinase 2	Homo sapiens	93-97
25510910-9	2015	Glucose-6-phosphate dehydrogenase activity was shown to be differentially modulated by NaB in the cell lines investigated: the enzyme was inhibited in MCF-7 cells, whereas in T-47D and MDA-MB-231 cells, G6PDH was activated.	nab	87-90	hexose-6-phosphate dehydrogenase/glucose 1-dehydrogenase	Homo sapiens	203-208
25737447-6	2015	Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31).	nab	44-47	microRNA 31	Homo sapiens	123-133
26029934-3	2015	OBJECTIVE: To report on experience with nab-paclitaxel for human epidermal growth factor receptor 2 (HER2)-negative MBC and identify patient characteristics affecting nab-paclitaxel treatment patterns in the community practice setting.	nab	40-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	65-99
26029934-3	2015	OBJECTIVE: To report on experience with nab-paclitaxel for human epidermal growth factor receptor 2 (HER2)-negative MBC and identify patient characteristics affecting nab-paclitaxel treatment patterns in the community practice setting.	nab	40-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	101-105
26029934-13	2015	CONCLUSIONS: In the community setting, nab-paclitaxel 100 mg/m2 weekly was the most commonly used starting dose for patients with HER2-negative MBC, including those with aggressive disease characteristics.	nab	39-42	erb-b2 receptor tyrosine kinase 2	Homo sapiens	130-134
25737447-6	2015	Specifically, we show that sodium butyrate (NaB) and panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31).	nab	44-47	microRNA 31	Homo sapiens	127-133
25830625-2	2015	Here, using electrophysiological techniques in brain slices from animals of the high anxiety-related behavior (HAB) and normal anxiety-related behavior (NAB) mouse model, we show that basal neurotransmission at ventral hippocampal CA3-CA1 synapses is weaker in HAB compared to NAB mice.	nab	153-156	carbonic anhydrase 3	Mus musculus	231-238
25854569-1	2015	OBJECTIVE: To investigate molecular mechanisms of posttranslational regulation of sodium butyrate (NaB) on indoleamine 2, 3-dioxygenase (IDO) expression induced by interferon gamma (IFN-gamma) in CNE2 nasopharyngeal carcinoma cells.	nab	99-102	indoleamine 2,3-dioxygenase 1	Homo sapiens	107-135
25854569-1	2015	OBJECTIVE: To investigate molecular mechanisms of posttranslational regulation of sodium butyrate (NaB) on indoleamine 2, 3-dioxygenase (IDO) expression induced by interferon gamma (IFN-gamma) in CNE2 nasopharyngeal carcinoma cells.	nab	99-102	indoleamine 2,3-dioxygenase 1	Homo sapiens	137-140
25854569-1	2015	OBJECTIVE: To investigate molecular mechanisms of posttranslational regulation of sodium butyrate (NaB) on indoleamine 2, 3-dioxygenase (IDO) expression induced by interferon gamma (IFN-gamma) in CNE2 nasopharyngeal carcinoma cells.	nab	99-102	interferon gamma	Homo sapiens	164-191
25854569-3	2015	RESULTS: Western blotting demonstrated that while the cells were treated with IFN-gamma and NaB compared with IFN-gamma treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-gamma and NaB compared with the ones treated with IFN-gamma only, acetylation and ubiquitination of IDO increased significantly.	nab	92-95	interferon gamma	Homo sapiens	110-119
25854569-3	2015	RESULTS: Western blotting demonstrated that while the cells were treated with IFN-gamma and NaB compared with IFN-gamma treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-gamma and NaB compared with the ones treated with IFN-gamma only, acetylation and ubiquitination of IDO increased significantly.	nab	92-95	indoleamine 2,3-dioxygenase 1	Homo sapiens	154-157
25854569-3	2015	RESULTS: Western blotting demonstrated that while the cells were treated with IFN-gamma and NaB compared with IFN-gamma treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-gamma and NaB compared with the ones treated with IFN-gamma only, acetylation and ubiquitination of IDO increased significantly.	nab	92-95	interferon gamma	Homo sapiens	110-119
25854569-3	2015	RESULTS: Western blotting demonstrated that while the cells were treated with IFN-gamma and NaB compared with IFN-gamma treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-gamma and NaB compared with the ones treated with IFN-gamma only, acetylation and ubiquitination of IDO increased significantly.	nab	92-95	interferon gamma	Homo sapiens	110-119
25854569-3	2015	RESULTS: Western blotting demonstrated that while the cells were treated with IFN-gamma and NaB compared with IFN-gamma treatment only, the expression of IDO protein increased significantly; furthermore, in the co-immunoprecipitation assay, while the cells were treated with IFN-gamma and NaB compared with the ones treated with IFN-gamma only, acetylation and ubiquitination of IDO increased significantly.	nab	92-95	indoleamine 2,3-dioxygenase 1	Homo sapiens	379-382
25854569-4	2015	Western blotting showed that the cells treated with NaB and IFN-gamma presented with lower IDO protein expression than the ones treated with NaB, IFN-gamma and bortezomib simultaneously.	nab	52-55	indoleamine 2,3-dioxygenase 1	Homo sapiens	91-94
25854569-4	2015	Western blotting showed that the cells treated with NaB and IFN-gamma presented with lower IDO protein expression than the ones treated with NaB, IFN-gamma and bortezomib simultaneously.	nab	52-55	interferon gamma	Homo sapiens	146-155
25854569-4	2015	Western blotting showed that the cells treated with NaB and IFN-gamma presented with lower IDO protein expression than the ones treated with NaB, IFN-gamma and bortezomib simultaneously.	nab	141-144	interferon gamma	Homo sapiens	60-69
25854569-5	2015	CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-gamma in a dose-dependent manner, and the combined treatment of IFN-gamma and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.	nab	12-15	indoleamine 2,3-dioxygenase 1	Homo sapiens	54-57
25854569-5	2015	CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-gamma in a dose-dependent manner, and the combined treatment of IFN-gamma and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.	nab	12-15	interferon gamma	Homo sapiens	69-78
25854569-5	2015	CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-gamma in a dose-dependent manner, and the combined treatment of IFN-gamma and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.	nab	12-15	indoleamine 2,3-dioxygenase 1	Homo sapiens	207-210
25854569-5	2015	CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-gamma in a dose-dependent manner, and the combined treatment of IFN-gamma and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.	nab	151-154	indoleamine 2,3-dioxygenase 1	Homo sapiens	54-57
25854569-5	2015	CONCLUSION: NaB could down-regulate the expression of IDO induced by IFN-gamma in a dose-dependent manner, and the combined treatment of IFN-gamma and NaB could promote the acetylation and ubiquitination of IDO in CNE2 nasopharyngeal carcinoma cells.	nab	151-154	indoleamine 2,3-dioxygenase 1	Homo sapiens	207-210
25931813-14	2015	CONCLUSION: Our results showed that single-agent nab-paclitaxel 260 mg/m(2) every 3 weeks is an effective and well tolerated regimen as second-line chemotherapy in HER2-negative, taxane-pretreated MBC patients, and that it produced interesting values of objective response rate and progression-free survival without the concern of significant toxicity.	nab	49-52	erb-b2 receptor tyrosine kinase 2	Homo sapiens	164-168
25682147-5	2015	Moderate positive phenotypic correlations were found between NAb levels in milk and in plasma: 0.18 for IgG and 0.40 for IgM.	nab	61-64	IgM	Bos taurus	121-124
25682147-7	2015	However, high genetic correlations were found for NAb in milk and plasma: 0.81 for IgG and 0.79 for IgM.	nab	50-53	IgM	Bos taurus	100-103
25682147-8	2015	Heritabilities (SE in parentheses) for NAb measured in plasma [0.15 (0.05) for IgG and 0.25 (0.06) for IgM] were higher than heritabilities of NAb measured in milk [0.08 (0.03) for IgG and 0.23 (0.05) for IgM].	nab	39-42	IgM	Bos taurus	103-106
27239491-6	2015	alpha2-Macroglobulin, fibrinogen gamma-chain (FGG), and complement factor H-related protein 1 were confirmed to be associated with NAB.	nab	131-134	alpha-2-macroglobulin	Homo sapiens	0-20
27239491-6	2015	alpha2-Macroglobulin, fibrinogen gamma-chain (FGG), and complement factor H-related protein 1 were confirmed to be associated with NAB.	nab	131-134	fibrinogen gamma chain	Homo sapiens	22-44
27239491-6	2015	alpha2-Macroglobulin, fibrinogen gamma-chain (FGG), and complement factor H-related protein 1 were confirmed to be associated with NAB.	nab	131-134	fibrinogen gamma chain	Homo sapiens	46-49
27239491-6	2015	alpha2-Macroglobulin, fibrinogen gamma-chain (FGG), and complement factor H-related protein 1 were confirmed to be associated with NAB.	nab	131-134	complement factor H related 1	Homo sapiens	56-93
27239491-7	2015	In an independent cohort, FGG plasma levels combined with age predicted NAB had a sensitivity of 59% and specificity of 78%.	nab	72-75	fibrinogen gamma chain	Homo sapiens	26-29
27239491-8	2015	CONCLUSION: A single blood protein, FGG, combined with age, was shown to relate to NAB and therefore could have potential for enrichment of clinical trial populations.	nab	83-86	fibrinogen gamma chain	Homo sapiens	36-39
25830625-2	2015	Here, using electrophysiological techniques in brain slices from animals of the high anxiety-related behavior (HAB) and normal anxiety-related behavior (NAB) mouse model, we show that basal neurotransmission at ventral hippocampal CA3-CA1 synapses is weaker in HAB compared to NAB mice.	nab	277-280	carbonic anhydrase 3	Mus musculus	231-238
25678799-0	2015	Efficacy of nab-paclitaxel plus trastuzumab in a long-surviving heavily pretreated HER2-positive breast cancer patient with brain metastases.	nab	12-15	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-87
25540368-6	2015	These data suggest that vaccination with a mixture of clade C Env trimers represents a promising strategy to augment vaccine-elicited NAb responses.	nab	134-137	endogenous retrovirus group K member 20	Homo sapiens	62-65
25678799-7	2015	Herein, we report a lengthy progression-free survival with the combination trastuzumab/nanoparticle albumin-bound (nab)-paclitaxel in a heavily pretreated HER2-positive BC patient with BM.	nab	115-118	erb-b2 receptor tyrosine kinase 2	Homo sapiens	155-159
25678799-12	2015	In conclusion, weekly nab-paclitaxel plus trastuzumab may represent a valuable option in the treatment of HER2-positive MBC with BM after radiotherapy and is effective and associated with a good toxicity profile, even in heavily pretreated patients.	nab	22-25	erb-b2 receptor tyrosine kinase 2	Homo sapiens	106-110
25459532-8	2015	Previous studies have shown that FVIII complexed with OPLS lowered Nab development against FVIII following subcutaneous administration.	nab	67-70	coagulation factor VIII	Homo sapiens	33-38
25065563-5	2015	We hypothesized that the combination of neoadjuvant nab-paclitaxel followed by vinorelbine could represent a nonanthracycline-based treatment option for early-stage Her2-overexpressing breast cancer.	nab	52-55	erb-b2 receptor tyrosine kinase 2	Homo sapiens	165-169
25548915-6	2014	Furthermore, NaB enhanced the acetylation of SMC gene-associated H3K9 and H4, and decreased the expression of HDAC2 and down-regulated the recruitment of HDAC2 to the promoter regions of SMC specific genes.	nab	13-16	histone deacetylase 2	Rattus norvegicus	110-115
26064905-9	2015	Moreover, 10 mg/kg NaB treatment markedly restored the levels of MDA, SOD, IL-1beta, TNF-alpha, and IL-8.	nab	19-22	interleukin 1 beta	Mus musculus	75-83
26064905-9	2015	Moreover, 10 mg/kg NaB treatment markedly restored the levels of MDA, SOD, IL-1beta, TNF-alpha, and IL-8.	nab	19-22	tumor necrosis factor	Mus musculus	85-94
26064905-9	2015	Moreover, 10 mg/kg NaB treatment markedly restored the levels of MDA, SOD, IL-1beta, TNF-alpha, and IL-8.	nab	19-22	chemokine (C-X-C motif) ligand 15	Mus musculus	100-104
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	caspase 3	Mus musculus	89-98
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	BCL2-associated X protein	Mus musculus	103-106
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	B cell leukemia/lymphoma 2	Mus musculus	136-141
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	thymoma viral proto-oncogene 1	Mus musculus	145-148
26064905-10	2015	10 mg/kg NaB treatment also remarkably inhibited the apoptosis, decreasing the levels of caspase-3 and Bax and increasing the levels of Bcl-2, p-Akt, and BDNF.	nab	9-12	brain derived neurotrophic factor	Mus musculus	154-158
26064905-11	2015	This study suggested that NaB exerts neuroprotective effects on cerebral I/R injury by antioxidant, anti-inflammatory, and antiapoptotic properties and BDNF-PI3K/Akt pathway is involved in antiapoptotic effect.	nab	26-29	brain derived neurotrophic factor	Mus musculus	152-156
26064905-11	2015	This study suggested that NaB exerts neuroprotective effects on cerebral I/R injury by antioxidant, anti-inflammatory, and antiapoptotic properties and BDNF-PI3K/Akt pathway is involved in antiapoptotic effect.	nab	26-29	thymoma viral proto-oncogene 1	Mus musculus	162-165
26349241-4	2015	In the present paper, we studied the effect of NaB on the DNA repair through Gadd45a protein modulation.	nab	47-50	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	77-84
26349241-5	2015	Our results indicate that suppression of Gadd45alpha reduces the DNA repair efficiency, in both basal, and NaB-dependent.	nab	107-110	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	41-52
26349241-6	2015	However NaB-induced supression of DNA repair is reduced in Gadd45-expressing transformed cells.	nab	8-11	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	59-65
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	growth arrest and DNA-damage-inducible 45 alpha	Mus musculus	33-39
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	45-48
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	49-53
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	98-101
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	102-106
26349241-9	2015	NaB amplified the interaction of Gadd45 with p21/Waf1 protein, thereby reducing the amount of the p21/Waf1 in complex with PCNA.	nab	0-3	proliferating cell nuclear antigen	Mus musculus	123-127
25548915-6	2014	Furthermore, NaB enhanced the acetylation of SMC gene-associated H3K9 and H4, and decreased the expression of HDAC2 and down-regulated the recruitment of HDAC2 to the promoter regions of SMC specific genes.	nab	13-16	histone deacetylase 2	Rattus norvegicus	154-159
25548915-8	2014	These results demonstrated that NaB effectively promotes MSC differentiation into SMCs, possibly by the marked inhibition of HDAC2 expression and disassociation of HDAC2 recruitment to SMC specific genes in MSCs, which further induces high levels of H3K9ace and H4ace and the enhanced expression of target genes, and this strategy could potentially be applied in clinical tissue engineering and cell transplantation.	nab	32-35	histone deacetylase 2	Rattus norvegicus	125-130
25548915-8	2014	These results demonstrated that NaB effectively promotes MSC differentiation into SMCs, possibly by the marked inhibition of HDAC2 expression and disassociation of HDAC2 recruitment to SMC specific genes in MSCs, which further induces high levels of H3K9ace and H4ace and the enhanced expression of target genes, and this strategy could potentially be applied in clinical tissue engineering and cell transplantation.	nab	32-35	histone deacetylase 2	Rattus norvegicus	164-169
25286028-7	2014	Moreover, HDACi chemicals Trichostatin A (TSA) and sodium butyrate (NaB) potently inhibited Bmi1 and triggered similar phenotypic changes reminiscent of Bmi1 silencing, although TSA treatment seemed paradoxically to induce some epithelial-mesenchymal transition-like changes in tongue cancer cells.	nab	68-71	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	92-96
25286028-7	2014	Moreover, HDACi chemicals Trichostatin A (TSA) and sodium butyrate (NaB) potently inhibited Bmi1 and triggered similar phenotypic changes reminiscent of Bmi1 silencing, although TSA treatment seemed paradoxically to induce some epithelial-mesenchymal transition-like changes in tongue cancer cells.	nab	68-71	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	153-157
25286028-8	2014	Importantly, NaB-induced antitumor effects were partially attenuated by enforced Bmi1 overexpression in vitro.	nab	13-16	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	81-85
25286028-9	2014	Genetic Bmi1 silencing and pharmacological inhibition of Bmi1 by NaB treatment significantly impaired tumor growth in a tongue cancer xenograft model.	nab	65-68	BMI1 proto-oncogene, polycomb ring finger	Homo sapiens	57-61
25368265-1	2014	AIM: To evaluate the predictive value of the expression of the secreted protein acidic and rich in cysteine (SPARC) for nab-paclitaxel in metastatic breast cancer (MBC).	nab	120-123	secreted protein acidic and cysteine rich	Homo sapiens	63-107
25450683-5	2014	The NAb-positive sera also inhibited the IFN-alpha-dependent induction of interferon-stimulated genes, MxA and OAS-1, in a dose-dependent manner.	nab	4-7	interferon alpha 1	Homo sapiens	41-50
25450683-5	2014	The NAb-positive sera also inhibited the IFN-alpha-dependent induction of interferon-stimulated genes, MxA and OAS-1, in a dose-dependent manner.	nab	4-7	MX dynamin like GTPase 1	Homo sapiens	103-106
25450683-5	2014	The NAb-positive sera also inhibited the IFN-alpha-dependent induction of interferon-stimulated genes, MxA and OAS-1, in a dose-dependent manner.	nab	4-7	2'-5'-oligoadenylate synthetase 1	Homo sapiens	111-116
25450683-8	2014	However, in the presence of anti-IFN-alpha NAb-positive sera, even when IFN-alpha was combined with TVR, the levels of HCV-RNA exhibited a time-course similar to that with TVR monotherapy, and HCV with TVR-resistant mutations emerged.	nab	43-46	interferon alpha 1	Homo sapiens	33-42
25450683-8	2014	However, in the presence of anti-IFN-alpha NAb-positive sera, even when IFN-alpha was combined with TVR, the levels of HCV-RNA exhibited a time-course similar to that with TVR monotherapy, and HCV with TVR-resistant mutations emerged.	nab	43-46	interferon alpha 1	Homo sapiens	72-81
25450683-9	2014	In conclusion, our findings suggest that the presence of IFN-alpha NAb decreases the antiviral effects of IFN-alpha and may be related to the development of TVR-resistant mutated viruses.	nab	67-70	interferon alpha 1	Homo sapiens	57-66
25450683-9	2014	In conclusion, our findings suggest that the presence of IFN-alpha NAb decreases the antiviral effects of IFN-alpha and may be related to the development of TVR-resistant mutated viruses.	nab	67-70	interferon alpha 1	Homo sapiens	106-115
25450683-1	2014	Although the development of anti-interferon (IFN)-alpha neutralizing antibodies (NAbs) is likely to be a common clinical problem for patients with various diseases treated with IFN, anti-IFN-alpha NAb has been exceptionally considered to have no clinical significance in the treatment of chronic hepatitis C with pegylated IFN-alpha (Peg-IFN-alpha).	nab	81-84	interferon alpha 1	Homo sapiens	45-48
25450683-1	2014	Although the development of anti-interferon (IFN)-alpha neutralizing antibodies (NAbs) is likely to be a common clinical problem for patients with various diseases treated with IFN, anti-IFN-alpha NAb has been exceptionally considered to have no clinical significance in the treatment of chronic hepatitis C with pegylated IFN-alpha (Peg-IFN-alpha).	nab	81-84	interferon alpha 1	Homo sapiens	177-180
25450683-1	2014	Although the development of anti-interferon (IFN)-alpha neutralizing antibodies (NAbs) is likely to be a common clinical problem for patients with various diseases treated with IFN, anti-IFN-alpha NAb has been exceptionally considered to have no clinical significance in the treatment of chronic hepatitis C with pegylated IFN-alpha (Peg-IFN-alpha).	nab	81-84	interferon alpha 1	Homo sapiens	177-180
25450683-1	2014	Although the development of anti-interferon (IFN)-alpha neutralizing antibodies (NAbs) is likely to be a common clinical problem for patients with various diseases treated with IFN, anti-IFN-alpha NAb has been exceptionally considered to have no clinical significance in the treatment of chronic hepatitis C with pegylated IFN-alpha (Peg-IFN-alpha).	nab	81-84	interferon alpha 1	Homo sapiens	177-180
25450683-2	2014	However, we recently clarified that the presence of NAb was associated with a non-response to the Peg-IFN plus ribavirin (RBV) therapy.	nab	52-55	interferon alpha 1	Homo sapiens	102-105
25450683-4	2014	Anti-IFN-alpha NAb-positive sera specifically inhibited the anti-HCV effects of IFN-alpha, without any effect on the activity of IFN-beta in vitro.	nab	15-18	interferon alpha 1	Homo sapiens	5-14
25450683-4	2014	Anti-IFN-alpha NAb-positive sera specifically inhibited the anti-HCV effects of IFN-alpha, without any effect on the activity of IFN-beta in vitro.	nab	15-18	interferon alpha 1	Homo sapiens	80-89
25368265-1	2014	AIM: To evaluate the predictive value of the expression of the secreted protein acidic and rich in cysteine (SPARC) for nab-paclitaxel in metastatic breast cancer (MBC).	nab	120-123	secreted protein acidic and cysteine rich	Homo sapiens	109-114
25158305-6	2014	Post-treatment with NaB significantly decreased plasma glucose, creatinine, urea, histological alterations including the fibrosis and collagen deposition as well as decreased the HDACs activity, expression of eNOS, iNOS, alpha-SMA, collagen I, fibronectin, TGFbeta-1, NFkappaB, apoptosis and DNA damage in the diabetic kidney.	nab	20-23	nitric oxide synthase 3	Rattus norvegicus	209-213
25158305-6	2014	Post-treatment with NaB significantly decreased plasma glucose, creatinine, urea, histological alterations including the fibrosis and collagen deposition as well as decreased the HDACs activity, expression of eNOS, iNOS, alpha-SMA, collagen I, fibronectin, TGFbeta-1, NFkappaB, apoptosis and DNA damage in the diabetic kidney.	nab	20-23	nitric oxide synthase 2	Rattus norvegicus	215-219
25158305-6	2014	Post-treatment with NaB significantly decreased plasma glucose, creatinine, urea, histological alterations including the fibrosis and collagen deposition as well as decreased the HDACs activity, expression of eNOS, iNOS, alpha-SMA, collagen I, fibronectin, TGFbeta-1, NFkappaB, apoptosis and DNA damage in the diabetic kidney.	nab	20-23	fibronectin 1	Rattus norvegicus	244-255
25158305-6	2014	Post-treatment with NaB significantly decreased plasma glucose, creatinine, urea, histological alterations including the fibrosis and collagen deposition as well as decreased the HDACs activity, expression of eNOS, iNOS, alpha-SMA, collagen I, fibronectin, TGFbeta-1, NFkappaB, apoptosis and DNA damage in the diabetic kidney.	nab	20-23	transforming growth factor, beta 1	Rattus norvegicus	257-266
24753077-5	2014	Primary Ewing sarcoma tumors expressed the transport protein SPARC, previously associated with nab-paclitaxel activity.	nab	95-98	secreted protein acidic and cysteine rich	Homo sapiens	61-66
25618518-5	2014	As indicated by the behavioral despair test, chronic administration of NaB had antidepressant-like effects in the FSL and was accompanied by increased levels of TET1.	nab	71-74	tet methylcytosine dioxygenase 1	Rattus norvegicus	161-165
24886956-6	2014	We conclude that immunisation with bacterially-expressed VP2 domains can induce strong serotype-specific NAb responses.	nab	105-108	VP2	Bluetongue virus	57-60
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	135-139
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	204-208
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	nitric oxide synthase 2, inducible	Mus musculus	249-253
24946862-10	2014	However, oral treatment of MPTP-intoxicated mice with cinnamon powder and NaB reduced the expression of iNOS and protected Parkin/DJ-1 in the nigra.	nab	74-77	nitric oxide synthase 2, inducible	Mus musculus	104-108
24946862-10	2014	However, oral treatment of MPTP-intoxicated mice with cinnamon powder and NaB reduced the expression of iNOS and protected Parkin/DJ-1 in the nigra.	nab	74-77	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	130-134
24946862-6	2014	However, cinnamon metabolite NaB abrogated IL-1beta-induced loss of these proteins.	nab	29-32	interleukin 1 beta	Mus musculus	43-51
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	81-84	interleukin 1 beta	Mus musculus	28-36
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	81-84	nitric oxide synthase 2, inducible	Mus musculus	59-63
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	135-139
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	204-208
24946862-8	2014	Furthermore, suppression of IL-1beta-induced expression of iNOS in astrocytes by NaB and reversal of NaB-mediated protection of Parkin/DJ-1 by DETA-NONOate in astrocytes indicate that NaB protects Parkin/DJ-1 in activated astrocytes via suppressing iNOS.	nab	101-104	nitric oxide synthase 2, inducible	Mus musculus	249-253
25070040-4	2014	The HDAC inhibitor sodium butyrate (NaB) potentiated the pro-senescent effect of Rsv and Quer in human and rat glioma cell lines but not in normal rat astrocytes.	nab	36-39	histone deacetylase 9	Homo sapiens	4-8
25071742-4	2014	Neutralizing antibodies (NAbs) to both E1 and E2 have been described with the major NAb target being E2.	nab	25-28	small nucleolar RNA, H/ACA box 73A	Homo sapiens	39-48
24577510-5	2014	Microarray profiling showed a synergistic action of NaB/VP-16 combination through the differential regulation of 1,413 genes.	nab	52-55	host cell factor C1	Homo sapiens	56-61
24829409-4	2014	Heterologous NAb titers, primarily to tier 1 HIV-1 isolates, elicited during the trivalent HIV-1 env prime, were significantly increased by the SIVmac239 gp140 protein boost in rabbits.	nab	13-16	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	97-100
24829409-6	2014	These results provide a proof of concept that a distally related retroviral SIV Env protein boost can increase pre-existing NAb responses against HIV-1.	nab	124-127	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	80-83
24444338-4	2014	We made a comparison between 2 bioassays; myxovirus resistance protein A (MxA) gene expression assay (MGA) and iLite  anti-Human IFNbeta bioassay, to measure IFNbeta-specific NAb titers in 44 MS patients.	nab	175-178	interferon beta 1	Homo sapiens	158-165
24444338-5	2014	We further studied how NAb titers affected in vivo transcription of IFN-induced genes myxovirus resistant 1 (MX1) and C-X-C motif chemokine 10 (CXCL10), in addition to serum CXCL10 protein levels.	nab	23-26	interferon alpha 1	Homo sapiens	68-71
24444338-5	2014	We further studied how NAb titers affected in vivo transcription of IFN-induced genes myxovirus resistant 1 (MX1) and C-X-C motif chemokine 10 (CXCL10), in addition to serum CXCL10 protein levels.	nab	23-26	MX dynamin like GTPase 1	Homo sapiens	109-112
24444338-5	2014	We further studied how NAb titers affected in vivo transcription of IFN-induced genes myxovirus resistant 1 (MX1) and C-X-C motif chemokine 10 (CXCL10), in addition to serum CXCL10 protein levels.	nab	23-26	C-X-C motif chemokine ligand 10	Homo sapiens	118-142
24444338-7	2014	MX1 and CXCL10 gene expression was strongly induced by IFNbeta and NAb positivity significantly reduced this expression.	nab	67-70	MX dynamin like GTPase 1	Homo sapiens	0-3
24444338-7	2014	MX1 and CXCL10 gene expression was strongly induced by IFNbeta and NAb positivity significantly reduced this expression.	nab	67-70	C-X-C motif chemokine ligand 10	Homo sapiens	8-14
24444338-8	2014	A NAb titer of 150 TRU/mL was observed to be a biological cut-point applicable to both assays, since MX1 and CXCL10 expression was greatly reduced or blocked in patients above this titer level.	nab	2-5	MX dynamin like GTPase 1	Homo sapiens	101-104
24444338-8	2014	A NAb titer of 150 TRU/mL was observed to be a biological cut-point applicable to both assays, since MX1 and CXCL10 expression was greatly reduced or blocked in patients above this titer level.	nab	2-5	C-X-C motif chemokine ligand 10	Homo sapiens	109-115
24577510-6	2014	Comparing VP-16 treatment with the NaB/VP-16 combination, 318 genes were deregulated: 250 genes were downregulated, and 68 were upregulated when compared with untreated cells.	nab	35-38	host cell factor C1	Homo sapiens	10-15
24067278-0	2014	SPARC independent drug delivery and antitumour effects of nab-paclitaxel in genetically engineered mice.	nab	58-61	secreted acidic cysteine rich glycoprotein	Mus musculus	0-5
24067278-8	2014	The interaction of plasma SPARC and albumin-bound drugs is observed at low doses of nab-paclitaxel but is saturated at therapeutic doses in murine tumours.	nab	84-87	secreted acidic cysteine rich glycoprotein	Mus musculus	26-31
24748646-5	2014	RESULTS: The combined presence of DRB1*07/DQA1*02 with A*26 or B*14 was found in 20% of patients with NAbs at high titres, but only in 5.4% of NAb-negative patients (p=0.00052, OR (95% CI) 4.34 (1.85 to 10.13)).	nab	102-105	major histocompatibility complex, class II, DR beta 1	Homo sapiens	34-38
24748646-5	2014	RESULTS: The combined presence of DRB1*07/DQA1*02 with A*26 or B*14 was found in 20% of patients with NAbs at high titres, but only in 5.4% of NAb-negative patients (p=0.00052, OR (95% CI) 4.34 (1.85 to 10.13)).	nab	102-105	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	42-46
24654922-6	2014	RESULTS: Patients on nab-paclitaxel + gemcitabine spent a significantly longer time in every state and experienced significantly greater overall Q-TWiST (+1.7 months [95% CI = 0.8, 2.7]) than those receiving gemcitabine alone (8.2 months [95% CI = 7.5, 8.9] vs 6.5 months [95% CI = 5.8, 7.0]), assuming base-case utilities of TOX/REL = 0.50.	nab	21-24	twist family bHLH transcription factor 1	Homo sapiens	147-152
24737289-6	2014	In the CRC cell lines, NaB treatment led to the upregulation of SELENBP1, CEA and AKP when compared with the untreated cells (2.24- to 4.82-fold).	nab	23-26	selenium binding protein 1	Homo sapiens	64-72
24737289-6	2014	In the CRC cell lines, NaB treatment led to the upregulation of SELENBP1, CEA and AKP when compared with the untreated cells (2.24- to 4.82-fold).	nab	23-26	CEA cell adhesion molecule 3	Homo sapiens	74-77
24696491-6	2014	Here we further report that an RNA interference-based knockdown of KAP1 in KSHV-infected primary effusion lymphoma (PEL) cells disrupted viral episome stability and abrogated sub-G1/G1 arrest of the cell cycle while increasing the efficiency of KSHV lytic reactivation by hypoxia or using the chemical 12-O-tetradecanoylphorbol-13-acetate (TPA) or sodium butyrate (NaB).	nab	365-368	tripartite motif containing 28	Homo sapiens	67-71
24610280-7	2014	Administration of CDRI-08/NaB resulted in activation of extracellular signal-regulated kinase ERK/CREB signaling cascade and up-regulation of p300, Ac-H3 and Ac-H4 levels, and down-regulation of HDACs (1, 2) and protein phosphatases (PP1alpha, PP2A) in hippocampus following CFC.	nab	26-29	cAMP responsive element binding protein 1	Rattus norvegicus	98-102
24654922-6	2014	RESULTS: Patients on nab-paclitaxel + gemcitabine spent a significantly longer time in every state and experienced significantly greater overall Q-TWiST (+1.7 months [95% CI = 0.8, 2.7]) than those receiving gemcitabine alone (8.2 months [95% CI = 7.5, 8.9] vs 6.5 months [95% CI = 5.8, 7.0]), assuming base-case utilities of TOX/REL = 0.50.	nab	21-24	thymocyte selection associated high mobility group box	Homo sapiens	326-329
24334704-6	2014	Our data show that Atro segregates ORs expressed in the Nba OSN classes and helps establish the Nab fate during OSN development.	nab	96-99	Grunge	Drosophila melanogaster	19-23
24530320-11	2014	NaB treatment improved the beta-cell proliferation, function and glucose homeostasis as well as reduced beta-cell apoptosis in juvenile diabetic rat by the modulation of p38/ERK MAPK and apoptotic pathway.	nab	0-3	mitogen activated protein kinase 14	Rattus norvegicus	170-173
24530320-11	2014	NaB treatment improved the beta-cell proliferation, function and glucose homeostasis as well as reduced beta-cell apoptosis in juvenile diabetic rat by the modulation of p38/ERK MAPK and apoptotic pathway.	nab	0-3	Eph receptor B1	Rattus norvegicus	174-177
24530320-11	2014	NaB treatment improved the beta-cell proliferation, function and glucose homeostasis as well as reduced beta-cell apoptosis in juvenile diabetic rat by the modulation of p38/ERK MAPK and apoptotic pathway.	nab	0-3	mitogen activated protein kinase 3	Rattus norvegicus	178-182
24847251-12	2014	The author believes that this case is the first report of a robust response to nab-paclitaxel monotherapy in triple-negative BRCA1-positive breast cancer, and that it supports further studies of nab-paclitaxel in this aggressive indication.	nab	79-82	BRCA1 DNA repair associated	Homo sapiens	125-130
24568633-2	2014	We report here that sodium butyrate (NaB), a small-molecule inhibitor of histone deacetylases (HDACs), upregulates transcriptional levels of the miR-302/367 cluster by enhancing Oct4 transcriptional activity at the miR-302/367 cluster promoter.	nab	37-40	POU class 5 homeobox 1	Homo sapiens	178-182
24568633-3	2014	NaB does not affect the OCT4 DNA-binding domain; instead it enhances transactivity of the OCT4 transactivation domains.	nab	0-3	POU class 5 homeobox 1	Homo sapiens	90-94
24568633-4	2014	We elucidate that OCT4 transcriptional activity is usually dampened by its associated HDACs in cells and can be derepressed by NaB by impairing the interaction between Oct4 and HDACs, which leads to an elevated expression of the miR-302/367 cluster.	nab	127-130	POU class 5 homeobox 1	Homo sapiens	18-22
24568633-4	2014	We elucidate that OCT4 transcriptional activity is usually dampened by its associated HDACs in cells and can be derepressed by NaB by impairing the interaction between Oct4 and HDACs, which leads to an elevated expression of the miR-302/367 cluster.	nab	127-130	POU class 5 homeobox 1	Homo sapiens	168-172
24608124-3	2014	Carriage of HLA-DRB1*15 was associated with increased risk of developing NAbs and high NAb titers.	nab	73-76	major histocompatibility complex, class II, DR beta 1	Homo sapiens	12-20
24608124-4	2014	After stratification based on type of IFNbeta preparation, HLA-DRB1*15 carriage was observed to increase the risk of developing NAbs as well as high NAb titers against both subcutaneous and intramuscular IFNbeta-1a.	nab	128-131	major histocompatibility complex, class II, DR beta 1	Homo sapiens	59-67
24608124-5	2014	Furthermore, in patients receiving subcutaneous IFNbeta-1a carriage of HLA-DQA1*05 decreased the risk for high NAb titers.	nab	111-114	major histocompatibility complex, class II, DQ alpha 1	Homo sapiens	71-79
24608124-6	2014	In IFNbeta-1b treated patients, HLA-DRB1*04 increased the risk of developing high NAb titers, and in a subgroup analysis of DRB1*04 alleles the risk for NAbs was increased in DRB1*04:01 carriers.	nab	82-85	major histocompatibility complex, class II, DR beta 1	Homo sapiens	32-40
24608124-6	2014	In IFNbeta-1b treated patients, HLA-DRB1*04 increased the risk of developing high NAb titers, and in a subgroup analysis of DRB1*04 alleles the risk for NAbs was increased in DRB1*04:01 carriers.	nab	82-85	major histocompatibility complex, class II, DR beta 1	Homo sapiens	36-40
23628985-12	2014	These results show that a panel of blood-based biomarkers is able to accurately predict NAB, supporting the hypothesis for a relationship between a blood-based signature and Abeta accumulation, therefore, providing a platform for developing a population-based screen.	nab	88-91	amyloid beta precursor protein	Homo sapiens	174-179
24614336-8	2014	Intracerebroventricular infusion of oxytocin (OXT, 0.1 microg/5 microl) inhibited aggressive behavior in adult NAB and LAB, but not HAB females.	nab	111-114	oxytocin/neurophysin I prepropeptide	Rattus norvegicus	36-44
24614336-8	2014	Intracerebroventricular infusion of oxytocin (OXT, 0.1 microg/5 microl) inhibited aggressive behavior in adult NAB and LAB, but not HAB females.	nab	111-114	oxytocin/neurophysin I prepropeptide	Rattus norvegicus	46-49
24614336-9	2014	Adolescent NAB rats that had been aggressive towards their intruder showed increased pERK immunoreactivity (IR) in the hypothalamic attack area and reduced pERK-IR in OXT neurons in the paraventricular hypothalamic nucleus compared to non-aggressive NAB rats.	nab	11-14	oxytocin/neurophysin I prepropeptide	Rattus norvegicus	167-170
24484617-2	2014	The chemotherapeutic agent nanoparticle albumin-encapsulated (NAB)-paclitaxel has been postulated to exploit SPARC expression to target neoplastic cells.	nab	62-65	secreted protein acidic and cysteine rich	Homo sapiens	109-114
24247978-6	2014	Apelin-13 treatment inhibited diabetes-, high glucose- and NaB-induced elevation of inflammatory factors, and histone hyperacetylation by upregulation of histone deacetylase 1.	nab	59-62	apelin	Mus musculus	0-6
24346096-1	2014	INTRODUCTION: nab-Paclitaxel (nab-P) is approved, in the United States, in combination with carboplatin for the first-line treatment of advanced non-small-cell lung cancer, based on a randomized phase 3 trial of nab-P plus carboplatin (nab-P/C) versus solvent-based paclitaxel plus carboplatin (sb-P/C).	nab	14-17	selenium binding protein 1	Homo sapiens	295-301
24346096-1	2014	INTRODUCTION: nab-Paclitaxel (nab-P) is approved, in the United States, in combination with carboplatin for the first-line treatment of advanced non-small-cell lung cancer, based on a randomized phase 3 trial of nab-P plus carboplatin (nab-P/C) versus solvent-based paclitaxel plus carboplatin (sb-P/C).	nab	30-33	selenium binding protein 1	Homo sapiens	295-301
24346096-11	2014	CONCLUSION: In this trial of patients receiving first-line treatment for advanced non-small-cell lung cancer, nab-P/C was associated with statistically and clinically significant reductions in patient-reported neuropathy, neuropathic pain in the hands and feet, and hearing loss compared with sb-P/C.	nab	110-113	selenium binding protein 1	Homo sapiens	293-299
24158909-4	2013	Three chemical genetic screens in wild-type yeast cells established that NAB promoted endosomal transport events dependent on the E3 ubiquitin ligase Rsp5/Nedd4.	nab	73-76	NEDD4 family E3 ubiquitin-protein ligase	Saccharomyces cerevisiae S288C	150-154
23516101-3	2013	Here we show that the HDAC inhibitor sodium butyrate (NaB) markedly increases cell death and reduces colony formation in human MB cell lines.	nab	54-57	histone deacetylase 9	Homo sapiens	22-26
23516101-4	2013	In addition, NaB increased the mRNA expression of Gria2, a neuronal differentiation marker, in D283 and DAOY cells and reduced the number of neurospheres in D283 cell cultures.	nab	13-16	glutamate ionotropic receptor AMPA type subunit 2	Homo sapiens	50-55
23989978-9	2013	In vivo, nab-paclitaxel showed antitumor activity in both rhabdomyosarcoma (RH4 and RD) and neuroblastoma [SK-N-BE(2) and CHLA-20] xenograft models.	nab	9-12	Rh blood group D antigen	Homo sapiens	76-79
23989978-12	2013	In the RH4 model, increased local relapse-free intervals were observed with nab-paclitaxel treatment (37.7 +- 3.2 days) comparing with paclitaxel (13.6 +- 2.07 days).	nab	76-79	Rh blood group D antigen	Homo sapiens	7-10
23942267-4	2013	Our previous studies revealed that NaB could inhibit IFN-gamma induced IDO expression in nasopharyngeal carcinoma cells, CNE2.	nab	35-38	interferon gamma	Homo sapiens	53-62
24042258-9	2013	BEZ235 and nab-paclitaxel caused an increase in PARP-1 and caspase-3 cleavage.	nab	11-14	poly (ADP-ribose) polymerase family, member 1	Mus musculus	48-54
24042258-9	2013	BEZ235 and nab-paclitaxel caused an increase in PARP-1 and caspase-3 cleavage.	nab	11-14	caspase 3	Mus musculus	59-68
23942267-4	2013	Our previous studies revealed that NaB could inhibit IFN-gamma induced IDO expression in nasopharyngeal carcinoma cells, CNE2.	nab	35-38	indoleamine 2,3-dioxygenase 1	Homo sapiens	71-74
23942267-5	2013	In the present study, we aim to investigate to the mechanism of NaB interfering with the interferon-gamma (IFN-gamma)-mediated IDO expression signaling transduction.	nab	64-67	interferon gamma	Homo sapiens	89-105
23942267-5	2013	In the present study, we aim to investigate to the mechanism of NaB interfering with the interferon-gamma (IFN-gamma)-mediated IDO expression signaling transduction.	nab	64-67	interferon gamma	Homo sapiens	107-116
23942267-5	2013	In the present study, we aim to investigate to the mechanism of NaB interfering with the interferon-gamma (IFN-gamma)-mediated IDO expression signaling transduction.	nab	64-67	indoleamine 2,3-dioxygenase 1	Homo sapiens	127-130
23942267-8	2013	KEY FINDINGS: We found that NaB inhibited IFN-gamma-induced IDO expression in CNE2 cells via decreasing phosphorylation and nuclear translocation of STAT1, but not via down-regulation of IFN-gamma-receptor (IFNGR).	nab	28-31	interferon gamma	Homo sapiens	42-51
23942267-8	2013	KEY FINDINGS: We found that NaB inhibited IFN-gamma-induced IDO expression in CNE2 cells via decreasing phosphorylation and nuclear translocation of STAT1, but not via down-regulation of IFN-gamma-receptor (IFNGR).	nab	28-31	indoleamine 2,3-dioxygenase 1	Homo sapiens	60-63
23942267-8	2013	KEY FINDINGS: We found that NaB inhibited IFN-gamma-induced IDO expression in CNE2 cells via decreasing phosphorylation and nuclear translocation of STAT1, but not via down-regulation of IFN-gamma-receptor (IFNGR).	nab	28-31	signal transducer and activator of transcription 1	Homo sapiens	149-154
23942267-8	2013	KEY FINDINGS: We found that NaB inhibited IFN-gamma-induced IDO expression in CNE2 cells via decreasing phosphorylation and nuclear translocation of STAT1, but not via down-regulation of IFN-gamma-receptor (IFNGR).	nab	28-31	interferon gamma receptor 1	Homo sapiens	207-212
23942267-9	2013	Immunoprecipitation assays revealed that NaB increased STAT1 acetylation.	nab	41-44	signal transducer and activator of transcription 1	Homo sapiens	55-60
23942267-11	2013	SIGNIFICANCE: These results suggest that NaB inhibited IFN-gamma-induced IDO expression via STAT1 increased acetylation, decreased phosphorylation, and reduced nuclear translocation.	nab	41-44	interferon gamma	Homo sapiens	55-64
23942267-11	2013	SIGNIFICANCE: These results suggest that NaB inhibited IFN-gamma-induced IDO expression via STAT1 increased acetylation, decreased phosphorylation, and reduced nuclear translocation.	nab	41-44	indoleamine 2,3-dioxygenase 1	Homo sapiens	73-76
23942267-11	2013	SIGNIFICANCE: These results suggest that NaB inhibited IFN-gamma-induced IDO expression via STAT1 increased acetylation, decreased phosphorylation, and reduced nuclear translocation.	nab	41-44	signal transducer and activator of transcription 1	Homo sapiens	92-97
23942267-12	2013	These provided new evidence for the anti-tumor action of NaB and potential drug targets to reduce the IDO-induced immune tolerance.	nab	57-60	indoleamine 2,3-dioxygenase 1	Homo sapiens	102-105
23831137-5	2013	This NAb assay utilizes an electrochemiluminescence detection platform and is based on the first step involved in all IFN-beta-induced biological activities, namely the binding of IFN-beta to its receptor, which is inhibited when NAbs are present.	nab	5-8	interferon beta 1	Homo sapiens	118-126
23803690-8	2013	Tumor stromal density was decreased by nab-paclitaxel and to a lesser extent by docetaxel as measured through reduction in alpha-smooth muscle actin, S100A4 and collagen 1 expression.	nab	39-42	S100 calcium binding protein A4	Homo sapiens	150-156
22833396-8	2013	Western blot analysis of DRG neurons from NaB-treated rats showed a 2.2-fold increase in phosphorylated ERK1/2 (pEKR1/2) and 1.9-fold increase in phosphorylated voltage-gated potassium channel subunit 4.2 (pKv4.2).	nab	42-45	mitogen activated protein kinase 3	Rattus norvegicus	104-110
23831137-5	2013	This NAb assay utilizes an electrochemiluminescence detection platform and is based on the first step involved in all IFN-beta-induced biological activities, namely the binding of IFN-beta to its receptor, which is inhibited when NAbs are present.	nab	5-8	interferon beta 1	Homo sapiens	180-188
23831137-6	2013	Using this approach, NAb titers in clinical samples from multiple sclerosis patients treated with IFN-beta were determined and compared with those obtained using existing cell-based NAb assays.	nab	21-24	interferon beta 1	Homo sapiens	98-106
23907428-14	2013	CONCLUSION: These data suggest that nab-paclitaxel and gemcitabine decreases CAF content inducing a marked alteration in cancer stroma that results in tumour softening.	nab	36-39	lysine acetyltransferase 2B	Homo sapiens	77-80
24086397-11	2013	Expression of the anti-apoptosis gene Bcl-xl and Bcl-2 in DU145 cells are decreased and expression of the pro-apoptosis gene Bax and Bak increased after NaB treatment.	nab	153-156	BCL2 like 1	Homo sapiens	38-44
24086397-11	2013	Expression of the anti-apoptosis gene Bcl-xl and Bcl-2 in DU145 cells are decreased and expression of the pro-apoptosis gene Bax and Bak increased after NaB treatment.	nab	153-156	BCL2 apoptosis regulator	Homo sapiens	49-54
24086397-11	2013	Expression of the anti-apoptosis gene Bcl-xl and Bcl-2 in DU145 cells are decreased and expression of the pro-apoptosis gene Bax and Bak increased after NaB treatment.	nab	153-156	BCL2 associated X, apoptosis regulator	Homo sapiens	125-128
24086397-11	2013	Expression of the anti-apoptosis gene Bcl-xl and Bcl-2 in DU145 cells are decreased and expression of the pro-apoptosis gene Bax and Bak increased after NaB treatment.	nab	153-156	BCL2 antagonist/killer 1	Homo sapiens	133-136
24086397-12	2013	Further studies have demonstrated that NaB up-regulated the expression of ANXA1 and that the tumor inhibition action of NaB was reduced markedly through knockdown of the ANXA1 gene in DU145 cells.	nab	39-42	annexin A1	Homo sapiens	74-79
24086397-12	2013	Further studies have demonstrated that NaB up-regulated the expression of ANXA1 and that the tumor inhibition action of NaB was reduced markedly through knockdown of the ANXA1 gene in DU145 cells.	nab	120-123	annexin A1	Homo sapiens	170-175
24086397-14	2013	CONCLUSION: Our results support a significant correlation between NaB functions and ANXA1 expression in prostate cancer, and pave the way for further studying the molecular mechanism of NaB actions in cancers.	nab	66-69	annexin A1	Homo sapiens	84-89
24086397-14	2013	CONCLUSION: Our results support a significant correlation between NaB functions and ANXA1 expression in prostate cancer, and pave the way for further studying the molecular mechanism of NaB actions in cancers.	nab	186-189	annexin A1	Homo sapiens	84-89
23615664-5	2013	We demonstrate that the enabling effects of exercise and NaB on subthreshold OLM learning are dependent on hippocampal BDNF upregulation, and are blocked by hippocampal infusion of BDNF short-interfering RNA.	nab	57-60	brain derived neurotrophic factor	Mus musculus	119-123
23615664-5	2013	We demonstrate that the enabling effects of exercise and NaB on subthreshold OLM learning are dependent on hippocampal BDNF upregulation, and are blocked by hippocampal infusion of BDNF short-interfering RNA.	nab	57-60	brain derived neurotrophic factor	Mus musculus	181-185
23615664-6	2013	Exercise and NaB increased bdnf transcripts I and IV, and the increases were associated with BDNF promoter acetylation on H4K8 but not H4K12.	nab	13-16	brain derived neurotrophic factor	Mus musculus	27-31
23615664-6	2013	Exercise and NaB increased bdnf transcripts I and IV, and the increases were associated with BDNF promoter acetylation on H4K8 but not H4K12.	nab	13-16	brain derived neurotrophic factor	Mus musculus	93-97
23475543-1	2013	This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS.	nab	135-138	brain derived neurotrophic factor	Homo sapiens	293-326
23874931-9	2013	Our results demonstrate heightened autologous NAb responses against gp120/gp41 can associate with a greater risk of HIV-1 MTCT and more specifically in those infants infected IU.	nab	46-49	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	68-73
23575901-6	2013	The NaB-treated group displayed the highest ALP activity and expression of osteo- and odontogenic-related genes and proteins compared to the other groups and baseline.	nab	4-7	alkaline phosphatase, placental	Homo sapiens	44-47
23232980-3	2013	TLR2 up-regulation by poly I:C was also reduced by IL-6Ralpha-nAb and inhibitors of Jak2, Stat3 and NF-kappaB phosphorylation, whereas RANTES secretion was unaffected, but abolished following NF-kappaB inhibition.	nab	62-65	toll like receptor 2	Homo sapiens	0-4
23232980-3	2013	TLR2 up-regulation by poly I:C was also reduced by IL-6Ralpha-nAb and inhibitors of Jak2, Stat3 and NF-kappaB phosphorylation, whereas RANTES secretion was unaffected, but abolished following NF-kappaB inhibition.	nab	62-65	interleukin 6 receptor	Homo sapiens	51-61
23475543-1	2013	This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS.	nab	135-138	brain derived neurotrophic factor	Homo sapiens	328-332
23475543-1	2013	This study underlines the importance of cinnamon, a widely-used food spice and flavoring material, and its metabolite sodium benzoate (NaB), a widely-used food preservative and a FDA-approved drug against urea cycle disorders in humans, in increasing the levels of neurotrophic factors [e.g., brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3)] in the CNS.	nab	135-138	neurotrophin 3	Homo sapiens	338-352
23475543-2	2013	NaB, but not sodium formate (NaFO), dose-dependently induced the expression of BDNF and NT-3 in primary human neurons and astrocytes.	nab	0-3	brain derived neurotrophic factor	Homo sapiens	79-83
23475543-6	2013	Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB.	nab	95-98	cAMP responsive element binding protein 1	Mus musculus	58-62
23475543-6	2013	Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB.	nab	114-117	cAMP responsive element binding protein 1	Mus musculus	58-62
23475543-6	2013	Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB.	nab	114-117	cAMP responsive element binding protein 1	Mus musculus	183-187
23475543-6	2013	Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB.	nab	114-117	brain derived neurotrophic factor	Mus musculus	248-252
23475543-6	2013	Furthermore, activation of cAMP response element binding (CREB) protein, but not NF-kappaB, by NaB, abrogation of NaB-induced expression of neurotrophic factors by siRNA knockdown of CREB and the recruitment of CREB and CREB-binding protein to the BDNF promoter by NaB suggest that NaB exerts its neurotrophic effect through the activation of CREB.	nab	114-117	cAMP responsive element binding protein 1	Mus musculus	183-187
23475543-8	2013	These results highlight a novel neutrophic property of cinnamon and its metabolite NaB via PKA - CREB pathway, which may be of benefit for various neurodegenerative disorders.	nab	83-86	cAMP responsive element binding protein 1	Mus musculus	97-101
23403953-6	2013	ID2 knockdown cells were more susceptible to histone deacethylase (HDAC) inhibitors including sodium butyrate (NaB), sodium 4-phenyl-butyrate, tricostatin A, suberoylanilide hydroxamic acid, MS-275, apicidin and HC-toxin.	nab	111-114	inhibitor of DNA binding 2	Homo sapiens	0-3
23503510-3	2013	The aim of our study was to analyze the 5-aza-2"-deoxycytidine (Aza-dC) and sodium butyrate (NaB) effects on CaP cells with modified AR gene expression.	nab	93-96	androgen receptor	Homo sapiens	133-135
23503510-9	2013	The co-treatment with Aza-dC and NaB was the most effective in demethylation and re-expression of the AR gene.	nab	33-36	androgen receptor	Homo sapiens	102-104
23696823-8	2013	In vitro studies revealed that treatment with sodium butyrate (NaB) also activated AMPK and AKT and enhanced Nrf2 expression by precluding ubiquitination, thereby increasing the half-life of the Nrf2 protein.	nab	63-66	AKT serine/threonine kinase 1	Rattus norvegicus	92-95
23696823-8	2013	In vitro studies revealed that treatment with sodium butyrate (NaB) also activated AMPK and AKT and enhanced Nrf2 expression by precluding ubiquitination, thereby increasing the half-life of the Nrf2 protein.	nab	63-66	NFE2 like bZIP transcription factor 2	Rattus norvegicus	109-113
23696823-8	2013	In vitro studies revealed that treatment with sodium butyrate (NaB) also activated AMPK and AKT and enhanced Nrf2 expression by precluding ubiquitination, thereby increasing the half-life of the Nrf2 protein.	nab	63-66	NFE2 like bZIP transcription factor 2	Rattus norvegicus	195-199
23696823-9	2013	Pharmacological studies and siRNA knockdown experiments showed that NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mammalian TOR complex 2 and phosphorylation of AKT at Ser473 and subsequent induction of Nrf2 expression and activation.	nab	68-71	sirtuin 1	Homo sapiens	154-163
23696823-9	2013	Pharmacological studies and siRNA knockdown experiments showed that NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mammalian TOR complex 2 and phosphorylation of AKT at Ser473 and subsequent induction of Nrf2 expression and activation.	nab	68-71	AKT serine/threonine kinase 1	Homo sapiens	249-252
23696823-9	2013	Pharmacological studies and siRNA knockdown experiments showed that NaB-mediated AMPK activation induced the phosphorylation and nuclear translocation of Sirtuin 1, leading to the increased assembly of mammalian TOR complex 2 and phosphorylation of AKT at Ser473 and subsequent induction of Nrf2 expression and activation.	nab	68-71	NFE2 like bZIP transcription factor 2	Homo sapiens	291-295
23403953-8	2013	NaB-induced apoptosis was inversely correlated with ID2 expression.	nab	0-3	inhibitor of DNA binding 2	Homo sapiens	52-55
23403953-9	2013	Expression of the anti-apoptotic mRNA BCL2 was induced by NaB in control cells, but this induction of BCL2 was inhibited by ID2 knockdown and strengthened by ID2 overexpression.	nab	58-61	BCL2 apoptosis regulator	Homo sapiens	38-42
23403953-10	2013	Expression of another anti-apoptotic mRNA, BCL2L1, was decreased by NaB administration and then partially recovered.	nab	68-71	BCL2 like 1	Homo sapiens	43-49
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	MX dynamin like GTPase 1	Homo sapiens	78-81
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	interferon alpha inducible protein 27	Homo sapiens	83-88
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	TNF superfamily member 10	Homo sapiens	117-122
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	interleukin 10	Homo sapiens	90-94
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	interferon alpha 1	Homo sapiens	166-175
25877635-9	2013	We found a significantly increased expression of a number of genes, including MX1, IFI27, IL10 and TNFSF10 (encoding TRAIL) in the NAb-positive patients treated with IFN-alpha.	nab	131-134	TNF superfamily member 10	Homo sapiens	99-106
23468623-3	2013	Here we characterized the earliest nAb responses in a subtype A HIV-1 infected Rwandan seroconverter who later developed moderate cross-clade nAb breadth, using (i) envelope (Env) glycoproteins from the transmitted/founder virus and twenty longitudinal nAb escape variants, (ii) longitudinal autologous plasma, and (iii) autologous monoclonal antibodies (mAbs).	nab	35-38	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	175-178
23468623-11	2013	Our data demonstrate that this subject"s first recognized nAb epitope elicited strain-specific mAbs, which incrementally acquired autologous breadth, and directed later B cell responses to target distinct portions of Env.	nab	58-61	endogenous retrovirus group K member 20	Homo sapiens	217-220
23460921-5	2013	Nab-paclitaxel treatment increased expression of the mitotic-spindle associated phospho-stathmin irrespective of the baseline total or phosphorylated stathmin level, and induced mitotic cell death as confirmed through increased expression of cleaved-PARP and caspase-3.	nab	0-3	stathmin 1	Homo sapiens	88-96
22763852-4	2013	NaB did not cause significant cell death at 100 muM but promoted the expression of the osteoblast phenotype (Runx2, osterix, osteocalcin, and bone sialoprotein).	nab	0-3	RUNX family transcription factor 2	Homo sapiens	109-114
22763852-4	2013	NaB did not cause significant cell death at 100 muM but promoted the expression of the osteoblast phenotype (Runx2, osterix, osteocalcin, and bone sialoprotein).	nab	0-3	Sp7 transcription factor	Homo sapiens	116-123
22763852-4	2013	NaB did not cause significant cell death at 100 muM but promoted the expression of the osteoblast phenotype (Runx2, osterix, osteocalcin, and bone sialoprotein).	nab	0-3	bone gamma-carboxyglutamate protein	Homo sapiens	125-136
22763852-5	2013	NaB significantly inhibited the LPS-induced production of reactive oxygen species and the expression of pro-inflammatory cytokines (IL-1beta and TNF-alpha).	nab	0-3	interleukin 1 beta	Homo sapiens	132-140
22763852-5	2013	NaB significantly inhibited the LPS-induced production of reactive oxygen species and the expression of pro-inflammatory cytokines (IL-1beta and TNF-alpha).	nab	0-3	tumor necrosis factor	Homo sapiens	145-154
23379109-3	2013	Preclinical data indicated an increase of drug accumulation in tumor tissues via nab-paclitaxel administration which appears to be related to direct interaction with albumin-binding proteins including stromal SPARC.	nab	81-84	secreted protein acidic and cysteine rich	Homo sapiens	209-214
23142458-6	2013	The expression of EGR1 in UT-7/EPO cells in response to rHuEPO was comparable to the proliferative response measured by (3)H-thymidine incorporation and could be inhibited by serum from a patient with NAb-mediated PRCA in a dilution-dependent manner.	nab	201-204	early growth response 1	Homo sapiens	18-22
23142458-6	2013	The expression of EGR1 in UT-7/EPO cells in response to rHuEPO was comparable to the proliferative response measured by (3)H-thymidine incorporation and could be inhibited by serum from a patient with NAb-mediated PRCA in a dilution-dependent manner.	nab	201-204	erythropoietin	Homo sapiens	31-34
24623075-5	2013	At low density, IGF1R nAb reduced development to the blastocyst stage, hatching, and total cell numbers in blastocysts and increased the number of apoptotic cells in blastocysts, suggesting that autocrine IGF1 signalling is occurring, even at low density.	nab	22-25	insulin-like growth factor I receptor	Mus musculus	16-21
24623075-5	2013	At low density, IGF1R nAb reduced development to the blastocyst stage, hatching, and total cell numbers in blastocysts and increased the number of apoptotic cells in blastocysts, suggesting that autocrine IGF1 signalling is occurring, even at low density.	nab	22-25	insulin-like growth factor 1	Mus musculus	16-20
23460921-5	2013	Nab-paclitaxel treatment increased expression of the mitotic-spindle associated phospho-stathmin irrespective of the baseline total or phosphorylated stathmin level, and induced mitotic cell death as confirmed through increased expression of cleaved-PARP and caspase-3.	nab	0-3	poly(ADP-ribose) polymerase 1	Homo sapiens	250-254
23460921-5	2013	Nab-paclitaxel treatment increased expression of the mitotic-spindle associated phospho-stathmin irrespective of the baseline total or phosphorylated stathmin level, and induced mitotic cell death as confirmed through increased expression of cleaved-PARP and caspase-3.	nab	0-3	caspase 3	Homo sapiens	259-268
22684624-7	2012	RESULTS: NaB decreased FD-40 flux, increased TEER and TJ protein Claudin-1 expression, induced ZO-1 and Occludin redistribution in cellular membrane, and reversed the damage effect after calcium (Ca(2+)) switch assay.	nab	9-12	claudin 1	Homo sapiens	65-74
22684624-7	2012	RESULTS: NaB decreased FD-40 flux, increased TEER and TJ protein Claudin-1 expression, induced ZO-1 and Occludin redistribution in cellular membrane, and reversed the damage effect after calcium (Ca(2+)) switch assay.	nab	9-12	tight junction protein 1	Homo sapiens	95-99
22684624-7	2012	RESULTS: NaB decreased FD-40 flux, increased TEER and TJ protein Claudin-1 expression, induced ZO-1 and Occludin redistribution in cellular membrane, and reversed the damage effect after calcium (Ca(2+)) switch assay.	nab	9-12	occludin	Homo sapiens	104-112
22684624-8	2012	Silencing Claudin-1 prevented protective function of NaB from enhancing intestinal barrier integrity.	nab	53-56	claudin 1	Homo sapiens	10-19
22684624-9	2012	Further studies demonstrated that NaB increased Claudin-1 transcription by facilitating the interaction between transcription factor SP1 and a specific motif within the promoter region of Claudin-1.	nab	34-37	claudin 1	Homo sapiens	48-57
22684624-9	2012	Further studies demonstrated that NaB increased Claudin-1 transcription by facilitating the interaction between transcription factor SP1 and a specific motif within the promoter region of Claudin-1.	nab	34-37	claudin 1	Homo sapiens	188-197
22684624-10	2012	This SP1 binding motif was located upstream of the coding region (-138 to -76 bp) and indispensable for the transcription of Claudin-1 following NaB treatment.	nab	145-148	claudin 1	Homo sapiens	125-134
22684624-12	2012	CONCLUSIONS: NaB enhanced intestinal barrier function through increasing Claudin-1 transcription via facilitating the association between SP1 and Claudin-1 promoter.	nab	13-16	claudin 1	Homo sapiens	73-82
22684624-12	2012	CONCLUSIONS: NaB enhanced intestinal barrier function through increasing Claudin-1 transcription via facilitating the association between SP1 and Claudin-1 promoter.	nab	13-16	claudin 1	Homo sapiens	146-155
23715237-12	2012	CONCLUSIONS: This rabbit model demonstrates that ISG15 expression evaluated with flow cytometry can be used as a detection assay for NAb.	nab	133-136	ubiquitin-like protein ISG15	Oryctolagus cuniculus	49-54
22718114-4	2012	During a chronic UVB exposure regimen, pre-treatment with a lentiviral vector overexpressing TIMP-1 or concomitant administration of an anti-TIMP-1-neutralizing antibody (NAB) led to photoprotection or more severe photodamage, respectively.	nab	171-174	TIMP metallopeptidase inhibitor 1	Homo sapiens	141-147
22718114-5	2012	Overexpression of TIMP-1 resulted in significant inhibition of UVB-induced ECM degradation, as well as suppression of decreased skin elasticity and roughness, whereas the NAB-mediated inhibition of TIMP-1 had opposite effects.	nab	171-174	TIMP metallopeptidase inhibitor 1	Homo sapiens	198-204
22577035-9	2012	RESULTS: IgM anti-AC NAb dose-dependently suppressed the production of DNA IC- and RNA IC-induced interleukin-6 and DNA IC-induced tumor necrosis factor alpha, as well as the RNA IC-induced up-regulation of CD86 and CD40 on DCs.	nab	21-24	interleukin 6	Homo sapiens	98-111
22577035-9	2012	RESULTS: IgM anti-AC NAb dose-dependently suppressed the production of DNA IC- and RNA IC-induced interleukin-6 and DNA IC-induced tumor necrosis factor alpha, as well as the RNA IC-induced up-regulation of CD86 and CD40 on DCs.	nab	21-24	CD86 molecule	Homo sapiens	207-211
22577035-9	2012	RESULTS: IgM anti-AC NAb dose-dependently suppressed the production of DNA IC- and RNA IC-induced interleukin-6 and DNA IC-induced tumor necrosis factor alpha, as well as the RNA IC-induced up-regulation of CD86 and CD40 on DCs.	nab	21-24	CD40 molecule	Homo sapiens	216-220
22577035-10	2012	IgM NAb-mediated inhibition was associated with suppression of IC-mediated p38 MAPK activation and nuclear localization.	nab	4-7	mitogen-activated protein kinase 14	Homo sapiens	75-78
22954172-7	2012	Sensitivity increased significantly for NAB combined with cytological tumor markers compared with NAB alone (CYFRA 21-1: 95% versus 83.5%, p &lt; 0.001, CEA: 92.1% versus 83.5%, p = 0.002, SCC: 91.4% versus 83.5%, p = 0.003).	nab	40-43	CEA cell adhesion molecule 3	Homo sapiens	153-156
22669487-6	2012	Like NaB, NaAC inhibited LPS-induced NF-kappaB activation.	nab	5-8	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	37-46
22954172-7	2012	Sensitivity increased significantly for NAB combined with cytological tumor markers compared with NAB alone (CYFRA 21-1: 95% versus 83.5%, p &lt; 0.001, CEA: 92.1% versus 83.5%, p = 0.002, SCC: 91.4% versus 83.5%, p = 0.003).	nab	40-43	serpin family B member 3	Homo sapiens	189-192
22825819-5	2012	Results showed that overall 72% of healthy adults were Ad5 seropositive, and 46.4% with baseline Ad5 NAb titers of &gt;200 in China.	nab	101-104	Alzheimer disease, familial, type 5	Homo sapiens	97-100
22740394-4	2012	The molecular determinants of NAb escape were distinct, even when comparing two maternal variants to the transmitted infant virus within one pair, in which insertions in V4 of gp120 and substitutions in HR2 of gp41 conferred neutralization resistance.	nab	30-33	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	176-181
22287540-7	2012	Compared with controls STATs signalling patterns were modulated in treated NAb-negative patients and inhibited in all treated NAb-positive patients independently of NAb titres.	nab	75-78	signal transducer and activator of transcription 1	Homo sapiens	23-28
22749601-5	2012	We hypothesize that Env protein escape variants stimulate broad NAb development in vivo and could generate such NAbs when used as immunogens.	nab	64-67	endogenous retrovirus group K member 20	Homo sapiens	20-23
22287540-7	2012	Compared with controls STATs signalling patterns were modulated in treated NAb-negative patients and inhibited in all treated NAb-positive patients independently of NAb titres.	nab	126-129	signal transducer and activator of transcription 1	Homo sapiens	23-28
22287540-7	2012	Compared with controls STATs signalling patterns were modulated in treated NAb-negative patients and inhibited in all treated NAb-positive patients independently of NAb titres.	nab	126-129	signal transducer and activator of transcription 1	Homo sapiens	23-28
21796630-7	2012	NaB restored the DPT expression in OSCC-derived cells.	nab	0-3	dermatopontin	Homo sapiens	17-20
22290116-6	2012	NaB administered following weak extinction induced behavioral extinction, infralimbic histone acetylation and c-Fos expression consistent with strong extinction.	nab	0-3	FBJ osteosarcoma oncogene	Mus musculus	110-115
22013146-2	2012	Persistency depends on NAb titers, which differ between IFNbeta preparations.	nab	23-26	interferon beta 1	Homo sapiens	56-63
21701815-5	2012	Here we delineate that NaB is also capable of increasing the level of DJ-1 in primary mouse and human astrocytes and human neurons highlighting another novel neuroprotective effect of this compound.	nab	23-26	Parkinson disease (autosomal recessive, early onset) 7	Mus musculus	70-74
21701815-10	2012	Together, these results suggest that NaB upregulates DJ-1 via modulation of mevalonate metabolites and that p21(ras), but not p21(rac), is involved in the regulation of DJ-1.	nab	37-40	Parkinsonism associated deglycase	Homo sapiens	53-57
22246241-10	2012	Sodium butyrate (NaB) induced demethylation             and histone modification at the promoter region of SFRP1/2 restoring the SFRP             expression in human gastric cancer cells.	nab	17-20	secreted frizzled related protein 1	Homo sapiens	107-114
22703536-9	2012	CONCLUSIONS: There are considerable differences in the detection and quantification of IFNB-induced NAbs among laboratories offering NAb testing for clinical practice using different assay methods.	nab	100-103	interferon beta 1	Homo sapiens	87-91
22013146-3	2012	OBJECTIVE: This study evaluated IFNbeta preparation-specific NAb cut-off titers during early treatment for prediction of NAb persistency.	nab	61-64	interferon beta 1	Homo sapiens	32-39
22013146-3	2012	OBJECTIVE: This study evaluated IFNbeta preparation-specific NAb cut-off titers during early treatment for prediction of NAb persistency.	nab	121-124	interferon beta 1	Homo sapiens	32-39
22013146-8	2012	NAb frequency significantly decreased by 40.7% in the IFNbeta-1a and by 60% in the IFNbeta-1b group at follow-up after a mean time of 75.4 months on treatment, and median NAb titers decreased significantly in both groups.	nab	0-3	interferon beta 1	Homo sapiens	54-61
22469747-6	2012	Consistently, infusion of DNMT inhibitor, 5-azacytidine (5-azaC), or histone deacetylases (HDACs) inhibitor, sodium butyrate (NaB), into the mPFC could interfere with LTP-associated demethylation and acetylation of reelin and bdnf genes, and the induction of LTP as well.	nab	126-129	reelin	Rattus norvegicus	215-221
22013146-9	2012	During baseline, NAb titers of &gt;258 neutralizing units (NU) had a sensitivity of 81.3% and a specificity of 90.9% in the IFNbeta-1a group, whereas titers of &gt;460 NU had a sensitivity of 100% and a specificity of 91.7% in the IFNbeta-1b group to predict persistency at follow-up.	nab	17-20	interferon beta 1	Homo sapiens	124-131
22013146-11	2012	CONCLUSION: IFNbeta preparation-specific NAb cut-off titers for prediction of NAb persistency, which may be useful in individual treatment decision making, are provided.	nab	41-44	interferon beta 1	Homo sapiens	12-19
22013146-11	2012	CONCLUSION: IFNbeta preparation-specific NAb cut-off titers for prediction of NAb persistency, which may be useful in individual treatment decision making, are provided.	nab	78-81	interferon beta 1	Homo sapiens	12-19
22131152-8	2012	The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P &lt; 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P &lt; 0.05).	nab	42-45	host cell factor C1	Homo sapiens	46-59
21359953-10	2012	The combination of lapatinib and nab-paclitaxel was well tolerated and provided good efficacy in women with HER2 positive breast cancer.	nab	33-36	erb-b2 receptor tyrosine kinase 2	Homo sapiens	108-112
22585996-0	2012	nab-Paclitaxel potentiates gemcitabine activity by reducing cytidine deaminase levels in a mouse model of pancreatic cancer.	nab	0-3	cytidine deaminase	Mus musculus	60-78
21699495-6	2012	Furthermore, down-regulation of STIM1 (stromal interaction molecule 1) by RNA interference or pharmacological blockade of the SOCC (store-operated Ca2+ channel) by 2-APB (2-aminoethoxydiphenyl borate) or SKF-96365 inhibited NaB-induced extracellular Ca2+ influx and apoptosis in HCT-116 cells.	nab	224-227	stromal interaction molecule 1	Homo sapiens	32-37
21699495-6	2012	Furthermore, down-regulation of STIM1 (stromal interaction molecule 1) by RNA interference or pharmacological blockade of the SOCC (store-operated Ca2+ channel) by 2-APB (2-aminoethoxydiphenyl borate) or SKF-96365 inhibited NaB-induced extracellular Ca2+ influx and apoptosis in HCT-116 cells.	nab	224-227	stromal interaction molecule 1	Homo sapiens	39-69
22131152-8	2012	The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P &lt; 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P &lt; 0.05).	nab	42-45	BCL2 like 11	Homo sapiens	98-101
22131152-8	2012	The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P &lt; 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P &lt; 0.05).	nab	42-45	caspase 3	Homo sapiens	139-148
22131152-8	2012	The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P &lt; 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P &lt; 0.05).	nab	42-45	caspase 9	Homo sapiens	153-162
22131152-8	2012	The apoptotic effects on BL cell lines of NaB/VP-16 and NaB/CDDP were followed by upregulation of Bim protein (P &lt; 0.05), activation of caspase-3 and caspase-9, followed by Mcl-1 downregulation (P &lt; 0.05).	nab	42-45	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	176-181
22124136-3	2012	In this work, we demonstrate that TSA, VPA, and NaB inhibited IFN-gamma production by CD56(dim) and CD56(bright) NK cells and NK cell-mediated cytotoxicity against K562 target cells.	nab	48-51	interferon gamma	Homo sapiens	62-71
21839127-5	2012	Specialized nanotechnological techniques like desolvation, emulsification, thermal gelation and recently nano-spray drying, nab-technology and self-assembly that have been investigated for fabrication of albumin nanoparticles, are also discussed.	nab	124-127	albumin	Homo sapiens	204-211
22302795-3	2012	Previous studies have shown Chd4 interacts with Nab (NGFI-A/Egr-binding) corepressors, which are required for early growth response 2 (Egr2/Krox20), to direct peripheral nerve myelination by Schwann cells.	nab	48-51	chromodomain helicase DNA binding protein 4	Mus musculus	28-32
22302795-3	2012	Previous studies have shown Chd4 interacts with Nab (NGFI-A/Egr-binding) corepressors, which are required for early growth response 2 (Egr2/Krox20), to direct peripheral nerve myelination by Schwann cells.	nab	48-51	early growth response 1	Mus musculus	53-59
22302795-3	2012	Previous studies have shown Chd4 interacts with Nab (NGFI-A/Egr-binding) corepressors, which are required for early growth response 2 (Egr2/Krox20), to direct peripheral nerve myelination by Schwann cells.	nab	48-51	early growth response 1	Mus musculus	60-63
22302795-3	2012	Previous studies have shown Chd4 interacts with Nab (NGFI-A/Egr-binding) corepressors, which are required for early growth response 2 (Egr2/Krox20), to direct peripheral nerve myelination by Schwann cells.	nab	48-51	early growth response 2	Mus musculus	135-139
22302795-3	2012	Previous studies have shown Chd4 interacts with Nab (NGFI-A/Egr-binding) corepressors, which are required for early growth response 2 (Egr2/Krox20), to direct peripheral nerve myelination by Schwann cells.	nab	48-51	early growth response 2	Mus musculus	140-146
22381755-3	2012	The changes in the intracellular localization of stromal interaction molecule (STIM1) and Orai1 following NaB treatment were detected by immunofluorescence technique.	nab	106-109	stromal interaction molecule 1	Homo sapiens	79-84
22381755-3	2012	The changes in the intracellular localization of stromal interaction molecule (STIM1) and Orai1 following NaB treatment were detected by immunofluorescence technique.	nab	106-109	ORAI calcium release-activated calcium modulator 1	Homo sapiens	90-95
22381755-5	2012	RESULTS: NaB induced apoptosis and caused translocation and colocalization of STIM1 and Orai1 in HCT-116 cells.	nab	9-12	stromal interaction molecule 1	Homo sapiens	78-83
22381755-5	2012	RESULTS: NaB induced apoptosis and caused translocation and colocalization of STIM1 and Orai1 in HCT-116 cells.	nab	9-12	ORAI calcium release-activated calcium modulator 1	Homo sapiens	88-93
22381755-6	2012	CONCLUSION: The apoptosis of human colon cancer cells induced by NaB is correlated to the redistribution of STIM1 and Orai1.	nab	65-68	stromal interaction molecule 1	Homo sapiens	108-113
22381755-6	2012	CONCLUSION: The apoptosis of human colon cancer cells induced by NaB is correlated to the redistribution of STIM1 and Orai1.	nab	65-68	ORAI calcium release-activated calcium modulator 1	Homo sapiens	118-123
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	nab	139-142	zinc finger protein 148	Homo sapiens	46-52
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	nab	139-142	tumor protein p53	Homo sapiens	56-59
22214764-8	2012	Functionally, the cytoplasmic accumulation of ZBP-89 by p53(G245D) significantly abrogated the induction of p21 caused by sodium butyrate (NaB) treatment and protected cells from TSA-induced death.	nab	139-142	cyclin dependent kinase inhibitor 1A	Homo sapiens	108-111
21495876-8	2012	Drawing on these analyses, we outline strategies for improving Env as a component of a vaccine aimed at inducing strong and sustained NAb responses.	nab	134-137	endogenous retrovirus group K member 20	Homo sapiens	63-66
21659904-6	2012	RESULTS: Change in interleukin-6 was significantly reduced in NAB compared with PL immediately after the race (median (interquartile range) = 23.9 (15.9-38.7) vs 31.6 (18.5-53.3) ng   L(-1), P = 0.03).	nab	62-65	interleukin 6	Homo sapiens	19-32
22773978-7	2012	TGF-beta NAb resulted in a reduced subretinal fibrosis areas by 65% compared to animals from control group at day 7.	nab	9-12	transforming growth factor, beta 1	Mus musculus	0-8
22156929-3	2012	SPARC (secreted protein acidic rich in cysteine) is an albumin-binding matrix-associated protein that is proposed to act as a mechanism for the increased efficacy of a nanoparticle albumin-bound preparation of the antimicrotubular drug Paclitaxel (nab-paclitaxel).	nab	248-251	secreted protein acidic and cysteine rich	Homo sapiens	0-5
23209707-6	2012	The critical reliance on Abeta"s conformational state for NAb binding, and not a linear sequence epitope, was confirmed by the antibody"s nM reactivity with plate-immobilized protofibrills, and weak uM binding to synthetic Abeta monomers and peptide fragments.	nab	58-61	amyloid beta precursor protein	Homo sapiens	25-30
23251616-6	2012	Sodium butyrate (NaB) at a concentration of 1 mM reduces Caco-2 cell proliferation, increases differentiation and increases GSTA1 activity 4-fold by 72 hours.	nab	17-20	glutathione S-transferase alpha 1	Homo sapiens	124-129
23251616-7	2012	In contrast, 10 mM NaB causes significant toxicity in preconfluent cells via apoptosis through caspase-3 activation with reduced GSTA1 activity.	nab	19-22	caspase 3	Homo sapiens	95-104
23251616-7	2012	In contrast, 10 mM NaB causes significant toxicity in preconfluent cells via apoptosis through caspase-3 activation with reduced GSTA1 activity.	nab	19-22	glutathione S-transferase alpha 1	Homo sapiens	129-134
23251616-9	2012	While 10 mM NaB causes GSTA1-JNK complex dissociation, phosphorylation of JNK is not altered.	nab	12-15	glutathione S-transferase alpha 1	Homo sapiens	23-28
23251616-9	2012	While 10 mM NaB causes GSTA1-JNK complex dissociation, phosphorylation of JNK is not altered.	nab	12-15	mitogen-activated protein kinase 8	Homo sapiens	29-32
21685230-8	2011	MxA expression was inhibited in a dose-dependent fashion in NAb positive samples.	nab	60-63	MX dynamin like GTPase 1	Homo sapiens	0-3
29147265-3	2011	Methods: The HBA-71 monoclonal antibody directed to the CD99/MIC2 antigen was used to stain a human osteoblast cell line as well as the two EFT cell lines KAL and EW-2 after pretreatment of the cells with the differentiation inducers calcitriol and the histone deacetylase (HDAC) inhibitors sodium butyrate (NaB), sodium phenylacetate (NaPA) as well as N, N"-hexamethylen-bis-acetamide (HMBA).	nab	308-311	CD99 molecule (Xg blood group)	Homo sapiens	13-19
23077563-8	2012	The MEKK1 gene transferred by MiLV significantly elevated the sensitivity of B95-8 cells and transplanted tumor to the treatment of Ganciclovir (GCV) and sodium butyrate (NaB).	nab	171-174	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	4-9
21887460-4	2011	To elucidate whether combined treatment with NaB and trastuzumab exerts anti-tumor effects on a HER2-overexpressing breast cancer cell line, SKBR3 cells were treated with NaB alone or in combination with trastuzumab, and the effects on proliferation and cell cycle progression were analyzed.	nab	45-48	erb-b2 receptor tyrosine kinase 2	Homo sapiens	96-100
21887460-6	2011	The growth-inhibitory effect of the combination of NaB and trastuzumab was accompanied by elevated mRNA and protein levels of the cyclin-dependent kinase inhibitor p27Kip1.	nab	51-54	cyclin dependent kinase inhibitor 1B	Homo sapiens	164-171
21887460-8	2011	In conclusion, trastuzumab significantly improved the antitumor effect of NaB on HER2-overexpressing breast cancer cell line in vitro.	nab	74-77	erb-b2 receptor tyrosine kinase 2	Homo sapiens	81-85
21751234-3	2011	Using the well-established mouse ESC culture, we demonstrated that HDAC inhibitors, both trichostatin A (TSA,50  nmol/L) and sodium butyrate (NaB, 200  micromol/L) that causes the pronounced reduction of HDAC4 activity, decreased cell death and increased viability of ESCs in response to oxidant stress.	nab	142-145	histone deacetylase 4	Mus musculus	204-209
21685230-9	2011	Mean MxA level post-IFN-beta: NAb negative 2330 (95% CI 1940-2719), NAb 20-99 NU 1533 (95% CI 741-2324), NAb 100-600 NU 832 (186-1478) and NAb &gt; 600 NU 101 (95% CI 0-224).	nab	30-33	MX dynamin like GTPase 1	Homo sapiens	5-8
21685230-10	2011	NAb titre and MxA level correlated strongly: MxA pre- (Spearman r = -0.72, p &lt; 0.0001), MxA post- (Spearman r = -0.79, p &lt; 0.0001) and MxA induction (Spearman r = -0.67, p = 0.0004).	nab	0-3	MX dynamin like GTPase 1	Homo sapiens	45-48
21685230-10	2011	NAb titre and MxA level correlated strongly: MxA pre- (Spearman r = -0.72, p &lt; 0.0001), MxA post- (Spearman r = -0.79, p &lt; 0.0001) and MxA induction (Spearman r = -0.67, p = 0.0004).	nab	0-3	MX dynamin like GTPase 1	Homo sapiens	45-48
21685230-10	2011	NAb titre and MxA level correlated strongly: MxA pre- (Spearman r = -0.72, p &lt; 0.0001), MxA post- (Spearman r = -0.79, p &lt; 0.0001) and MxA induction (Spearman r = -0.67, p = 0.0004).	nab	0-3	MX dynamin like GTPase 1	Homo sapiens	45-48
21862562-0	2011	MAB-10/NAB acts with LIN-29/EGR to regulate terminal differentiation and the transition from larva to adult in C. elegans.	nab	7-10	NAB transcription cofactor mab-10	Caenorhabditis elegans	0-6
21836637-5	2011	Here, we show that Krox20 functions as a SUMO ligase for its coregulators--the Nab proteins--and that Nab sumoylation negatively modulates Krox20 transcriptional activity in vivo.	nab	79-82	early growth response 2	Homo sapiens	19-25
21862562-0	2011	MAB-10/NAB acts with LIN-29/EGR to regulate terminal differentiation and the transition from larva to adult in C. elegans.	nab	7-10	Zinc finger transcription factor lin-29	Caenorhabditis elegans	21-27
21862562-3	2011	Here, we identify a new heterochronic gene, mab-10, and show that mab-10 encodes a NAB (NGFI-A-binding protein) transcriptional co-factor.	nab	83-86	NAB transcription cofactor mab-10	Caenorhabditis elegans	66-72
21862562-4	2011	MAB-10 acts with LIN-29 to control the expression of genes required to regulate a subset of differentiation events during the larval-to-adult transition, and we show that the NAB-interaction domain of LIN-29 is conserved in Kruppel-family EGR (early growth response) proteins.	nab	175-178	NAB transcription cofactor mab-10	Caenorhabditis elegans	0-6
21862562-4	2011	MAB-10 acts with LIN-29 to control the expression of genes required to regulate a subset of differentiation events during the larval-to-adult transition, and we show that the NAB-interaction domain of LIN-29 is conserved in Kruppel-family EGR (early growth response) proteins.	nab	175-178	Zinc finger transcription factor lin-29	Caenorhabditis elegans	201-207
21847061-8	2011	The sensitivity increased significantly for NAB combined with a tumor marker compared with NAB alone (100% for CYFRA 21-1, 92.9% for CEA, and 94.2% for SCC; p = 0.001, p = 0.025, and p = 0.014, respectively).	nab	44-47	CEA cell adhesion molecule 3	Homo sapiens	133-136
21221878-4	2011	Furthermore, sodium butyrate (NaB), an inducer of cellular differentiation, increased the expression of beta-casein, a milk-related differentiation marker, together with up-regulation of NDRG1 in breast cancer cells.	nab	30-33	casein beta	Homo sapiens	104-115
21221878-4	2011	Furthermore, sodium butyrate (NaB), an inducer of cellular differentiation, increased the expression of beta-casein, a milk-related differentiation marker, together with up-regulation of NDRG1 in breast cancer cells.	nab	30-33	N-myc downstream regulated 1	Homo sapiens	187-192
21847061-8	2011	The sensitivity increased significantly for NAB combined with a tumor marker compared with NAB alone (100% for CYFRA 21-1, 92.9% for CEA, and 94.2% for SCC; p = 0.001, p = 0.025, and p = 0.014, respectively).	nab	44-47	serpin family B member 3	Homo sapiens	152-155
21847061-10	2011	CONCLUSION: Evaluation of tumor markers CYFRA 21-1, CEA, and SCC in the cytological fluid can improve the diagnostic performance of CT-guided NAB for NSCLC.	nab	142-145	CEA cell adhesion molecule 3	Homo sapiens	52-55
21847061-10	2011	CONCLUSION: Evaluation of tumor markers CYFRA 21-1, CEA, and SCC in the cytological fluid can improve the diagnostic performance of CT-guided NAB for NSCLC.	nab	142-145	serpin family B member 3	Homo sapiens	61-64
21619905-4	2011	As expected, Ad5 NAb titers were both frequent and high magnitude in sub-Saharan Africa and Southeast Asia.	nab	17-20	Alzheimer disease, familial, type 5	Homo sapiens	13-16
21671178-6	2011	The average number of gamma-H2AX foci per cell receiving the combined treatment was significantly increased at different time points, and the expression levels of Ku70 mRNA and protein were suppressed by NaB in a dose-dependent manner.	nab	204-207	X-ray repair cross complementing 6	Homo sapiens	163-167
21671178-7	2011	It was concluded that enhanced radiosensitivity induced by NaB involves an inhibited expression of Ku70 and an increase in gamma-H2AX foci, which suggests decreased ability in DSB repair.	nab	59-62	X-ray repair cross complementing 6	Homo sapiens	99-103
21912547-2	2011	The generation of flat revertants of v-K-ras-transformed renal cells by exposure to the histone deacetylase inhibitor sodium butyrate (NaB) was previously found to be dependent on transcriptional activation of the PAI-1 (SERPINE1) gene (encoding the type-1 inhibitor of urokinase and tissue-type plasminogen activators).	nab	135-138	serpin family E member 1	Homo sapiens	214-219
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	MAX dimerization protein 1	Homo sapiens	80-84
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	selenoprotein P	Homo sapiens	86-91
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	93-98
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	early growth response 1	Homo sapiens	111-115
21411522-13	2011	Changes in cellular gene expression in response to VPA, NaB, or TSA were globally similar as assessed by human genome arrays; however, VPA selectively stimulated the expression of some cellular genes, such as MEF2D, YY1, and ZEB1, that could repress the EBV lytic cycle.	nab	56-59	myocyte enhancer factor 2D	Homo sapiens	209-214
21411522-13	2011	Changes in cellular gene expression in response to VPA, NaB, or TSA were globally similar as assessed by human genome arrays; however, VPA selectively stimulated the expression of some cellular genes, such as MEF2D, YY1, and ZEB1, that could repress the EBV lytic cycle.	nab	56-59	YY1 transcription factor	Homo sapiens	216-219
21411522-13	2011	Changes in cellular gene expression in response to VPA, NaB, or TSA were globally similar as assessed by human genome arrays; however, VPA selectively stimulated the expression of some cellular genes, such as MEF2D, YY1, and ZEB1, that could repress the EBV lytic cycle.	nab	56-59	zinc finger E-box binding homeobox 1	Homo sapiens	225-229
21411530-3	2011	One major reason for such a meager NAb response is the phenomenon of glycan shielding involving GP5, a major glycoprotein carrying one major neutralizing epitope.	nab	35-38	glycoprotein V platelet	Homo sapiens	96-99
21430056-7	2011	This study is the first to explore the use of a collection of HIV-1 env quasispecies variants as immunogens and to present evidence that it is possible to educate the B-cell response by sequential exposure to native HIV-1 quasispecies env variants derived from an individual with a broadened NAb response.	nab	292-295	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	235-238
21385866-0	2011	The NAB-Brk signal bifurcates at JNK to independently induce apoptosis and compensatory proliferation.	nab	4-7	brinker	Drosophila melanogaster	8-11
21385866-0	2011	The NAB-Brk signal bifurcates at JNK to independently induce apoptosis and compensatory proliferation.	nab	4-7	basket	Drosophila melanogaster	33-36
21385866-6	2011	We have previously shown that elimination of misspecified cells due to reduced Dpp signaling is achieved by the interaction of the co-repressor NAB with the transcriptional repressor Brk, which in turn induces Jun N-terminal kinase-dependent apoptosis.	nab	144-147	brinker	Drosophila melanogaster	183-186
21385866-8	2011	Our findings indicate that the NAB primary signal activates JNK, which in turn transmits two independent signals.	nab	31-34	basket	Drosophila melanogaster	60-63
21488133-4	2011	Using radiolabeled NaB((3) H)H(4) and Raney nickel as well as sulfhydryl assay (Ellman"s reagent), we confirmed that CDA could conjugate with cysteine through a thioether linkage.	nab	19-22	cytidine deaminase	Homo sapiens	117-120
21240457-11	2011	Gene silencing of the microtubule regulatory gene STMN1 by RNAi suggested a distinct synergistic effect in the combined treatment with nab-paclitaxel.	nab	135-138	stathmin 1	Homo sapiens	50-55
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	signal transducer and activator of transcription 3	Homo sapiens	66-71
21411522-11	2011	The levels and kinetics of specific cellular transcripts, such as Stat3, Frmd6, Mad1, Sepp1, c-fos, c-jun, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.	nab	141-144	FERM domain containing 6	Homo sapiens	73-78
21625361-5	2011	Thus, the PDE-D performs better than the M06-2x for the observed NAB@C(60) pi-stacked complexes.	nab	65-68	phosphodiesterase 6D	Homo sapiens	10-15
20851496-7	2011	We observed that monocytes stimulated to differentiate in the presence of NaB displayed colony formation and dendritic cell morphology, lost CD14 and showed decreased secretion of IL-1beta.	nab	74-77	CD14 molecule	Homo sapiens	141-145
20851496-7	2011	We observed that monocytes stimulated to differentiate in the presence of NaB displayed colony formation and dendritic cell morphology, lost CD14 and showed decreased secretion of IL-1beta.	nab	74-77	interleukin 1 beta	Homo sapiens	180-188
20851496-9	2011	Being a natural short chain fatty acid, NaB may regulate CD1a acquisition independently of its HDAC inhibitory activity.	nab	40-43	CD1a molecule	Homo sapiens	57-61
20851496-11	2011	On the other hand, CD1a can also be induced by toll like receptors 2 (TLR 2) agonists, such as Pam3Cys, and NaB inhibited this effect.	nab	108-111	CD1a molecule	Homo sapiens	19-23
20851496-11	2011	On the other hand, CD1a can also be induced by toll like receptors 2 (TLR 2) agonists, such as Pam3Cys, and NaB inhibited this effect.	nab	108-111	toll like receptor 2	Homo sapiens	47-68
20851496-11	2011	On the other hand, CD1a can also be induced by toll like receptors 2 (TLR 2) agonists, such as Pam3Cys, and NaB inhibited this effect.	nab	108-111	toll like receptor 2	Homo sapiens	70-75
20851496-12	2011	Our data suggest that the histone deacetylase inhibitor NaB instead of impairing DC differentiation inhibits the acquisition of CD1a induced both by cytokines and by TLR 2 agonist stimulus.	nab	56-59	CD1a molecule	Homo sapiens	128-132
20851496-12	2011	Our data suggest that the histone deacetylase inhibitor NaB instead of impairing DC differentiation inhibits the acquisition of CD1a induced both by cytokines and by TLR 2 agonist stimulus.	nab	56-59	toll like receptor 2	Homo sapiens	166-171
20851496-13	2011	Furthermore, this occurs at the transcriptional level as NaB led to a decrease in mRNA levels of CD1a and upregulation of CD1d.	nab	57-60	CD1a molecule	Homo sapiens	97-101
20851496-13	2011	Furthermore, this occurs at the transcriptional level as NaB led to a decrease in mRNA levels of CD1a and upregulation of CD1d.	nab	57-60	CD1d molecule	Homo sapiens	122-126
21152868-3	2011	In the present study, we investigated the effects of the histone deacetylase inhibitors (HDACis), trichostatin A (TSA) and sodium butyrate (NaB), on PHB expression in the thyroid tumor cell lines, TPC-1 and FRO.	nab	140-143	prohibitin 1	Homo sapiens	149-152
21152868-4	2011	Both TSA and NaB increased PHB mRNA levels.	nab	13-16	prohibitin 1	Homo sapiens	27-30
21912547-2	2011	The generation of flat revertants of v-K-ras-transformed renal cells by exposure to the histone deacetylase inhibitor sodium butyrate (NaB) was previously found to be dependent on transcriptional activation of the PAI-1 (SERPINE1) gene (encoding the type-1 inhibitor of urokinase and tissue-type plasminogen activators).	nab	135-138	serpin family E member 1	Homo sapiens	221-229
21912547-3	2011	NaB-initiated PAI-1 expression preceded induced cell spreading and entry into G(1) arrest.	nab	0-3	serpin family E member 1	Homo sapiens	14-19
21912547-7	2011	These data suggest that high-level PAI-1 expression suppresses growth of chronic ras-oncogene transformed cells and is likely a major cytostatic effector of NaB exposure.	nab	157-160	serpin family E member 1	Homo sapiens	35-40
21673991-2	2011	Oral treatment of Shigella infected rabbits with sodium butyrate (NaB) reduces clinical severity and counteracts the downregulation of cathelicidin (CAP-18) in the large intestinal epithelia.	nab	66-69	antimicrobial protein CAP18	Oryctolagus cuniculus	149-155
21789245-7	2011	NaB inhibited the expression of glucose transporter type 1 (GLUT 1), but substantially increased mitochondria bound hexokinase (HK) activity.	nab	0-3	solute carrier family 2 member 1	Homo sapiens	32-58
21789245-7	2011	NaB inhibited the expression of glucose transporter type 1 (GLUT 1), but substantially increased mitochondria bound hexokinase (HK) activity.	nab	0-3	solute carrier family 2 member 1	Homo sapiens	60-66
21789245-7	2011	NaB inhibited the expression of glucose transporter type 1 (GLUT 1), but substantially increased mitochondria bound hexokinase (HK) activity.	nab	0-3	hexokinase 1	Homo sapiens	116-126
21789245-7	2011	NaB inhibited the expression of glucose transporter type 1 (GLUT 1), but substantially increased mitochondria bound hexokinase (HK) activity.	nab	0-3	hexokinase 1	Homo sapiens	128-130
21789245-8	2011	NaB induced increase in HK activity was associated to isoform HK I and was accompanied by 1.5 fold increase in HK I mRNA expression and cognate protein biosynthesis.	nab	0-3	hexokinase 1	Homo sapiens	24-26
21789245-8	2011	NaB induced increase in HK activity was associated to isoform HK I and was accompanied by 1.5 fold increase in HK I mRNA expression and cognate protein biosynthesis.	nab	0-3	hexokinase 1	Homo sapiens	62-66
21789245-8	2011	NaB induced increase in HK activity was associated to isoform HK I and was accompanied by 1.5 fold increase in HK I mRNA expression and cognate protein biosynthesis.	nab	0-3	hexokinase 1	Homo sapiens	111-115
21789245-13	2011	The high O(2) consumption in NaB-treated cells was shown to be unrelated to mitochondrial biogenesis since citrate synthase (CS) activity and the amount of mitochondrial DNA remained unchanged.	nab	29-32	citrate synthase	Homo sapiens	107-123
21789245-13	2011	The high O(2) consumption in NaB-treated cells was shown to be unrelated to mitochondrial biogenesis since citrate synthase (CS) activity and the amount of mitochondrial DNA remained unchanged.	nab	29-32	citrate synthase	Homo sapiens	125-127
21673991-4	2011	Since acute respiratory infections often cause secondary complications during shigellosis, the systemic effect of PB and NaB on CAP-18 expression in respiratory epithelia was also evaluated.	nab	121-124	antimicrobial protein CAP18	Oryctolagus cuniculus	128-134
21673991-10	2011	Both PB and NaB counteracted the downregulation of CAP-18 in lung epithelium.	nab	12-15	antimicrobial protein CAP18	Oryctolagus cuniculus	51-57
21673991-11	2011	The drug effect is suggested to be systemic as intravenous administration of NaB could also upregulate CAP-18 in the epithelia of lung, rectum and colon.	nab	77-80	antimicrobial protein CAP18	Oryctolagus cuniculus	103-109
21673991-13	2011	Enhancement of CAP-18 in the mucosal epithelia of the respiratory tract by PB or NaB is a novel discovery.	nab	81-84	antimicrobial protein CAP18	Oryctolagus cuniculus	15-21
20718712-2	2010	In this study, we aimed to determine whether NaB induced differentiation and regulated the expression of the mucosal factor MUC2 through the PTEN/PI3K (phosphoinositide 3-kinase) pathway.	nab	45-48	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	124-128
20718712-2	2010	In this study, we aimed to determine whether NaB induced differentiation and regulated the expression of the mucosal factor MUC2 through the PTEN/PI3K (phosphoinositide 3-kinase) pathway.	nab	45-48	phosphatase and tensin homolog	Homo sapiens	141-145
20718712-4	2010	NaB treatment markedly increased the expression of PTEN and MUC2, but it decreased the expression of PI3K.	nab	0-3	phosphatase and tensin homolog	Homo sapiens	51-55
20718712-4	2010	NaB treatment markedly increased the expression of PTEN and MUC2, but it decreased the expression of PI3K.	nab	0-3	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	60-64
20718712-6	2010	Hence, we conclude that NaB increased PTEN expression, promoted the expression of MUC2 and induced the differentiation of gastric cancer cells through the PTEN/PI3K signalling pathway.	nab	24-27	phosphatase and tensin homolog	Homo sapiens	38-42
20718712-6	2010	Hence, we conclude that NaB increased PTEN expression, promoted the expression of MUC2 and induced the differentiation of gastric cancer cells through the PTEN/PI3K signalling pathway.	nab	24-27	mucin 2, oligomeric mucus/gel-forming	Homo sapiens	82-86
20718712-6	2010	Hence, we conclude that NaB increased PTEN expression, promoted the expression of MUC2 and induced the differentiation of gastric cancer cells through the PTEN/PI3K signalling pathway.	nab	24-27	phosphatase and tensin homolog	Homo sapiens	155-159
20691806-3	2010	Sodium butyrate (NaB) has received much attention as a potential chemopreventive agent for cancer treatment due to its protective action against intracellular events including IFN-gamma-mediated signaling transduction.	nab	17-20	interferon gamma	Homo sapiens	176-185
20213511-2	2010	We investigated the effect of sodium butyrate (NaB) on pro-angiogenic and anti-angiogenic VEGF variants production in immortalized human lung microvascular endothelial cells (HLMEC).	nab	47-50	vascular endothelial growth factor A	Homo sapiens	90-94
20213511-5	2010	We found that NaB significantly increased the anti-angiogenic transcript and protein levels of the VEGF 121b, VEGF165b and VEGF189b variants in HLMEC cells.	nab	14-17	vascular endothelial growth factor A	Homo sapiens	99-103
20691806-4	2010	Therefore, the question remains whether IDO is a target of the anti-tumor action of NaB.	nab	84-87	indoleamine 2,3-dioxygenase 1	Homo sapiens	40-43
20691806-5	2010	In this study, we demonstrate for the first time that NaB down-regulated IDO via both transcriptional and post-transcriptional mechanisms.	nab	54-57	indoleamine 2,3-dioxygenase 1	Homo sapiens	73-76
20691806-6	2010	NaB repressed the activity of STAT1 to inhibit STAT1-driven transcriptional activity of IDO.	nab	0-3	signal transducer and activator of transcription 1	Homo sapiens	30-35
20691806-6	2010	NaB repressed the activity of STAT1 to inhibit STAT1-driven transcriptional activity of IDO.	nab	0-3	signal transducer and activator of transcription 1	Homo sapiens	47-52
20691806-6	2010	NaB repressed the activity of STAT1 to inhibit STAT1-driven transcriptional activity of IDO.	nab	0-3	indoleamine 2,3-dioxygenase 1	Homo sapiens	88-91
20691806-8	2010	Moreover, immunoprecipitation and immunoblotting assays showed that treatment of cells with NaB caused dramatic ubiquitination of total intracellular proteins, including IDO.	nab	92-95	indoleamine 2,3-dioxygenase 1	Homo sapiens	170-173
20691806-10	2010	These results suggest that NaB-induced STAT1 activity inhibition and ubiquitin/proteasome-dependent proteolysis are involved in the down-regulation of IDO.	nab	27-30	signal transducer and activator of transcription 1	Homo sapiens	39-44
20691806-10	2010	These results suggest that NaB-induced STAT1 activity inhibition and ubiquitin/proteasome-dependent proteolysis are involved in the down-regulation of IDO.	nab	27-30	indoleamine 2,3-dioxygenase 1	Homo sapiens	151-154
21176600-9	2010	The expression of p27(Kip1) was markedly up-regulated after being treated with NaB.	nab	79-82	zinc ribbon domain containing 2	Homo sapiens	18-21
20802016-8	2010	CONCLUSIONS: HVGGSSV-nab-paclitaxel was found to bind specifically to the tax-interacting protein-1 (TIP-1) receptor expressed in irradiated tumors, enhance bioavailability of paclitaxel, and significantly increase tumor growth delay as compared with controls in mouse models of lung cancer.	nab	21-24	Tax1 (human T cell leukemia virus type I) binding protein 3	Mus musculus	74-99
20802016-8	2010	CONCLUSIONS: HVGGSSV-nab-paclitaxel was found to bind specifically to the tax-interacting protein-1 (TIP-1) receptor expressed in irradiated tumors, enhance bioavailability of paclitaxel, and significantly increase tumor growth delay as compared with controls in mouse models of lung cancer.	nab	21-24	Tax1 (human T cell leukemia virus type I) binding protein 3	Mus musculus	101-106
20802016-9	2010	Here we show that targeting nab-paclitaxel to radiation-inducible TIP-1 results in increased tumor-specific drug delivery and enhanced biological efficacy in the treatment of cancer.	nab	28-31	Tax1 (human T cell leukemia virus type I) binding protein 3	Mus musculus	66-71
20935470-4	2010	While short treatment with the HDACI sodium butyrate (NaB) induced a reversible G(1) cell cycle arrest in both parental and p21(Waf1-/-) cells, long-term treatment led to dramatic changes in p21(Waf1+/+) cells only: cell cycle arrest became irreversible and cells become hypertrophic, SA-betaGal-positive and accumulated gammaH2AX foci associated with mTORC1 activation.	nab	54-57	cyclin dependent kinase inhibitor 1A	Homo sapiens	124-127
20935470-4	2010	While short treatment with the HDACI sodium butyrate (NaB) induced a reversible G(1) cell cycle arrest in both parental and p21(Waf1-/-) cells, long-term treatment led to dramatic changes in p21(Waf1+/+) cells only: cell cycle arrest became irreversible and cells become hypertrophic, SA-betaGal-positive and accumulated gammaH2AX foci associated with mTORC1 activation.	nab	54-57	cyclin dependent kinase inhibitor 1A	Homo sapiens	128-132
20935470-4	2010	While short treatment with the HDACI sodium butyrate (NaB) induced a reversible G(1) cell cycle arrest in both parental and p21(Waf1-/-) cells, long-term treatment led to dramatic changes in p21(Waf1+/+) cells only: cell cycle arrest became irreversible and cells become hypertrophic, SA-betaGal-positive and accumulated gammaH2AX foci associated with mTORC1 activation.	nab	54-57	cyclin dependent kinase inhibitor 1A	Homo sapiens	195-199
20935470-4	2010	While short treatment with the HDACI sodium butyrate (NaB) induced a reversible G(1) cell cycle arrest in both parental and p21(Waf1-/-) cells, long-term treatment led to dramatic changes in p21(Waf1+/+) cells only: cell cycle arrest became irreversible and cells become hypertrophic, SA-betaGal-positive and accumulated gammaH2AX foci associated with mTORC1 activation.	nab	54-57	H2A.X variant histone	Mus musculus	321-330
20935470-4	2010	While short treatment with the HDACI sodium butyrate (NaB) induced a reversible G(1) cell cycle arrest in both parental and p21(Waf1-/-) cells, long-term treatment led to dramatic changes in p21(Waf1+/+) cells only: cell cycle arrest became irreversible and cells become hypertrophic, SA-betaGal-positive and accumulated gammaH2AX foci associated with mTORC1 activation.	nab	54-57	CREB regulated transcription coactivator 1	Mus musculus	352-358
20935470-7	2010	In contrast, the knockout of the p21(Waf1) abolished most of the features of NaB-induced senescence, including irreversibility of cell cycle arrest, hypertrophy, additional focal adhesions and block of migration, gammaH2AX foci accumulation and SA-betaGal staining.	nab	77-80	cyclin dependent kinase inhibitor 1A	Homo sapiens	33-36
20935470-7	2010	In contrast, the knockout of the p21(Waf1) abolished most of the features of NaB-induced senescence, including irreversibility of cell cycle arrest, hypertrophy, additional focal adhesions and block of migration, gammaH2AX foci accumulation and SA-betaGal staining.	nab	77-80	cyclin dependent kinase inhibitor 1A	Homo sapiens	37-41
20524007-6	2010	Patients who developed NAbs had lower apoE levels before treatment, 67 (47-74) mg/L median (interquartile range), and at the moment of NAb analysis, 53 (50-84) mg/L, in comparison to those who remained NAb-negative, 83 (68-107) mg/L, P = 0.03, and 76 (66-87) mg/L, P = 0.04, respectively.	nab	23-26	apolipoprotein E	Homo sapiens	38-42
20524007-7	2010	When adjusting for age and smoking for a one-standard deviation decrease in apoE levels, a 5.6-fold increase in the odds of becoming NAb-positive was detected: odds ratios (OR) 0.18 (95% CI 0.04-0.77), P = 0.04.	nab	133-136	apolipoprotein E	Homo sapiens	76-80
20524007-8	2010	When adjusting for apoE, smoking habit became associated with NAb induction: OR 5.6 (95% CI 1.3-87), P = 0.03.	nab	62-65	apolipoprotein E	Homo sapiens	19-23
20524007-9	2010	These results suggest that apoE-containing lipoprotein metabolism and, possibly, tobacco smoking may be associated with risk of NAb production in female MS patients treated with IFN-beta.	nab	128-131	apolipoprotein E	Homo sapiens	27-31
20524007-9	2010	These results suggest that apoE-containing lipoprotein metabolism and, possibly, tobacco smoking may be associated with risk of NAb production in female MS patients treated with IFN-beta.	nab	128-131	interferon beta 1	Homo sapiens	178-186
21176600-9	2010	The expression of p27(Kip1) was markedly up-regulated after being treated with NaB.	nab	79-82	cyclin dependent kinase inhibitor 1B	Homo sapiens	22-26
21176600-10	2010	CONCLUSIONS: NaB treatment can inhibit the growth of oral squamous carcinoma cell line in vitro and induce cell cycle arrest, which might be associated with the increased expression of p27(Kip1) protein.	nab	13-16	zinc ribbon domain containing 2	Homo sapiens	185-188
21176600-10	2010	CONCLUSIONS: NaB treatment can inhibit the growth of oral squamous carcinoma cell line in vitro and induce cell cycle arrest, which might be associated with the increased expression of p27(Kip1) protein.	nab	13-16	cyclin dependent kinase inhibitor 1B	Homo sapiens	189-193
20860805-9	2010	Interestingly, we found that the sensitivity of Envs to contemporaneous autologous NAbs correlated positively with increased sensitivity to soluble CD4 and inversely with anti-CD4 antibody and Envs with increased NAb sensitivity were able to efficiently infect HeLa cells expressing low CD4.	nab	83-86	CD4 molecule	Homo sapiens	148-151
20860805-9	2010	Interestingly, we found that the sensitivity of Envs to contemporaneous autologous NAbs correlated positively with increased sensitivity to soluble CD4 and inversely with anti-CD4 antibody and Envs with increased NAb sensitivity were able to efficiently infect HeLa cells expressing low CD4.	nab	83-86	CD4 molecule	Homo sapiens	176-179
20860805-9	2010	Interestingly, we found that the sensitivity of Envs to contemporaneous autologous NAbs correlated positively with increased sensitivity to soluble CD4 and inversely with anti-CD4 antibody and Envs with increased NAb sensitivity were able to efficiently infect HeLa cells expressing low CD4.	nab	83-86	CD4 molecule	Homo sapiens	176-179
19900401-2	2010	Here we show that e2f1 expression is regulated through the Wnt/Tcf-pathway: e2f1 promoter activity is inhibited by sodium butyrate (NaB) and by overexpression of beta-catenin/Tcf.	nab	132-135	E2F transcription factor 1	Mus musculus	18-22
24683262-4	2010	OBJECTIVE: The aim of this study was to examine the ability of the histone deacetylase inhibitor, sodium butyrate (NaB), to modulate the expression of p53.	nab	115-118	tumor protein p53	Homo sapiens	151-154
24683262-10	2010	RESULTS: In the SW-1990 and JHP-1 cell lines, use of 1 mM NaB was found to induce histone acetylation and p53 expression compared with those not treated with NaB (P = 0.01 and P = 0.018, respectively).	nab	58-61	tumor protein p53	Homo sapiens	106-109
24683262-14	2010	CONCLUSION: This in vitro study found that NaB induced p53 expression in 2 pancreatic cancer cell lines (SW-1990 and JHP-1).	nab	43-46	tumor protein p53	Homo sapiens	55-58
20445436-11	2010	A randomized controlled trial for patients with active disease despite IFNB therapy showed that baseline NAb titers were reduced by subsequent intravenous methylprednisolone treatment, but the incidence of NAbs was too small to assess clinical relevance.	nab	105-108	interferon beta 1	Homo sapiens	71-75
19863349-1	2010	Histone deacetylase inhibitors (HDACI), e.g., sodium butyrate (NaB), have been suggested to upregulate the coxsackie and adenovirus receptor (CAR).	nab	63-66	CXADR Ig-like cell adhesion molecule	Homo sapiens	107-140
19863349-1	2010	Histone deacetylase inhibitors (HDACI), e.g., sodium butyrate (NaB), have been suggested to upregulate the coxsackie and adenovirus receptor (CAR).	nab	63-66	CXADR Ig-like cell adhesion molecule	Homo sapiens	142-145
19863349-3	2010	NaB treatment of colon cancer cells increased CAR expression preferentially in cell lines with low basic CAR levels.	nab	0-3	CXADR Ig-like cell adhesion molecule	Homo sapiens	46-49
19863349-3	2010	NaB treatment of colon cancer cells increased CAR expression preferentially in cell lines with low basic CAR levels.	nab	0-3	CXADR Ig-like cell adhesion molecule	Homo sapiens	105-108
20585851-0	2010	Final results of a phase II study of nab-paclitaxel, bevacizumab, and gemcitabine as first-line therapy for patients with HER2-negative metastatic breast cancer.	nab	37-40	erb-b2 receptor tyrosine kinase 2	Homo sapiens	122-126
20477957-4	2010	Increased abundance in Nep mRNA was observed in Nab.	nab	48-51	membrane metalloendopeptidase	Homo sapiens	23-26
20477957-7	2010	CONCLUSIONS: nep gene expression is up-regulated during the transition to the stationary phase in response to "factors" (metabolite and/or regulatory molecule) occurring in high-density cultures of Nab.	nab	198-201	membrane metalloendopeptidase	Homo sapiens	13-16
20378772-4	2010	Systemic injection with iRGD improved the therapeutic index of drugs of various compositions, including a small molecule (doxorubicin), nanoparticles (nab-paclitaxel and doxorubicin liposomes), and a monoclonal antibody (trastuzumab).	nab	151-154	interferon gamma inducible protein 47	Mus musculus	24-28
19900401-2	2010	Here we show that e2f1 expression is regulated through the Wnt/Tcf-pathway: e2f1 promoter activity is inhibited by sodium butyrate (NaB) and by overexpression of beta-catenin/Tcf.	nab	132-135	E2F transcription factor 1	Mus musculus	76-80
19900401-2	2010	Here we show that e2f1 expression is regulated through the Wnt/Tcf-pathway: e2f1 promoter activity is inhibited by sodium butyrate (NaB) and by overexpression of beta-catenin/Tcf.	nab	132-135	catenin (cadherin associated protein), beta 1	Mus musculus	162-174
19900401-4	2010	Being inserted into luciferase reporter vector, the identified element provides positive transcriptional regulation in response to beta-catenin/Tcf co-transfection and NaB treatment.	nab	168-171	catenin (cadherin associated protein), beta 1	Mus musculus	131-143
20568894-0	2010	Binding of AR to SMRT/N-CoR complex and its co-operation with PSA promoter in prostate cancer cells treated with natural histone deacetylase inhibitor NaB.	nab	151-154	androgen receptor	Homo sapiens	11-13
21178266-6	2010	We amplified immunoprecipitated DNA by conventional PCR and in the following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	185-188	androgen receptor	Homo sapiens	210-212
21178266-6	2010	We amplified immunoprecipitated DNA by conventional PCR and in the following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	185-188	nuclear receptor corepressor 2	Homo sapiens	213-217
21178266-6	2010	We amplified immunoprecipitated DNA by conventional PCR and in the following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	185-188	nuclear receptor corepressor 1	Homo sapiens	218-223
21178266-7	2010	The co-immunoprecipitation assay revealed increase in AR-SMRT formation in NaB treated cells.	nab	75-78	androgen receptor	Homo sapiens	54-56
21178266-7	2010	The co-immunoprecipitation assay revealed increase in AR-SMRT formation in NaB treated cells.	nab	75-78	nuclear receptor corepressor 2	Homo sapiens	57-61
21178266-9	2010	Furthermore, we estimated the reduced presence of HDAC2 and HDAC3 proteins by NaB and TSA treatment in AR-negative DU145 cell line.	nab	78-81	histone deacetylase 2	Homo sapiens	50-55
21178266-9	2010	Furthermore, we estimated the reduced presence of HDAC2 and HDAC3 proteins by NaB and TSA treatment in AR-negative DU145 cell line.	nab	78-81	histone deacetylase 3	Homo sapiens	60-65
21178266-10	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	androgen receptor	Homo sapiens	47-49
21178266-10	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	androgen receptor	Homo sapiens	118-120
21178266-10	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	nuclear receptor corepressor 2	Homo sapiens	190-194
21178266-11	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor protein.	nab	86-89	nuclear receptor corepressor 2	Homo sapiens	23-27
21178266-11	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor protein.	nab	86-89	nuclear receptor corepressor 1	Homo sapiens	28-33
21178266-11	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor protein.	nab	86-89	nuclear receptor corepressor 2	Homo sapiens	161-165
20568894-8	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	nuclear receptor corepressor 2	Homo sapiens	190-194
20568894-9	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor prote.	nab	86-89	nuclear receptor corepressor 2	Homo sapiens	23-27
20568894-9	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor prote.	nab	86-89	nuclear receptor corepressor 1	Homo sapiens	28-33
20568894-9	2010	We suggest that AR and SMRT/N-CoR corepressors may form a stable complex in vitro and NaB may facilitate the interaction between AR nuclear steroid receptor and SMRT corepressor prote.	nab	86-89	nuclear receptor corepressor 2	Homo sapiens	161-165
20568894-0	2010	Binding of AR to SMRT/N-CoR complex and its co-operation with PSA promoter in prostate cancer cells treated with natural histone deacetylase inhibitor NaB.	nab	151-154	nuclear receptor corepressor 2	Homo sapiens	17-21
20568894-0	2010	Binding of AR to SMRT/N-CoR complex and its co-operation with PSA promoter in prostate cancer cells treated with natural histone deacetylase inhibitor NaB.	nab	151-154	nuclear receptor corepressor 1	Homo sapiens	22-27
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	nuclear receptor corepressor 2	Homo sapiens	60-64
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	nuclear receptor corepressor 2	Homo sapiens	66-128
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	nuclear receptor corepressor 1	Homo sapiens	166-194
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	nuclear receptor corepressor 1	Homo sapiens	196-201
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	histone deacetylase 3	Homo sapiens	212-233
20568894-4	2010	We aimed to study the inhibitory effects of the corepressor SMRT (Silencing Mediator for Retinoid and Thyroid -hormone receptors) which forms a complex together with nuclear receptor corepressor (N-CoR) and with histone deacetylase 3 (HDAC3) on AR activity.The androgen-sensitive prostate cancer cell line LNCaP and androgen-insensitive prostate cancer cell line C4-2 both AR-positive, and androgen-insensitive DU145 and PC3 prostate cancer cell lines were treated with two HDACIs, sodium butyrate (NaB) and/or trichostatin A (TSA).	nab	499-502	histone deacetylase 3	Homo sapiens	235-240
20568894-5	2010	We amplified immunoprecipitated DNA by conventional PCR and in the -following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	186-189	androgen receptor	Homo sapiens	211-213
20568894-5	2010	We amplified immunoprecipitated DNA by conventional PCR and in the -following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	186-189	nuclear receptor corepressor 2	Homo sapiens	214-218
20568894-5	2010	We amplified immunoprecipitated DNA by conventional PCR and in the -following step we used the chromatin immunoprecipitation (ChIP) analysis coupled with quantitative PCR for monitoring NaB induced formation of AR-SMRT/N-CoR complex binding on the PSA promoter.	nab	186-189	nuclear receptor corepressor 1	Homo sapiens	219-224
20568894-6	2010	The co-immunoprecipitation assay revealed increase in AR-SMRT formation in NaB treated cells.	nab	75-78	androgen receptor	Homo sapiens	54-56
20568894-6	2010	The co-immunoprecipitation assay revealed increase in AR-SMRT formation in NaB treated cells.	nab	75-78	nuclear receptor corepressor 2	Homo sapiens	57-61
20568894-8	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	androgen receptor	Homo sapiens	47-49
20568894-8	2010	In conclusion, the inhibitory effect of NaB on AR gene expression seems to be specific and unique for prostate cancer AR-positive cell lines and corresponds with its ability to stimulate AR-SMRT complex formation.	nab	40-43	androgen receptor	Homo sapiens	118-120
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	74-77	MX dynamin like GTPase 1	Homo sapiens	13-16
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	74-77	C-C motif chemokine ligand 2	Homo sapiens	18-22
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	74-77	C-X-C motif chemokine ligand 10	Homo sapiens	24-30
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	74-77	interferon alpha inducible protein 27	Homo sapiens	35-40
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	129-132	MX dynamin like GTPase 1	Homo sapiens	13-16
19558503-13	2009	Induction of MxA, CCL2, CXCL10 and IFI27 was reduced in patients with low NAb levels and lost in patients with intermediate/high NAb levels.	nab	129-132	C-X-C motif chemokine ligand 10	Homo sapiens	24-30
19884577-5	2009	RESULTS: Treatment with IM IFNbeta-1a was associated with a lower rate of NAb formation among 718 patients screened (p &lt; 0.0001 vs SC IFNbeta-1a 22 microg, 44 microg, and IFNbeta-1b).	nab	74-77	interferon beta 1	Homo sapiens	27-34
19828617-1	2009	The nuclear magnetic resonance (NMR) structure of a globular domain of residues 1071 to 1178 within the previously annotated nucleic acid-binding region (NAB) of severe acute respiratory syndrome coronavirus nonstructural protein 3 (nsp3) has been determined, and N- and C-terminally adjoining polypeptide segments of 37 and 25 residues, respectively, have been shown to form flexibly extended linkers to the preceding globular domain and to the following, as yet uncharacterized domain.	nab	154-157	SH2 domain containing 3C	Homo sapiens	233-237
20004833-0	2009	Dag nab it!	nab	4-7	dystroglycan 1	Homo sapiens	0-3
19884577-6	2009	At baseline, patients who were binding antibody positive (BAb+)/neutralizing antibody positive (NAb+) had lower MxA, viperin, and IFIT-1 response compared with BAb-negative (BAb-)/NAb-negative (NAb-) patients (all p &lt; 0.0001).	nab	96-99	MX dynamin like GTPase 1	Homo sapiens	112-115
19884577-6	2009	At baseline, patients who were binding antibody positive (BAb+)/neutralizing antibody positive (NAb+) had lower MxA, viperin, and IFIT-1 response compared with BAb-negative (BAb-)/NAb-negative (NAb-) patients (all p &lt; 0.0001).	nab	96-99	radical S-adenosyl methionine domain containing 2	Homo sapiens	117-124
19884577-6	2009	At baseline, patients who were binding antibody positive (BAb+)/neutralizing antibody positive (NAb+) had lower MxA, viperin, and IFIT-1 response compared with BAb-negative (BAb-)/NAb-negative (NAb-) patients (all p &lt; 0.0001).	nab	96-99	interferon induced protein with tetratricopeptide repeats 1	Homo sapiens	130-136
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	nitric oxide synthase 2, inducible	Mus musculus	76-97
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	nitric oxide synthase 2, inducible	Mus musculus	99-103
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	tumor necrosis factor	Mus musculus	133-142
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	interleukin 1 beta	Mus musculus	147-155
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	integrin alpha M	Mus musculus	178-183
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	integrin alpha X	Mus musculus	185-190
19812204-3	2009	NaB, but not sodium formate, was found to inhibit LPS-induced expression of inducible NO synthase (iNOS), proinflammatory cytokines (TNF-alpha and IL-1beta) and surface markers (CD11b, CD11c, and CD68) in mouse microglia.	nab	0-3	CD68 antigen	Mus musculus	196-200
19812204-4	2009	Similarly, NaB also inhibited fibrillar amyloid beta (Abeta)-, prion peptide-, double-stranded RNA (polyinosinic-polycytidylic acid)-, HIV-1 Tat-, 1-methyl-4-phenylpyridinium(+)-, IL-1beta-, and IL-12 p40(2)-induced microglial expression of iNOS.	nab	11-14	interleukin 1 beta	Mus musculus	180-188
19812204-4	2009	Similarly, NaB also inhibited fibrillar amyloid beta (Abeta)-, prion peptide-, double-stranded RNA (polyinosinic-polycytidylic acid)-, HIV-1 Tat-, 1-methyl-4-phenylpyridinium(+)-, IL-1beta-, and IL-12 p40(2)-induced microglial expression of iNOS.	nab	11-14	nitric oxide synthase 2, inducible	Mus musculus	241-245
19812204-5	2009	In addition to microglia, NaB also suppressed the expression of iNOS in mouse peritoneal macrophages and primary human astrocytes.	nab	26-29	nitric oxide synthase 2, inducible	Mus musculus	64-68
19812204-9	2009	These results highlight a novel anti-inflammatory role of NaB via modulation of the mevalonate pathway and p21(ras).	nab	58-61	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	107-110
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-C motif chemokine ligand 1	Homo sapiens	9-13
19538176-0	2009	Nanoparticle albumin-bound (NAB) technology is a promising method for anti-cancer drug delivery.	nab	28-31	albumin	Homo sapiens	13-20
19538176-2	2009	Recently, nanoparticle albumin-bound (nab) paclitaxel (nab-paclitaxel; Abraxane) has been approved in 2006 for use in patients with metastatic breast cancer who have failed in the combination chemotherapy, and so the nab-technology has attracted much interest in the anti-cancer drug delivery system.	nab	38-41	albumin	Homo sapiens	23-30
19538176-2	2009	Recently, nanoparticle albumin-bound (nab) paclitaxel (nab-paclitaxel; Abraxane) has been approved in 2006 for use in patients with metastatic breast cancer who have failed in the combination chemotherapy, and so the nab-technology has attracted much interest in the anti-cancer drug delivery system.	nab	55-58	albumin	Homo sapiens	23-30
19538176-2	2009	Recently, nanoparticle albumin-bound (nab) paclitaxel (nab-paclitaxel; Abraxane) has been approved in 2006 for use in patients with metastatic breast cancer who have failed in the combination chemotherapy, and so the nab-technology has attracted much interest in the anti-cancer drug delivery system.	nab	55-58	albumin	Homo sapiens	23-30
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-C motif chemokine ligand 2	Homo sapiens	15-19
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-C motif chemokine ligand 7	Homo sapiens	21-25
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-X-C motif chemokine ligand 10	Homo sapiens	27-33
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-X-C motif chemokine ligand 11	Homo sapiens	35-41
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	C-C motif chemokine receptor 1	Homo sapiens	47-51
19667211-9	2009	RESULTS: CCL1, CCL2, CCL7, CXCL10, CXCL11, and CCR1 gene expression was strongly upregulated in interferon beta-treated, NAB-negative MS patients.	nab	121-124	interferon beta 1	Homo sapiens	96-111
19667211-12	2009	Accordingly, serum chemokine protein levels of interferon beta-treated, NAB-negative MS patients were significantly higher than in untreated or interferon beta-treated, NAB-positive MS patients.	nab	72-75	interferon beta 1	Homo sapiens	47-62
19667211-12	2009	Accordingly, serum chemokine protein levels of interferon beta-treated, NAB-negative MS patients were significantly higher than in untreated or interferon beta-treated, NAB-positive MS patients.	nab	169-172	interferon beta 1	Homo sapiens	144-159
19567243-5	2009	The NAb specificities for SOSIP antisera mapped in part to the CD4 binding site on gp120.	nab	4-7	CD4 molecule	Homo sapiens	63-66
19821084-5	2009	NaB and TSA could induce the apoptosis of HL-60 and K562 cells, and Z-VAD-FMK caused a marked decrease in apoptosis induced by HDAC inhibitors.	nab	0-3	histone deacetylase 9	Homo sapiens	127-131
19821084-7	2009	The results suggested that NaB and TSA induce distinct caspase-dependent apoptosis of human leukemic cells through down-regulating the expression of Daxx protein in vitro.	nab	27-30	death domain associated protein	Homo sapiens	149-153
19360904-3	2009	Consequently, trichostatin A (TSA), sodium butyrate (NaB), and valproic acid (VPA) stimulated glial fibrillary acidic protein (GFAP) gene expression, and their stimulatory effects on GFAP gene expression were inhibited by treatment of these cells with finasteride, an inhibitor of the enzyme producing 5alpha-reduced neurosteroids.	nab	53-56	glial fibrillary acidic protein	Rattus norvegicus	94-125
19360904-3	2009	Consequently, trichostatin A (TSA), sodium butyrate (NaB), and valproic acid (VPA) stimulated glial fibrillary acidic protein (GFAP) gene expression, and their stimulatory effects on GFAP gene expression were inhibited by treatment of these cells with finasteride, an inhibitor of the enzyme producing 5alpha-reduced neurosteroids.	nab	53-56	glial fibrillary acidic protein	Rattus norvegicus	127-131
19360904-3	2009	Consequently, trichostatin A (TSA), sodium butyrate (NaB), and valproic acid (VPA) stimulated glial fibrillary acidic protein (GFAP) gene expression, and their stimulatory effects on GFAP gene expression were inhibited by treatment of these cells with finasteride, an inhibitor of the enzyme producing 5alpha-reduced neurosteroids.	nab	53-56	glial fibrillary acidic protein	Rattus norvegicus	183-187
19567243-5	2009	The NAb specificities for SOSIP antisera mapped in part to the CD4 binding site on gp120.	nab	4-7	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	83-88
19465447-13	2009	NAB titers decreased significantly and transiently after infusion of 16 MIU IFNbeta-1b but not after both forms of 8 MIU applications.	nab	0-3	interferon beta 1	Homo sapiens	76-83
19432898-9	2009	Next, we investigated the cell death effect of endogenous p21 protein on cell fate using sodium butyrate (NaB).	nab	106-109	cyclin dependent kinase inhibitor 1A	Homo sapiens	58-61
19013255-3	2009	In this report, we demonstrate that the HDAC inhibitor NaB (sodium butyrate) was able to induce cell growth arrest and to increase HOXB13 expression in AR-negative prostate cancer cells.	nab	55-58	homeobox B13	Homo sapiens	131-137
19645322-7	2009	It was found that the MEK inhibitor decreased collagen biosynthesis and expression of MAP-kinases (ERK1, ERK2), while NaB counteracted the process.	nab	118-121	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
19340848-9	2009	Repeat administration of low-dose AAV.hRPE65.hRPE65 to both eyes of RPE65(-/-) mice resulted in transgene expression and functional rescue, but re-administration of high-dose AAV2 resulted in boosted NAb titres and variable transgene expression in the second injected eye.	nab	200-203	retinal pigment epithelium 65	Mus musculus	39-44
19013255-3	2009	In this report, we demonstrate that the HDAC inhibitor NaB (sodium butyrate) was able to induce cell growth arrest and to increase HOXB13 expression in AR-negative prostate cancer cells.	nab	55-58	androgen receptor	Homo sapiens	152-154
19412420-6	2009	Response to nab-paclitaxel was higher for SPARC-positive patients (10/12, 83%) than SPARC-negative patients (1/4, 25%).	nab	12-15	secreted protein acidic and cysteine rich	Homo sapiens	42-47
19412420-6	2009	Response to nab-paclitaxel was higher for SPARC-positive patients (10/12, 83%) than SPARC-negative patients (1/4, 25%).	nab	12-15	secreted protein acidic and cysteine rich	Homo sapiens	84-89
19412420-9	2009	If confirmed in larger studies, treatment with nab-paclitaxel may convert a poor prognosis SPARC-positive patient population into a group with better clinical outcomes.	nab	47-50	secreted protein acidic and cysteine rich	Homo sapiens	91-96
19719045-7	2009	It was found that the MEK inhibitor decreased collagen biosynthesis and expression of MAP-kinases (ERK1, ERK2), while NaB counteracted the process.	nab	118-121	mitogen-activated protein kinase kinase 7	Homo sapiens	22-25
19218566-7	2009	Nab was shown to act as a negative feedback modulator of the different Krox20 activating functions in the hindbrain.	nab	0-3	early growth response 2	Gallus gallus	71-77
19218566-8	2009	HCF-1 was found to bind to a Krox20 N-terminal region, which was shown to rely on multiple elements, including acidic domains, to convey Nab activation and Krox20 autoregulation.	nab	137-140	early growth response 2	Gallus gallus	29-35
19278300-10	2009	CONCLUSION: Use of an IFN-beta-1b dose higher than the currently approved 250-microg dose is associated with an increased probability of NAb disappearance.	nab	137-140	interferon beta 1	Homo sapiens	22-30
19028832-4	2009	Another 14 NAb-positive patients with a low MxA-mRNA response served as controls.	nab	11-14	MX dynamin like GTPase 1	Homo sapiens	44-47
19244508-7	2009	These studies describe a unique animal model of CMT, whereby weakness is due to conduction block or neuromuscular junction failure rather than secondary axon loss and demonstrate that the Egr2-Nab complex is critical for proper peripheral nerve myelination.	nab	193-196	early growth response 2	Mus musculus	188-192
19000020-7	2009	The excellent agreement observed between the theoretical prediction and experimental findings reinforces the validity of using as NAb unitage the titer based on 10-fold reduction of IFN activity, reportable as Tenfold Reduction Units (TRU)/mL, as previously recommended.	nab	130-133	interferon alpha 1	Homo sapiens	182-185
19000020-9	2009	The constant Ab method can be used as a quantitative, sensitive IFN NAb screening bioassay of any nature, and should be able to detect low levels of NAbs early in the course of IFN therapy.	nab	68-71	interferon alpha 1	Homo sapiens	64-67
18817816-8	2009	5-HT(1A) antagonist, WAY 100635, significantly block the antidepressant-like effects induced by NaB plus EB.	nab	96-99	5-hydroxytryptamine receptor 1A	Rattus norvegicus	0-7
19956429-5	2009	We hypothesized that the HDAC inhibitor Sodium Butyrate (NaB) might activate Notch1 in pheochromocytoma resulting in altered tumor cell proliferation.	nab	57-60	notch receptor 1	Rattus norvegicus	77-83
19956429-10	2009	Treatment with NaB led to a dose-dependent induction of Notch1 signaling, reduction of NE markers ASCL1 and CgA, and a significant reduction in cellular proliferation.	nab	15-18	notch receptor 1	Rattus norvegicus	56-62
19956429-10	2009	Treatment with NaB led to a dose-dependent induction of Notch1 signaling, reduction of NE markers ASCL1 and CgA, and a significant reduction in cellular proliferation.	nab	15-18	achaete-scute family bHLH transcription factor 1	Rattus norvegicus	98-103
19956429-10	2009	Treatment with NaB led to a dose-dependent induction of Notch1 signaling, reduction of NE markers ASCL1 and CgA, and a significant reduction in cellular proliferation.	nab	15-18	chromogranin A	Rattus norvegicus	108-111
19956429-11	2009	Levels of expression of cyclin D1, p21, cleaved PARP, and cleaved caspase 3 proteins indicated the presence of cell cycle arrest and apoptosis following NaB treatment.	nab	153-156	cyclin D1	Rattus norvegicus	24-33
19956429-11	2009	Levels of expression of cyclin D1, p21, cleaved PARP, and cleaved caspase 3 proteins indicated the presence of cell cycle arrest and apoptosis following NaB treatment.	nab	153-156	KRAS proto-oncogene, GTPase	Rattus norvegicus	35-38
19956429-12	2009	CONCLUSION: NaB activated Notch1 signaling, inhibited cellular proliferation, reduced NE markers, and induced cell cycle arrest and apoptosis in pheochromocytoma cells.	nab	12-15	notch receptor 1	Rattus norvegicus	26-32
18817816-11	2009	In conclusion, NaB may exert antidepressant-like effects in combination with EB in ovariectomized female rats through 5-HT(1A) receptor, via altering the expression of 5-HT(1A) in the hypothalamus.	nab	15-18	5-hydroxytryptamine receptor 1A	Rattus norvegicus	168-175
18817816-11	2009	In conclusion, NaB may exert antidepressant-like effects in combination with EB in ovariectomized female rats through 5-HT(1A) receptor, via altering the expression of 5-HT(1A) in the hypothalamus.	nab	15-18	5-hydroxytryptamine receptor 1A	Rattus norvegicus	118-125
19799355-0	2009	[Effect of histone deacetylases inhibitor sodium butyrate (NaB) on transformants E1A + cHa-Ras expressing wild type p53 with supressed transactivation function].	nab	59-62	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	116-119
19357765-2	2009	METHODOLOGY/ PRINCIPAL FINDINGS: In this study, microarray analysis, in situ hybridization, quantitative real-time PCR and immunohistochemistry revealed decreased expression of the vasopressin gene (Avp) in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei of adult LAB mice compared to HAB, NAB (normal anxiety-related behavior) and HABxLAB F1 intercross controls, without detecting differences in receptor expression or density.	nab	309-312	arginine vasopressin	Mus musculus	199-202
19799355-3	2009	NaB treatment increased p53 transcriptional activity and induced an irreversible G1/S cell cycle arrest in ERas(WT), but not in ERas(GSE56) cells.	nab	0-3	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	24-27
19799355-5	2009	p53 activity in transformants ERas(WT) increased both after irradiation or upon NaB treatment.	nab	80-83	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	0-3
21180570-3	2008	The principle in NAb in vitro assays is the utilization of cultured cell lines that are responsive to IFN-ss.	nab	17-20	interferon alpha 1	Homo sapiens	102-105
18718708-3	2008	Here, we show that the HDIs suberoylanilide hydroxamic acid (SAHA; vorinostat), sodium butyrate (NaB) and MS-275 sensitized DAOY and PC3 tumour cells for the cytotoxic effects of IL-2-activated PBMCs.	nab	97-100	interleukin 2	Homo sapiens	179-183
18955705-5	2008	Viral vector-mediated up-regulation of AVP V1a receptors (AVP-Rs) within the medial preoptic area of lactating NAB rats and chronic central AVP treatment of NAB and LAB dams improved, whereas local blockade of AVP-R expression by means of antisense oligodeoxynucleotides or central AVP-R antagonism impaired, maternal care in NAB dams.	nab	111-114	arginine vasopressin	Rattus norvegicus	58-61
18955705-7	2008	Treatment-induced impairment of AVP-mediated maternal behavior increased adult emotionality and impaired social interactions in male offspring of NAB dams.	nab	146-149	arginine vasopressin	Rattus norvegicus	32-35
19094453-1	2008	The development of neutralizing antibodies (NAbs) against interferon-beta(IFNbeta) reduces clinical efficacy and markers of bioactivity in patients with multiple sclerosis (MS), although it has also been shown that a poor response to IFNbeta coincided with unexpectedly low NAb levels.	nab	44-47	interferon beta 1	Homo sapiens	58-82
19094453-1	2008	The development of neutralizing antibodies (NAbs) against interferon-beta(IFNbeta) reduces clinical efficacy and markers of bioactivity in patients with multiple sclerosis (MS), although it has also been shown that a poor response to IFNbeta coincided with unexpectedly low NAb levels.	nab	44-47	interferon beta 1	Homo sapiens	74-81
18971450-8	2008	Upon prolonged treatment, NAb-negative patients displayed a state of decreased transmembrane IFNAR-2 expression (p &lt; or = 0.025), whereas levels of soluble IFNAR-2 were slightly increased (p &lt; 0.0001).	nab	26-29	interferon alpha and beta receptor subunit 2	Homo sapiens	93-100
18971450-10	2008	In NAb-positive patients, pretreatment expression levels of both transmembrane IFNAR-2 isoforms were significantly lower than in NAb-negative patients (p &lt; or = 0.0089).	nab	3-6	interferon alpha and beta receptor subunit 2	Homo sapiens	79-86
18971450-10	2008	In NAb-positive patients, pretreatment expression levels of both transmembrane IFNAR-2 isoforms were significantly lower than in NAb-negative patients (p &lt; or = 0.0089).	nab	129-132	interferon alpha and beta receptor subunit 2	Homo sapiens	79-86
18955705-5	2008	Viral vector-mediated up-regulation of AVP V1a receptors (AVP-Rs) within the medial preoptic area of lactating NAB rats and chronic central AVP treatment of NAB and LAB dams improved, whereas local blockade of AVP-R expression by means of antisense oligodeoxynucleotides or central AVP-R antagonism impaired, maternal care in NAB dams.	nab	111-114	arginine vasopressin	Rattus norvegicus	39-42
18955705-5	2008	Viral vector-mediated up-regulation of AVP V1a receptors (AVP-Rs) within the medial preoptic area of lactating NAB rats and chronic central AVP treatment of NAB and LAB dams improved, whereas local blockade of AVP-R expression by means of antisense oligodeoxynucleotides or central AVP-R antagonism impaired, maternal care in NAB dams.	nab	111-114	arginine vasopressin	Rattus norvegicus	58-61
18955705-5	2008	Viral vector-mediated up-regulation of AVP V1a receptors (AVP-Rs) within the medial preoptic area of lactating NAB rats and chronic central AVP treatment of NAB and LAB dams improved, whereas local blockade of AVP-R expression by means of antisense oligodeoxynucleotides or central AVP-R antagonism impaired, maternal care in NAB dams.	nab	111-114	arginine vasopressin	Rattus norvegicus	58-61
18955705-5	2008	Viral vector-mediated up-regulation of AVP V1a receptors (AVP-Rs) within the medial preoptic area of lactating NAB rats and chronic central AVP treatment of NAB and LAB dams improved, whereas local blockade of AVP-R expression by means of antisense oligodeoxynucleotides or central AVP-R antagonism impaired, maternal care in NAB dams.	nab	111-114	arginine vasopressin	Rattus norvegicus	58-61
18766004-9	2008	In these HER2-positive tumors, nab-paclitaxel was equal to or better than polysorbate-based docetaxel in tumors with medium to high SPARC levels (PC3 and HT29), but not in MDA-MB-231/HER2+ tumors with low SPARC expression.	nab	31-34	erb-b2 receptor tyrosine kinase 2	Homo sapiens	9-13
18766004-9	2008	In these HER2-positive tumors, nab-paclitaxel was equal to or better than polysorbate-based docetaxel in tumors with medium to high SPARC levels (PC3 and HT29), but not in MDA-MB-231/HER2+ tumors with low SPARC expression.	nab	31-34	erb-b2 receptor tyrosine kinase 2	Homo sapiens	183-187
18766004-9	2008	In these HER2-positive tumors, nab-paclitaxel was equal to or better than polysorbate-based docetaxel in tumors with medium to high SPARC levels (PC3 and HT29), but not in MDA-MB-231/HER2+ tumors with low SPARC expression.	nab	31-34	secreted protein acidic and cysteine rich	Homo sapiens	205-210
18766004-10	2008	These results demonstrated that the relative efficacy of nab-paclitaxel was significantly higher compared with polysorbate-based docetaxel in HER2-negative tumors (three of three) and in HER2-positive tumors with high levels of SPARC.	nab	57-60	erb-b2 receptor tyrosine kinase 2	Homo sapiens	142-146
18766004-10	2008	These results demonstrated that the relative efficacy of nab-paclitaxel was significantly higher compared with polysorbate-based docetaxel in HER2-negative tumors (three of three) and in HER2-positive tumors with high levels of SPARC.	nab	57-60	secreted protein acidic and cysteine rich	Homo sapiens	228-233
18505772-1	2008	OBJECTIVE: To establish whether multiple sclerosis (MS) patients, who have lost the therapeutic effect of interferon-beta (IFN-beta) owing to neutralizing antibodies (NAbs) and subsequently revert from a NAb-positive to a NAb-negative state under continued IFN-beta-1b therapy, regain clinical effect after reversion.	nab	167-170	interferon beta 1	Homo sapiens	123-131
18571155-4	2008	We report that in discs lacking zfh2 the limits of the expression domains of the genes tsh, nub, rn, dve and nab coincide, and expression of wg in the wing hinge, is lost.	nab	109-112	Zn finger homeodomain 2	Drosophila melanogaster	32-36
18571155-6	2008	Distal repression of zfh2 permits activation of nab in the wing blade and wg in the wing hinge.	nab	48-51	Zn finger homeodomain 2	Drosophila melanogaster	21-25
18519143-9	2008	Of note is that the escape mutants were more sensitive than the parental CC1/85 isolate to a subset of neutralizing monoclonal antibodies and to some sera from HIV-1-infected people, implying that sequence changes in Env that confer resistance to CCR5 inhibitors can increase the accessibility of some NAb epitopes.	nab	302-305	C-C motif chemokine receptor 5	Homo sapiens	247-251
18519143-10	2008	The need to preserve NAb resistance may therefore be a constraint upon how escape from CCR5 inhibitors occurs in vivo.	nab	21-24	C-C motif chemokine receptor 5	Homo sapiens	87-91
18081914-2	2008	Two to forty per cent of IFN-beta-treated multiple sclerosis (MS) patients develop IFN-beta-neutralizing antibodies (NAb) with subsequent attenuation of MxA protein induction.	nab	117-120	interferon beta 1	Homo sapiens	25-33
18081914-2	2008	Two to forty per cent of IFN-beta-treated multiple sclerosis (MS) patients develop IFN-beta-neutralizing antibodies (NAb) with subsequent attenuation of MxA protein induction.	nab	117-120	interferon beta 1	Homo sapiens	83-91
18081914-7	2008	Patients with NAb had low MxA levels, but in some patients, remaining MxA induction could be detected despite NAb.	nab	14-17	MX dynamin like GTPase 1	Homo sapiens	26-29
18505772-3	2008	However, some patients, who become NAb-positive under treatment with IFN-beta-1b, may revert to a NAb-negative state under continuous treatment.	nab	35-38	interferon beta 1	Homo sapiens	69-77
18505772-3	2008	However, some patients, who become NAb-positive under treatment with IFN-beta-1b, may revert to a NAb-negative state under continuous treatment.	nab	98-101	interferon beta 1	Homo sapiens	69-77
18505772-14	2008	CONCLUSION: Under NAb-positive periods, the clinical effect of IFN-beta was abolished.	nab	18-21	interferon beta 1	Homo sapiens	63-71
18455826-6	2008	However, blocking Akt activity by expressing its dominant negative form remarkably promoted NaB and GCV-mediated cytotoxicity via a thymidine kinase (TK)-independent mechanism.	nab	92-95	AKT serine/threonine kinase 1	Homo sapiens	18-21
18455826-7	2008	Interestingly, it was found that the constitutive activation of mitogen-activated protein kinase kinase kinase 1 (MEKK1) dramatically enhanced the sensitization of the cells to the combination of NaB and GCV, accompanied with an increase in TK expression in B95-8 cells.	nab	196-199	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	64-112
18455826-7	2008	Interestingly, it was found that the constitutive activation of mitogen-activated protein kinase kinase kinase 1 (MEKK1) dramatically enhanced the sensitization of the cells to the combination of NaB and GCV, accompanied with an increase in TK expression in B95-8 cells.	nab	196-199	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	114-119
18455826-8	2008	These results suggest that interfering with either the Akt or MEKK1 signaling pathway may be a useful therapeutic strategy to increase the sensitivity of EBV-positive tumor cells to the combination of NaB and GCV.	nab	201-204	AKT serine/threonine kinase 1	Homo sapiens	55-58
18455826-8	2008	These results suggest that interfering with either the Akt or MEKK1 signaling pathway may be a useful therapeutic strategy to increase the sensitivity of EBV-positive tumor cells to the combination of NaB and GCV.	nab	201-204	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	62-67
18456662-0	2008	Active gene repression by the Egr2.NAB complex during peripheral nerve myelination.	nab	35-38	early growth response 2	Homo sapiens	30-34
18456662-3	2008	The NAB (NGFI-A/Egr-binding) corepressors interact with Egr2 and are required for proper coordination of myelin formation.	nab	4-7	early growth response 1	Homo sapiens	9-15
18456662-3	2008	The NAB (NGFI-A/Egr-binding) corepressors interact with Egr2 and are required for proper coordination of myelin formation.	nab	4-7	early growth response 2	Homo sapiens	56-60
18456662-5	2008	To define the physiological role of NAB corepression in gene repression by Egr2, we tested whether the Egr2.NAB complex directly repressed specific target genes.	nab	36-39	early growth response 2	Homo sapiens	75-79
18456662-8	2008	In addition, NAB2 represses transcription by interaction with the chromodomain helicase DNA-binding protein 4 (CHD4) subunit of the nucleosome remodeling and deacetylase chromatin remodeling complex, and we demonstrate that CHD4 occupies NAB-repressed promoters in a developmentally regulated manner in vivo.	nab	13-16	chromodomain helicase DNA binding protein 4	Homo sapiens	66-109
18456662-8	2008	In addition, NAB2 represses transcription by interaction with the chromodomain helicase DNA-binding protein 4 (CHD4) subunit of the nucleosome remodeling and deacetylase chromatin remodeling complex, and we demonstrate that CHD4 occupies NAB-repressed promoters in a developmentally regulated manner in vivo.	nab	13-16	chromodomain helicase DNA binding protein 4	Homo sapiens	111-115
18456662-8	2008	In addition, NAB2 represses transcription by interaction with the chromodomain helicase DNA-binding protein 4 (CHD4) subunit of the nucleosome remodeling and deacetylase chromatin remodeling complex, and we demonstrate that CHD4 occupies NAB-repressed promoters in a developmentally regulated manner in vivo.	nab	13-16	chromodomain helicase DNA binding protein 4	Homo sapiens	224-228
18426395-5	2008	This study suggests that high levels of NAb and stable epitopes in gp120 could play a crucial role in protection against disease progression.	nab	40-43	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	67-72
18524893-0	2008	Disruption of Krox20-Nab interaction in the mouse leads to peripheral neuropathy with biphasic evolution.	nab	21-24	early growth response 2	Mus musculus	14-20
18524893-2	2008	Krox20 is known to interact with cofactors of the Nab family and a mutation affecting isoleucine 268, which prevents this interaction, has been shown to result in congenital hypomyelinating neuropathy in humans.	nab	50-53	early growth response 2	Homo sapiens	0-6
17986500-9	2008	CONCLUSIONS: MRI activity and NAb occurrence during the first 6 months of interferon beta treatment were reliable predictors of long term clinical response, particularly when combined.	nab	30-33	interferon beta 1	Homo sapiens	74-89
18452462-9	2008	The Bcl-2 expression in bladder cancer cells is decreased and caspase-3 expression increased after NaB treatment.	nab	99-102	BCL2 apoptosis regulator	Homo sapiens	4-9
18452462-9	2008	The Bcl-2 expression in bladder cancer cells is decreased and caspase-3 expression increased after NaB treatment.	nab	99-102	caspase 3	Homo sapiens	62-71
18844115-8	2008	After treated with NaB the mRNA and protein expressions of p16 gene were increased in both cells.	nab	19-22	cyclin dependent kinase inhibitor 2A	Homo sapiens	59-62
18844115-9	2008	CONCLUSION: NaB inhibits the growth of human gastric cancer cells by blocking cell cycles, inducing apoptosis and upregulating the expression of p16 gene by increasing acetylation and reducing methylation.	nab	12-15	cyclin dependent kinase inhibitor 2A	Homo sapiens	145-148
18426595-10	2008	In patients testing positive for NAbs (NAb+) to IFN beta-1a 44 mcg sc tiw, changes in BOD were smaller than in NAb negative (NAb-) patients, but similar to those receiving IFN beta-1a, 30 mcg im qw.	nab	33-36	interferon beta 1	Homo sapiens	48-56
18426595-10	2008	In patients testing positive for NAbs (NAb+) to IFN beta-1a 44 mcg sc tiw, changes in BOD were smaller than in NAb negative (NAb-) patients, but similar to those receiving IFN beta-1a, 30 mcg im qw.	nab	39-42	interferon beta 1	Homo sapiens	48-56
18426595-10	2008	In patients testing positive for NAbs (NAb+) to IFN beta-1a 44 mcg sc tiw, changes in BOD were smaller than in NAb negative (NAb-) patients, but similar to those receiving IFN beta-1a, 30 mcg im qw.	nab	39-42	interferon beta 1	Homo sapiens	48-56
18516298-6	2008	VEGF-A protected MDA-MB-231 cells against nab-paclitaxel cytotoxicity, whereas bevacizumab sensitized cells to the effect of the drug.	nab	42-45	vascular endothelial growth factor A	Homo sapiens	0-6
18420982-1	2008	High levels of natural antibodies (NAb) binding the alpha-Gal residue (Galalpha1-3Galbeta1-4GlcNAc) are found in poultry (and humans), which is probably reflected by high levels of natural agglutinating antibodies (Ab) to rabbit red blood cells (RRBC) in plasma from chickens (and humans).	nab	35-38	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	52-61
18420982-8	2008	Our data confirm the presence of high levels of (preexisting) NAb in the plasma of chickens directed to the alpha-Gal residue.	nab	62-65	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	108-117
18420982-9	2008	The decreased responsiveness to alpha-Gal-bearing antigens in the current study shows that, in addition to immune-enhancing features, NAb may also have suppressive effects on specific immune responses, which substantiates the regulatory role of innate immunity (NAb) in mounting specific immune responses.	nab	134-137	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	32-41
18420982-9	2008	The decreased responsiveness to alpha-Gal-bearing antigens in the current study shows that, in addition to immune-enhancing features, NAb may also have suppressive effects on specific immune responses, which substantiates the regulatory role of innate immunity (NAb) in mounting specific immune responses.	nab	262-265	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	32-41
18844115-1	2008	OBJECTIVE: To investigate the effects of sodium butyrate (NaB), a histone deacetylase inhibitor (HDACI), on the proliferation of human gastric cancer cells and the expression of p16, an important negative-regulatory factor of the cell cycle G1.	nab	58-61	cyclin dependent kinase inhibitor 2A	Homo sapiens	178-181
18197126-6	2008	In addition, a higher proportion of defective clones was found among the env genes of NAb- patients (25% to 93%)-particularly those with lower viral loads and low levels of env diversity-than among those of NAb+ patients (7% to 19%).	nab	86-89	endogenous retrovirus group K member 20	Homo sapiens	73-76
18197126-6	2008	In addition, a higher proportion of defective clones was found among the env genes of NAb- patients (25% to 93%)-particularly those with lower viral loads and low levels of env diversity-than among those of NAb+ patients (7% to 19%).	nab	86-89	endogenous retrovirus group K member 20	Homo sapiens	173-176
18203293-0	2008	Regulation of demethylation and re-expression of RASSF1A gene in gastric cancer cell lines by combined treatment of 5-Aza-CdR and NaB.	nab	130-133	Ras association domain family member 1	Homo sapiens	49-56
17986510-2	2008	The frequency of Nabs varies depending on IFN-beta product and the Nab assay used.	nab	17-20	interferon beta 1	Homo sapiens	42-50
18203293-6	2008	The combined treatment of 5-Aza-CdR and NaB induced complete demethylation of RASSF1A gene, leading to a significantly higher re-expression of the mRNA and protein of RASSF1A than those treated with 5-Aza-CdR alone (P&lt;0.05).	nab	40-43	Ras association domain family member 1	Homo sapiens	78-85
18203293-6	2008	The combined treatment of 5-Aza-CdR and NaB induced complete demethylation of RASSF1A gene, leading to a significantly higher re-expression of the mRNA and protein of RASSF1A than those treated with 5-Aza-CdR alone (P&lt;0.05).	nab	40-43	Ras association domain family member 1	Homo sapiens	167-174
17941058-8	2008	CD81-negative HepG2 hepatoma cells were resistant to cell-free virus infection but became infected after coculturing with JFH-infected cells in the presence of nAb, confirming that CD81-independent routes of cell-cell transmission exist.	nab	160-163	CD81 molecule	Homo sapiens	0-4
17784815-5	2007	NAb titers obtained using IFN-beta1b averaged 3-5-fold lower than titers of the same sample assayed using either IFN-beta1a or human fibroblast-derived IFN-beta.	nab	0-3	interferon beta 1	Homo sapiens	26-34
17911184-5	2008	Patients with NAb titres of up to 150 TRU/ml (ten times reduction units per ml) still had retained IFNbeta bioactivity, whereas greatly reduced levels of IFNbeta bioactivity were found in patients with NAbs of 150-600 TRU/ml.	nab	14-17	interferon beta 1	Homo sapiens	99-106
17911184-8	2008	CONCLUSION: There is a stepwise loss of IFNbeta bioactivity with increasing NAb titres and it is possible to identify functionally critical NAb titre levels that are useful to support treatment decisions at the individual patient level.	nab	76-79	interferon beta 1	Homo sapiens	40-47
18751946-1	2008	PURPOSE: Hyperacute rejection (HAR) mediated by the natural antibody (nAb) against Gal alpha 1-3Gal beta-4-GlcNAc (alpha Gal) is the major obstacle in xenogeneic organ transplantation.	nab	70-73	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	87-113
18751946-1	2008	PURPOSE: Hyperacute rejection (HAR) mediated by the natural antibody (nAb) against Gal alpha 1-3Gal beta-4-GlcNAc (alpha Gal) is the major obstacle in xenogeneic organ transplantation.	nab	70-73	glycoprotein galactosyltransferase alpha 1, 3	Mus musculus	115-124
18096076-4	2007	RESULTS: To test the mechanism of NAB regulation in Schwann cells, transfection assays revealed that both Nab1 and Nab2 promoters are activated by Egr2 expression.	nab	34-37	NGFI-A binding protein 1	Homo sapiens	106-110
18096076-4	2007	RESULTS: To test the mechanism of NAB regulation in Schwann cells, transfection assays revealed that both Nab1 and Nab2 promoters are activated by Egr2 expression.	nab	34-37	NGFI-A binding protein 2	Homo sapiens	115-119
18096076-4	2007	RESULTS: To test the mechanism of NAB regulation in Schwann cells, transfection assays revealed that both Nab1 and Nab2 promoters are activated by Egr2 expression.	nab	34-37	early growth response 2	Homo sapiens	147-151
18001282-3	2007	Both osmotically stimulated peripheral secretion and intra-paraventricular nucleus (PVN) release of AVP were found decreased in LAB animals compared with normal anxiety (NAB) or high anxiety (HAB) controls.	nab	170-173	arginine vasopressin	Mus musculus	100-103
19140343-1	2008	We studied the role of JNK1,2 stress-kinases in the regulation of premature senescence program, stimulated by the inhibitor of histone deacetylase, sodium butyrate (NaB).	nab	165-168	mitogen-activated protein kinase 8	Mus musculus	23-27
18323252-11	2007	Strong correlation between NaB concentration and cell viability after 24 h was noticed (correlation coefficient was 0.94 and 0.98 for C6 and HepG2, respectively).	nab	27-30	complement C6	Homo sapiens	134-146
17486365-6	2007	SAHA and NaB induced mitochondrial depolarisation as well as caspase-9 and -3 activities, and their cytotoxic effects could be significantly reduced by the pan-caspase inhibitor z-VAD-fmk.	nab	9-12	caspase 9	Homo sapiens	61-77
17662004-5	2007	It is concluded that NAb titres are important for the biological response to IFN-beta.	nab	21-24	interferon beta 1	Homo sapiens	77-85
17457510-5	2007	NAb testing is a critical component of care for MS patients because it provides information on one of the most important factors determining clinical responsiveness to IFNbeta therapy.	nab	0-3	interferon beta 1	Homo sapiens	168-175
17540780-3	2007	In this study, we have investigated the effect of sodium butyrate (NaB) and IFN-gamma/TNF-alpha on human NHE3 promoter activity.	nab	67-70	solute carrier family 9 member A3	Homo sapiens	105-109
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	35-38	solute carrier family 9 member A3	Homo sapiens	76-80
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	35-38	solute carrier family 9 member A3	Homo sapiens	197-201
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	35-38	interferon gamma	Homo sapiens	290-299
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	35-38	tumor necrosis factor	Homo sapiens	300-309
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	157-160	solute carrier family 9 member A3	Homo sapiens	76-80
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	157-160	solute carrier family 9 member A3	Homo sapiens	197-201
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	157-160	interferon gamma	Homo sapiens	290-299
17540780-4	2007	In transient transfection studies, NaB (5 mM) led to 10-fold stimulation of NHE3 promoter activity after incubation for 24 h. With 5"-deletion analysis, the NaB-responsive region was mapped to the NHE3 core promoter, bp -95 to + 5, which we had shown previously to confer responsiveness to IFN-gamma/TNF-alpha.	nab	157-160	tumor necrosis factor	Homo sapiens	300-309
17540780-5	2007	The stimulatory effect of NaB on the NHE3 promoter was reduced by 60% in the presence of IFN-gamma/TNF-alpha.	nab	26-29	solute carrier family 9 member A3	Homo sapiens	37-41
17540780-5	2007	The stimulatory effect of NaB on the NHE3 promoter was reduced by 60% in the presence of IFN-gamma/TNF-alpha.	nab	26-29	interferon gamma	Homo sapiens	89-98
17540780-5	2007	The stimulatory effect of NaB on the NHE3 promoter was reduced by 60% in the presence of IFN-gamma/TNF-alpha.	nab	26-29	tumor necrosis factor	Homo sapiens	99-108
17540780-7	2007	Knockdown of Sp1 and Sp3 expression with small interfering RNA (siRNA) resulted in a significant resistance to NaB effects.	nab	111-114	Sp3 transcription factor	Homo sapiens	21-24
17540780-9	2007	Gel mobility shift assays with nuclear proteins from NaB-treated cells showed enhanced binding of Sp1 and Sp3 to the NHE3 promoter.	nab	53-56	Sp3 transcription factor	Homo sapiens	106-109
17540780-9	2007	Gel mobility shift assays with nuclear proteins from NaB-treated cells showed enhanced binding of Sp1 and Sp3 to the NHE3 promoter.	nab	53-56	solute carrier family 9 member A3	Homo sapiens	117-121
17540780-10	2007	The phosphatase inhibitor okadaic acid (200 nM) blocked the stimulatory effect of NaB on the NHE3 promoter.	nab	82-85	solute carrier family 9 member A3	Homo sapiens	93-97
17540780-11	2007	NaB effects on the NHE3 promoter were significantly attenuated by protein phosphatase (PP)1alpha- and PP2Aalpha-specific siRNA transfection.	nab	0-3	solute carrier family 9 member A3	Homo sapiens	19-23
17540780-11	2007	NaB effects on the NHE3 promoter were significantly attenuated by protein phosphatase (PP)1alpha- and PP2Aalpha-specific siRNA transfection.	nab	0-3	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	87-96
17540780-11	2007	NaB effects on the NHE3 promoter were significantly attenuated by protein phosphatase (PP)1alpha- and PP2Aalpha-specific siRNA transfection.	nab	0-3	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	102-111
17540780-12	2007	Our data suggest that the differential regulation of NHE3 gene expression by NaB and IFN-gamma/TNF-alpha is mediated through alternative pathways that converge on Sp1/Sp3.	nab	77-80	solute carrier family 9 member A3	Homo sapiens	53-57
17540780-12	2007	Our data suggest that the differential regulation of NHE3 gene expression by NaB and IFN-gamma/TNF-alpha is mediated through alternative pathways that converge on Sp1/Sp3.	nab	77-80	Sp3 transcription factor	Homo sapiens	167-170
17579047-6	2007	Furthermore, we observed that NaB switched the differentiation of myelin basic protein-primed T cells from Th1 to Th2 mode, enriched regulatory T cell population, and down-regulated the expression of various contact molecules in T cells.	nab	30-33	negative elongation factor complex member C/D, Th1l	Mus musculus	107-110
17579047-6	2007	Furthermore, we observed that NaB switched the differentiation of myelin basic protein-primed T cells from Th1 to Th2 mode, enriched regulatory T cell population, and down-regulated the expression of various contact molecules in T cells.	nab	30-33	heart and neural crest derivatives expressed 2	Mus musculus	114-117
17344314-3	2007	Our previously published observations indicated that this induction is Ser/Thr kinase dependent and that NaB-responsive elements were localized within -320/-34 bp of the rat NHE3 promoter.	nab	105-108	solute carrier family 9 member A3	Rattus norvegicus	174-178
17344314-4	2007	Here we further delineate the mechanism of NaB-mediated NHE3 gene transcription.	nab	43-46	solute carrier family 9 member A3	Rattus norvegicus	56-60
17344314-5	2007	Transient and stable transfection of Caco-2 cells with NHE3 gene reporter constructs identified Sp binding site SpB at position -58/-55 nt as critical for NaB-mediated induction.	nab	155-158	surfactant protein B	Homo sapiens	112-115
17344314-6	2007	Gel mobility shift (GMSA) and DNA affinity precipitation assays indicated NaB-induced binding of Sp3 and decreased binding of Sp1 to SpB element.	nab	74-77	Sp3 transcription factor	Rattus norvegicus	97-100
17344314-6	2007	Gel mobility shift (GMSA) and DNA affinity precipitation assays indicated NaB-induced binding of Sp3 and decreased binding of Sp1 to SpB element.	nab	74-77	surfactant protein B	Rattus norvegicus	133-136
17344314-7	2007	While no changes in expression of Sp1 or Sp3 were noted, NaB induced phosphorylation of Sp1 and acetylation of Sp3.	nab	57-60	Sp3 transcription factor	Rattus norvegicus	111-114
17344314-11	2007	GMSA identified a protein-DNA complex with a -196/-175 nt probe; this interaction was not affected by NaB treatment, thus suggesting that in response to NaB Sp3 binding to site SpB precedes and results in recruitment of the putative factor to this upstream site.	nab	153-156	Sp3 transcription factor	Rattus norvegicus	157-160
17344314-11	2007	GMSA identified a protein-DNA complex with a -196/-175 nt probe; this interaction was not affected by NaB treatment, thus suggesting that in response to NaB Sp3 binding to site SpB precedes and results in recruitment of the putative factor to this upstream site.	nab	153-156	surfactant protein B	Rattus norvegicus	177-180
17420930-4	2007	Significantly lower pre- and post-dose blood levels of IFN induced markers, except for postdose PKR-mRNA (p = 0.09), were seen in NAB+ compared with NAB-patients and between patients with high (&gt; 200 t(1/10)) and low ( pound 200 t(1/10)) NAB titers.	nab	130-133	interferon alpha 1	Homo sapiens	55-58
17692727-17	2007	The proportions of NAb+ patients with high NAb titers (&gt;1000 NU/mL) at week 48 were 11.1% in the RNF study and 19.5% in the EVIDENCE study.	nab	19-22	tripartite motif containing 31	Homo sapiens	100-103
17420930-4	2007	Significantly lower pre- and post-dose blood levels of IFN induced markers, except for postdose PKR-mRNA (p = 0.09), were seen in NAB+ compared with NAB-patients and between patients with high (&gt; 200 t(1/10)) and low ( pound 200 t(1/10)) NAB titers.	nab	149-152	interferon alpha 1	Homo sapiens	55-58
17548440-2	2007	However, data from pivotal trials of IFN-beta in MS suggest that NAb-positive patients may have a reduced relapse rate during the first six to 12 months of therapy.	nab	65-68	interferon beta 1	Homo sapiens	37-45
17548440-6	2007	This is in accordance with observations in randomised studies of the three different IFN-beta preparations, showing that patients who become NAb-positive have lower relapse rates during the first six or 12 months of therapy.	nab	141-144	interferon beta 1	Homo sapiens	85-93
17407191-6	2007	These results lend further support to the idea that polymorphic carbohydrates of the Gal alpha1,3Gal/ABO type serve as important targets for NAb and C" and that their expression on virus has influenced their evolution by contributing to protection against viral transmission within as well as between species.	nab	141-144	ABO, alpha 1-3-N-acetylgalactosaminyltransferase and alpha 1-3-galactosyltransferase	Homo sapiens	89-104
17420930-5	2007	A significant inverse correlation between NAB titer and pre-dose levels of the above IFN-induced markers was found.	nab	42-45	interferon alpha 1	Homo sapiens	85-88
17420930-4	2007	Significantly lower pre- and post-dose blood levels of IFN induced markers, except for postdose PKR-mRNA (p = 0.09), were seen in NAB+ compared with NAB-patients and between patients with high (&gt; 200 t(1/10)) and low ( pound 200 t(1/10)) NAB titers.	nab	149-152	interferon alpha 1	Homo sapiens	55-58
17161819-3	2007	In this study, three types of short chain fatty acids (sodium butyrate (NaB), sodium phenylbutyrate (NaPB), sodium phenylacetate (NaPA)) were found to have anti-inflammatory effects in IFN-gamma-stimulated RAW 264.7 cells.	nab	72-75	interferon gamma	Mus musculus	185-194
17131381-5	2007	Treatment of colon cancer cells SW480 with sodium butyrate (NaB), which induces colon cancer cell differentiation, can induce the upregulation of GCIP expression, suggesting that the protein functions as a negative regulator in cell proliferation.	nab	60-63	cyclin D1 binding protein 1	Homo sapiens	146-150
17439886-10	2007	In conclusion, NAbs to IFNbeta are common in a clinical setting and the IFNbeta preparations differ not only in NAb seroprevalence, but also in immunogenicity.	nab	15-18	interferon beta 1	Homo sapiens	23-30
17439886-10	2007	In conclusion, NAbs to IFNbeta are common in a clinical setting and the IFNbeta preparations differ not only in NAb seroprevalence, but also in immunogenicity.	nab	15-18	interferon beta 1	Homo sapiens	72-79
17082793-2	2007	The overall low expression levels of the Coxsackie and Adenovirus receptor and the presence of high anti-Ad5-neutralizing antibody (NAb) titers in the human population are considered detrimental for consistency of clinical results.	nab	132-135	Alzheimer disease, familial, type 5	Homo sapiens	105-108
17082793-6	2007	Our results demonstrate that the sero prevalence and the titers of NAb against Ad35 are significantly lower than against Ad5.	nab	67-70	Alzheimer disease, familial, type 5	Homo sapiens	121-124
17267498-11	2007	(ii) DNA vaccination with monomeric gp120-based antigens can elicit a consistent NAb response against the homologous neutralization-resistant virus by targeting epitopes outside the V1, V2, and V3 regions.	nab	81-84	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	36-41
17389300-4	2007	In addition, the rate of NAb production is probably less with IFNbeta-1a treatment than with IFNbeta-1b treatment, although the magnitude and persistence of this difference is difficult to determine (Level B).	nab	25-28	interferon beta 1	Homo sapiens	62-69
17389300-4	2007	In addition, the rate of NAb production is probably less with IFNbeta-1a treatment than with IFNbeta-1b treatment, although the magnitude and persistence of this difference is difficult to determine (Level B).	nab	25-28	interferon beta 1	Homo sapiens	93-100
17389300-8	2007	Although the finding of sustained high-titer NAbs (&gt;100 to 200 NU/mL) is associated with a reduction in the therapeutic effects of IFNbeta on radiographic and clinical measures of MS disease activity, there is insufficient information on the utilization of NAb testing to provide specific recommendations regarding when to test, which test to use, how many tests are necessary, or which cutoff titer to apply (Level U).	nab	45-48	interferon beta 1	Homo sapiens	134-141
17161819-5	2007	Their potency as anti-inflammatory agents was in the order of NaB&gt;NaPB&gt;NaPA.	nab	62-65	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	69-73
17161819-8	2007	The potency of NF-kappaB and ERK inhibition was also in the order of NaB&gt;NaPB&gt;NaPA.	nab	69-72	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	15-24
17161819-8	2007	The potency of NF-kappaB and ERK inhibition was also in the order of NaB&gt;NaPB&gt;NaPA.	nab	69-72	mitogen-activated protein kinase 1	Mus musculus	29-32
17161819-8	2007	The potency of NF-kappaB and ERK inhibition was also in the order of NaB&gt;NaPB&gt;NaPA.	nab	69-72	N-ethylmaleimide sensitive fusion protein attachment protein beta	Mus musculus	76-80
17432596-1	2007	We investigated the role of p38alpha stress-kinase in regulation of premature senescence program, stimulated by histone deacetylase inhibitor--sodium butyrate (NaB)--after application to rodent transformed cell lines.	nab	160-163	mitogen-activated protein kinase 14	Mus musculus	28-36
17016586-12	2006	Therefore, only subsets of molecular events that determine the PAX8 mRNA splicing heterogeneity in bladder tumours are sensitive to NaB treatment.	nab	132-135	paired box 8	Homo sapiens	63-67
17158768-6	2006	We could demonstrate that HDAC inhibition dose-dependently inhibited proliferation of both cell lines with IC50 values varying from the millimolar (NaB) to the micromolar (MS-275) and the nanomolar range (TSA).	nab	148-151	histone deacetylase 9	Homo sapiens	26-30
16541197-2	2006	Confluent human dermal fibroblasts were treated with 2 mM and 4 mM of sodium butyrate (NaB) for 48 h. It was found that butyrate induced collagen biosynthesis and prolidase activity independently of alpha2beta1 integrin signaling.	nab	87-90	peptidase D	Homo sapiens	163-172
17009592-4	2006	The results indicated that a group of heat shock protein (hsp) genes were upregulated by 3 mM NaB within the first 24 hours of exposure.	nab	94-97	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	38-56
17009592-4	2006	The results indicated that a group of heat shock protein (hsp) genes were upregulated by 3 mM NaB within the first 24 hours of exposure.	nab	94-97	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	58-61
17009592-5	2006	Because the transcription of hsp genes is under the control of heat shock factors (HSFs), we measured the effects of overexpressed HSF-1 on the responses of HT 29 cells to NaB.	nab	172-175	heat shock protein 90 beta family member 2, pseudogene	Homo sapiens	29-32
17009592-5	2006	Because the transcription of hsp genes is under the control of heat shock factors (HSFs), we measured the effects of overexpressed HSF-1 on the responses of HT 29 cells to NaB.	nab	172-175	heat shock transcription factor 1	Homo sapiens	131-136
17009592-6	2006	Overexpression of HSF-1 inhibited NaB-induced differentiation as measured by alkaline phosphatase activity and carcinoembryonic antigen expression.	nab	34-37	heat shock transcription factor 1	Homo sapiens	18-23
16574654-3	2006	To understand the molecular mechanisms underlying NAB repression, we found that EGR activity is modulated by at least two repression domains within NAB2, one of which uniquely requires interaction with the CHD4 (chromodomain helicase DNA-binding protein 4) subunit of the NuRD (nucleosome remodeling and deacetylase) chromatin remodeling complex.	nab	50-53	NGFI-A binding protein 2	Homo sapiens	148-152
16574654-3	2006	To understand the molecular mechanisms underlying NAB repression, we found that EGR activity is modulated by at least two repression domains within NAB2, one of which uniquely requires interaction with the CHD4 (chromodomain helicase DNA-binding protein 4) subunit of the NuRD (nucleosome remodeling and deacetylase) chromatin remodeling complex.	nab	50-53	chromodomain helicase DNA binding protein 4	Homo sapiens	206-210
16574654-3	2006	To understand the molecular mechanisms underlying NAB repression, we found that EGR activity is modulated by at least two repression domains within NAB2, one of which uniquely requires interaction with the CHD4 (chromodomain helicase DNA-binding protein 4) subunit of the NuRD (nucleosome remodeling and deacetylase) chromatin remodeling complex.	nab	50-53	chromodomain helicase DNA binding protein 4	Homo sapiens	212-255
16699007-7	2006	Histone deacetylase inhibitors, including sodium butyrate (NaB) and trichostatin A, caused the rapid dissociation of LANA from the ORF50 promoter.	nab	59-62	LANA	Human gammaherpesvirus 8	117-121
16699007-7	2006	Histone deacetylase inhibitors, including sodium butyrate (NaB) and trichostatin A, caused the rapid dissociation of LANA from the ORF50 promoter.	nab	59-62	ORF50	Human gammaherpesvirus 8	131-136
16699007-8	2006	NaB treatment of latently infected BCBL1 cells disrupted a stable interaction between LANA and the cellular proteins Sp1 and histone H2B.	nab	0-3	LANA	Human gammaherpesvirus 8	86-90
16699007-9	2006	We also found immunological and radiochemical evidence that LANA is subject to lysine acetylation after NaB treatment.	nab	104-107	LANA	Human gammaherpesvirus 8	60-64
16886664-7	2006	Targeted co-treatments of 1alpha25(OH)2D3 plus HDAC inhibitors (TSA, NaB) resulted in re-expression of antiproliferative target genes (e.g., GADD45alpha, p21(waf1/cip1)) and synergistic inhibition of proliferation.	nab	69-72	growth arrest and DNA damage inducible alpha	Homo sapiens	141-152
16886664-7	2006	Targeted co-treatments of 1alpha25(OH)2D3 plus HDAC inhibitors (TSA, NaB) resulted in re-expression of antiproliferative target genes (e.g., GADD45alpha, p21(waf1/cip1)) and synergistic inhibition of proliferation.	nab	69-72	cyclin dependent kinase inhibitor 1A	Homo sapiens	154-168
16632996-3	2006	TGF-beta is an important tumor suppressor in the gut and has many similar biologic activities as NaB.	nab	97-100	transforming growth factor, beta 1	Rattus norvegicus	0-8
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	183-186	mitogen-activated protein kinase 1	Homo sapiens	50-87
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	183-186	mitogen-activated protein kinase 1	Homo sapiens	89-92
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	183-186	sodium voltage-gated channel alpha subunit 4	Homo sapiens	149-154
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	275-278	mitogen-activated protein kinase 1	Homo sapiens	50-87
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	275-278	mitogen-activated protein kinase 1	Homo sapiens	89-92
16800929-1	2006	The study was purposed to investigate the role of extracellular signal-regulated kinase (ERK) pathway in the differentiation of human MDS cell lines SKM-1 induced by sodium butyrate (NaB), and to elucidate the molecular mechanism of differentiation in SKM-1 cells induced by NaB.	nab	275-278	sodium voltage-gated channel alpha subunit 4	Homo sapiens	252-257
16800929-3	2006	The effect of NaB in combination with the ERK inhibitor PD98059 on the proliferation/differentiation of SKM-1 cells was studied, and then the expression levels of the P21 and HDAC protein were detected by Western blot.	nab	14-17	sodium voltage-gated channel alpha subunit 4	Homo sapiens	104-109
16800929-4	2006	The results showed that the expression level of phosphorylated ERK was down-regulated by the 1 mmol/L NaB, and the level of total ERK had not changed.	nab	102-105	mitogen-activated protein kinase 1	Homo sapiens	63-66
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	0-3	sodium voltage-gated channel alpha subunit 4	Homo sapiens	99-104
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	0-3	H3 histone pseudogene 16	Homo sapiens	146-149
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	0-3	histone deacetylase 9	Homo sapiens	154-158
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	mitogen-activated protein kinase kinase 7	Homo sapiens	26-29
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	sodium voltage-gated channel alpha subunit 4	Homo sapiens	99-104
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	H3 histone pseudogene 16	Homo sapiens	146-149
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	histone deacetylase 9	Homo sapiens	154-158
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	mitogen-activated protein kinase kinase 7	Homo sapiens	26-29
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	sodium voltage-gated channel alpha subunit 4	Homo sapiens	99-104
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	H3 histone pseudogene 16	Homo sapiens	146-149
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	histone deacetylase 9	Homo sapiens	154-158
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	mitogen-activated protein kinase kinase 7	Homo sapiens	26-29
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	sodium voltage-gated channel alpha subunit 4	Homo sapiens	99-104
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	H3 histone pseudogene 16	Homo sapiens	146-149
16800929-5	2006	NaB or combination of the MEK inhibitor PD98059 with NaB could increase the differentiation of the SKM-1 cells and up-regulated the levels of the P21 and HDAC protein, but the effect of combination of NaB with PD98059 was higher than that of NaB alone.	nab	53-56	histone deacetylase 9	Homo sapiens	154-158
16632996-4	2006	Therefore, we hypothesized that the chemo-preventive effects of NaB are mediated in part by enhancing TGF-beta signaling and its tumor suppressor function in the gut.	nab	64-67	transforming growth factor, beta 1	Rattus norvegicus	102-110
16632996-5	2006	METHODS: The effects of NaB on Smad3 expression in rat intestinal epithelial (RIE-1) cells and 6 human colon cancer cell lines were examined.	nab	24-27	SMAD family member 3	Rattus norvegicus	31-36
16632996-6	2006	The effects of NaB on TGF-beta-induced Smad3 phosphorylation and plasminogen activator inhibitor-1 (PAI-1) and cyclooxygenase-2 (COX-2) gene expression were also examined in RIE-1 cells.	nab	15-18	transforming growth factor, beta 1	Rattus norvegicus	22-30
16632996-8	2006	RESULTS: NaB induced Smad3 in RIE-1 cells and in 4 human colon cancer cell lines.	nab	9-12	SMAD family member 3	Homo sapiens	21-26
16632996-9	2006	NaB enhanced TGF-beta-induced Smad3 phosphorylation and potentiated TGF-beta-induced PAI-1 expression.	nab	0-3	transforming growth factor, beta 1	Rattus norvegicus	13-21
16632996-9	2006	NaB enhanced TGF-beta-induced Smad3 phosphorylation and potentiated TGF-beta-induced PAI-1 expression.	nab	0-3	SMAD family member 3	Rattus norvegicus	30-35
16632996-9	2006	NaB enhanced TGF-beta-induced Smad3 phosphorylation and potentiated TGF-beta-induced PAI-1 expression.	nab	0-3	transforming growth factor, beta 1	Rattus norvegicus	68-76
16632996-9	2006	NaB enhanced TGF-beta-induced Smad3 phosphorylation and potentiated TGF-beta-induced PAI-1 expression.	nab	0-3	serpin family E member 1	Rattus norvegicus	85-90
16632996-10	2006	NaB and TGF-beta synergistically inhibited anchorage-independent growth of Akt-transformed RIE-1 cells.	nab	0-3	AKT serine/threonine kinase 1	Rattus norvegicus	75-78
16632996-11	2006	CONCLUSIONS: These results demonstrate that NaB induces Smad3 and potentiates TGF-beta signaling and its tumor suppressor activity in gut epithelial cells.	nab	44-47	SMAD family member 3	Rattus norvegicus	56-61
16632996-11	2006	CONCLUSIONS: These results demonstrate that NaB induces Smad3 and potentiates TGF-beta signaling and its tumor suppressor activity in gut epithelial cells.	nab	44-47	transforming growth factor, beta 1	Rattus norvegicus	78-86
16465425-3	2006	In this study, we investigated whether anticancer drugs could directly induce MVP protein or gene expression in the SW-620 human colorectal cancer cell line, in which MVP has been shown to be induced by the differentiation-inducing agent, sodium butyrate (NaB).	nab	256-259	major vault protein	Homo sapiens	167-170
16716107-6	2006	Immunogenicity of the AdH5-based vaccine was significantly attenuated or completely abolished when the preexisting anti-AdH5 NAb titer was higher than 40.	nab	125-128	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	22-26
16716107-6	2006	Immunogenicity of the AdH5-based vaccine was significantly attenuated or completely abolished when the preexisting anti-AdH5 NAb titer was higher than 40.	nab	125-128	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	120-124
16716107-7	2006	Because 27% of human serum samples from the United States tested so far have an anti-AdH5 NAb titer higher than 40, our results suggested that a significant percentage of humans with preexisting anti-AdH5 immunity would not be candidates for vaccination with an AdH5-based genetic vaccine.	nab	90-93	alcohol dehydrogenase 5 (class III), chi polypeptide	Homo sapiens	85-89
16734381-12	2006	Further experiments showed that Sp1, Sp3, CREB-binding protein (CBP), p300, and histone deacetylase (HDAC) were physically associated and HDAC inhibitors (trichostatin A or NaB) upregulated COL11A2 promoter activity and endogenous gene expression.	nab	173-176	Sp3 transcription factor	Homo sapiens	37-40
16734381-12	2006	Further experiments showed that Sp1, Sp3, CREB-binding protein (CBP), p300, and histone deacetylase (HDAC) were physically associated and HDAC inhibitors (trichostatin A or NaB) upregulated COL11A2 promoter activity and endogenous gene expression.	nab	173-176	CREB binding protein	Homo sapiens	42-62
16734381-12	2006	Further experiments showed that Sp1, Sp3, CREB-binding protein (CBP), p300, and histone deacetylase (HDAC) were physically associated and HDAC inhibitors (trichostatin A or NaB) upregulated COL11A2 promoter activity and endogenous gene expression.	nab	173-176	CREB binding protein	Homo sapiens	64-67
16734381-12	2006	Further experiments showed that Sp1, Sp3, CREB-binding protein (CBP), p300, and histone deacetylase (HDAC) were physically associated and HDAC inhibitors (trichostatin A or NaB) upregulated COL11A2 promoter activity and endogenous gene expression.	nab	173-176	E1A binding protein p300	Homo sapiens	70-74
16734381-12	2006	Further experiments showed that Sp1, Sp3, CREB-binding protein (CBP), p300, and histone deacetylase (HDAC) were physically associated and HDAC inhibitors (trichostatin A or NaB) upregulated COL11A2 promoter activity and endogenous gene expression.	nab	173-176	collagen type XI alpha 2 chain	Homo sapiens	190-197
16368144-9	2006	The anti-CS nAAbs by participating in the nAb network, could function in innate defense mechanisms and at the same time recognize a target antigen (nucleosome) in a systemic autoimmune disease.	nab	42-45	citrate synthase	Homo sapiens	9-11
16421483-7	2006	RESULTS: DAF knockout (KO) but not wild-type (WT) grafts showed hyperacute or acute humoral rejection in nonsensitized GalT KO mice with low levels of anti-alphaGal IgM NAb.	nab	169-172	CD55 molecule, decay accelerating factor for complement	Mus musculus	9-12
16466595-10	2006	The odds of relapse during a NAb+ period are between 1.51 and 1.58 (p &lt; 0.03) with the time to first relapse being shortened by an average of 244 days after 12 months of IFN-beta therapy.	nab	29-32	interferon beta 1	Homo sapiens	173-181
16461476-2	2006	This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats.	nab	70-73	trefoil factor 3	Rattus norvegicus	130-146
16461476-2	2006	This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats.	nab	70-73	trefoil factor 3	Rattus norvegicus	148-152
16461476-2	2006	This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats.	nab	70-73	interleukin 1 beta	Rattus norvegicus	155-172
16461476-2	2006	This study evaluates effects of topical treatment of sodium butyrate (NaB) and 5-aminosalicylic acid (5-ASA) on the expression of trefoil factor 3 (TFF3), interleukin 1beta (IL1beta), and nuclear factor kappaB (NFkappaB) in trinitrobenzene sulphonic acid (TNBS) induced colitis in rats.	nab	70-73	interleukin 1 beta	Rattus norvegicus	174-181
16461476-5	2006	RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression.	nab	22-25	myeloperoxidase	Rattus norvegicus	100-103
16461476-5	2006	RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression.	nab	22-25	trefoil factor 3	Rattus norvegicus	126-130
16461476-5	2006	RESULTS: Treatment of NaB, 5-ASA, and the combination improved diarrhoea, colonic damage score, and MPO activities, increased TFF3 mRNA expression, and decreased serum IL1beta production and tissue NFkappaB expression.	nab	22-25	interleukin 1 beta	Rattus norvegicus	168-175
16461476-7	2006	CONCLUSIONS: The combination of topical treatment of NaB and 5-ASA was effective for relieving and repairing colonic inflammation and the effects were related to stimulation of TFF3 mRNA expression and down-regulation of IL1beta production and NFkappaB expression.	nab	53-56	trefoil factor 3	Rattus norvegicus	177-181
16461476-7	2006	CONCLUSIONS: The combination of topical treatment of NaB and 5-ASA was effective for relieving and repairing colonic inflammation and the effects were related to stimulation of TFF3 mRNA expression and down-regulation of IL1beta production and NFkappaB expression.	nab	53-56	interleukin 1 beta	Rattus norvegicus	221-228
16421483-10	2006	These studies demonstrate the physiologic role of DAF in preventing humoral rejection in the presence of low levels of NAb and have implications for transplantation of discordant vascularized xenografts.	nab	119-122	CD55 molecule, decay accelerating factor for complement	Mus musculus	50-53
16305739-5	2005	NCoA3 gene expression is upregulated following NaB treatment of latently infected cells whereas IRF8 gene expression is strongly downregulated in the promonocytic cell line following NaB treatment.	nab	47-50	nuclear receptor coactivator 3	Homo sapiens	0-5
16305739-5	2005	NCoA3 gene expression is upregulated following NaB treatment of latently infected cells whereas IRF8 gene expression is strongly downregulated in the promonocytic cell line following NaB treatment.	nab	183-186	interferon regulatory factor 8	Homo sapiens	96-100
16305739-7	2005	Moreover, NCoA3 gene expression was also upregulated after treatment of U1 and ACH-2 cells with phorbol myristyl acetate (PMA) but not trichostatin A (TSA) and after treatment with NaB of two others HIV-1 latently infected cell lines (OM10.1 and J1.1).	nab	181-184	nuclear receptor coactivator 3	Homo sapiens	10-15
16083714-6	2005	The effect of CA-MEK on sodium butyrate (NaB)-induced apoptosis was evaluated by the Annexin V assay.	nab	41-44	annexin A5	Rattus norvegicus	85-94
16343270-11	2006	Treatment with NaB increased the expression of p21 in JeKo-1 and Hbl-2 cells, while in Granta 519 cells no effect was noted.	nab	15-18	H3 histone pseudogene 16	Homo sapiens	47-50
16343270-12	2006	The expression of p27 remained constant in all three cell lines after exposure to NaB.	nab	82-85	interferon alpha inducible protein 27	Homo sapiens	18-21