PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
35280925-7	2022	After co-injection with AAV overexpressing alpha-synuclein (aSyn) into mouse SN (PD model), we found that moderate miR-181a/b overexpression exacerbated aSyn-induced DA neuronal loss, whereas miR-181 inhibition was neuroprotective relative to controls (GFP alone and/or scrambled RNA).	Dopamine	166-168	microRNA 181a-2	Mus musculus	115-125
34538100-13	2021	In conclusion, downregulation of the miR-181a gene led to increased BP and salt sensitivity in mice.	Salts	75-79	microRNA 181a-2	Mus musculus	37-45
35201360-7	2022	The miRNA profile of MVs in BALF was altered after ozone exposure; thus, increases in miR-21, miR-145, mi320a, miR-155, let-7b, miR744, miR181, miR-17, miR-92a, and miR-199a-3p were observed, whereas miR-24-3p and miR-20 were reduced.	Ozone	51-56	microRNA 181a-2	Mus musculus	136-142
32338107-10	2020	Bioinformatics prediction and western blotting methods validated the targets of miR-181a in vitro.Results: Curcumin treatment alleviated cisplatin-induced nephrotoxicity as validated by the blood urea nitrogen (BUN) values, and histological analysis of kidneys.	Curcumin	107-115	microRNA 181a-2	Mus musculus	80-88
31185507-8	2021	Both DMOG and Ac-LETD-CHO increased HIF-1alpha expression paralleled with the suppression of miR-126-5p, miR-128-3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138-5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.	oxalylglycine	5-9	microRNA 181a-2	Mus musculus	120-127
31185507-8	2021	Both DMOG and Ac-LETD-CHO increased HIF-1alpha expression paralleled with the suppression of miR-126-5p, miR-128-3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138-5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.	ac-letd	14-21	microRNA 181a-2	Mus musculus	120-127
31185507-8	2021	Both DMOG and Ac-LETD-CHO increased HIF-1alpha expression paralleled with the suppression of miR-126-5p, miR-128-3p and miR-181 expression and upregulation of miR-26b, 106a-5p, 106b-5p, 135a-5p, 135b-5p, 138-5p, 199a-5p, 200a-3p and 200c-3p expression.We demonstrate a mechanistic link for the DMOG and Ac-LETD-CHO protection against hyperglycaemia-induced neuronal dysfunction, DNA damage and apoptosis and thereby propose that pharmacological agents mimicking these effects may represent a promising novel therapy for the hyperglycaemia-induced neuropathy.	CAV protocol	22-25	microRNA 181a-2	Mus musculus	120-127
32338107-12	2020	We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells.Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.	Curcumin	276-284	microRNA 181a-2	Mus musculus	142-150
32338107-10	2020	Bioinformatics prediction and western blotting methods validated the targets of miR-181a in vitro.Results: Curcumin treatment alleviated cisplatin-induced nephrotoxicity as validated by the blood urea nitrogen (BUN) values, and histological analysis of kidneys.	Cisplatin	137-146	microRNA 181a-2	Mus musculus	80-88
32338107-12	2020	We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells.Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.	Cisplatin	298-307	microRNA 181a-2	Mus musculus	142-150
32338107-10	2020	Bioinformatics prediction and western blotting methods validated the targets of miR-181a in vitro.Results: Curcumin treatment alleviated cisplatin-induced nephrotoxicity as validated by the blood urea nitrogen (BUN) values, and histological analysis of kidneys.	Urea	196-200	microRNA 181a-2	Mus musculus	80-88
32338107-10	2020	Bioinformatics prediction and western blotting methods validated the targets of miR-181a in vitro.Results: Curcumin treatment alleviated cisplatin-induced nephrotoxicity as validated by the blood urea nitrogen (BUN) values, and histological analysis of kidneys.	Nitrogen	201-209	microRNA 181a-2	Mus musculus	80-88
32338107-11	2020	At the molecular level, curcumin treatment decreased miR-181a expression level, which was induced by cisplatin and restored the in vivo expression of PTEN, which was suppressed by cisplatin.	Curcumin	24-32	microRNA 181a-2	Mus musculus	53-61
32338107-11	2020	At the molecular level, curcumin treatment decreased miR-181a expression level, which was induced by cisplatin and restored the in vivo expression of PTEN, which was suppressed by cisplatin.	Cisplatin	101-110	microRNA 181a-2	Mus musculus	53-61
32338107-11	2020	At the molecular level, curcumin treatment decreased miR-181a expression level, which was induced by cisplatin and restored the in vivo expression of PTEN, which was suppressed by cisplatin.	Cisplatin	180-189	microRNA 181a-2	Mus musculus	53-61
32338107-12	2020	We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells.Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.	Curcumin	193-201	microRNA 181a-2	Mus musculus	45-53
32338107-12	2020	We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells.Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.	Curcumin	193-201	microRNA 181a-2	Mus musculus	142-150
32338107-12	2020	We verified the direct regulation of PTEN by miR-181a in cultured human embryonic kidney 293T cells.Conclusions: We showed the involvement of miR-181a/PTEN axis in the renoprotective effect of curcumin against cisplatin-induced AKI, and provide new evidence on the ability of curcumin to alleviate cisplatin-induced nephrotoxicity.	Cisplatin	210-219	microRNA 181a-2	Mus musculus	142-150
32087004-6	2020	Additionally, Abeta treatment inhibited cLTP-dependent induction of translin and subsequent reduction of miR-181a, and cotreatment with miR-181a antagomir effectively reversed the effects elicited by Abeta but did not rescue translin levels, suggesting that the activity-dependent upregulation of translin was upstream of miR-181a.	cltp	40-44	microRNA 181a-2	Mus musculus	105-113
32297422-10	2020	miR-153 was elevated but miR-181a was reduced in LD BPA offspring.	bisphenol A	52-55	microRNA 181a-2	Mus musculus	25-33
32633406-0	2020	Morphine induces the apoptosis of mouse hippocampal neurons HT-22 through upregulating miR-181-5p.	Morphine	0-8	microRNA 181a-2	Mus musculus	87-94
32633406-6	2020	MiR-181-5p was upregulated and MAPK1 was downregulated in HT-22 cells by morphine induction.	Morphine	73-81	microRNA 181a-2	Mus musculus	0-7
32633406-7	2020	Knockdown of miR-181-5p enhanced viability and proliferative ability, as well as reduced apoptosis in morphine-induced HT-22 cells.	Morphine	102-110	microRNA 181a-2	Mus musculus	13-20
32633406-9	2020	Knockdown of MAPK1 was able to reverse the regulatory effects of miR-181-5p on morphine-induced phenotype changes of HT-22 cells.	Morphine	79-87	microRNA 181a-2	Mus musculus	65-72
32633406-10	2020	CONCLUSIONS: Morphine induces apoptosis of hippocampal neurons HT-22 by upregulating miR-181-5p to suppress the level of MAPK1.	Morphine	13-21	microRNA 181a-2	Mus musculus	85-92
31115560-3	2019	The MM cell line RPMI 8226 stably transduced with miR-181a mimics or inhibitor was established via lentiviral vectors.	rpmi 8226	17-26	microRNA 181a-2	Mus musculus	50-58
32087004-6	2020	Additionally, Abeta treatment inhibited cLTP-dependent induction of translin and subsequent reduction of miR-181a, and cotreatment with miR-181a antagomir effectively reversed the effects elicited by Abeta but did not rescue translin levels, suggesting that the activity-dependent upregulation of translin was upstream of miR-181a.	UNII-042A8N37WH	14-19	microRNA 181a-2	Mus musculus	105-113
30938884-10	2019	When we knocked down miR-181a and then treated cells with U0126 before ox-LDL stimulation, we found that U0126 reversed the increased activation of the MEK/ERK/NF-kappaB pathway and upregulation of NLRP3 inflammasome-related proteins (NLRP3, caspase-1, IL-18, IL-1beta) that resulted from miR-181a knockdown.	U 0126	58-63	microRNA 181a-2	Mus musculus	289-297
30938884-10	2019	When we knocked down miR-181a and then treated cells with U0126 before ox-LDL stimulation, we found that U0126 reversed the increased activation of the MEK/ERK/NF-kappaB pathway and upregulation of NLRP3 inflammasome-related proteins (NLRP3, caspase-1, IL-18, IL-1beta) that resulted from miR-181a knockdown.	U 0126	105-110	microRNA 181a-2	Mus musculus	21-29
30938884-10	2019	When we knocked down miR-181a and then treated cells with U0126 before ox-LDL stimulation, we found that U0126 reversed the increased activation of the MEK/ERK/NF-kappaB pathway and upregulation of NLRP3 inflammasome-related proteins (NLRP3, caspase-1, IL-18, IL-1beta) that resulted from miR-181a knockdown.	U 0126	105-110	microRNA 181a-2	Mus musculus	289-297
31563103-5	2020	Sixteen miRNAs in hippocampus of pups on PND 35 were significantly affected by MCLR exposure with the markedly decreased transcription of miR-181a-5p.	cyanoginosin LR	79-83	microRNA 181a-2	Mus musculus	138-146
31563103-6	2020	We then found that miR-181a-5p was down-regulated, accompanied by activation of ER stress after prenatal exposure to MCLR using qPCR analysis.	cyanoginosin LR	117-121	microRNA 181a-2	Mus musculus	19-27
31563103-7	2020	Furthermore, glucose-regulated protein, 78kDa/binding immunoglobulin protein (Grp78/BIP), a major ER chaperone and signaling regulator, was identified as a target of miR-181a-5p.	Glucose	13-20	microRNA 181a-2	Mus musculus	166-174
31563103-9	2020	Our findings indicate that the up-regulation of Grp78 mediated by inhibition of miR-181a-5p is a possible mechanism resulting in ER stress and cognitive impairment in pups following prenatal MCLR exposure.	cyanoginosin LR	191-195	microRNA 181a-2	Mus musculus	80-88
31341031-6	2019	Here, we report the results of systemic treatment with anti-miRNA oligonucleotides (AMOs) directed against miR-181a utilizing a nanopiece delivery platform (NP).	Oligonucleotides	66-82	microRNA 181a-2	Mus musculus	107-115
31413305-3	2019	One such substance, miR-181, reduces plasma triglyceride levels in mice by targeting isocitrate dehydrogenase 1.	Triglycerides	44-56	microRNA 181a-2	Mus musculus	20-27
28382720-4	2017	ADSCs were engineered to overexpress miRNA-181-5p (miR-181-5p-ADSCs) to selectively home exosomes to mouse hepatic stellate (HST-T6) cells or a CCl4-induced liver fibrosis murine model and compared with non-targeting control Caenorhabditis elegans miR-67 (cel-miR-67)-ADSCs.	Carbon Tetrachloride	144-148	microRNA 181a-2	Mus musculus	51-58
30565672-11	2019	RESULTS: ANRIL and Prox1 were downregulated, whereas miR-181a was upregulated in the diabetic wound healing mouse model and high glucose (HG)-induced LECs.	Glucose	129-136	microRNA 181a-2	Mus musculus	53-61
29737518-9	2018	Moreover, miR-181a mimics repressed foam cell formation, TC and TG levels induced by ox-LDL dramatically.	Technetium	57-59	microRNA 181a-2	Mus musculus	10-18
29737518-9	2018	Moreover, miR-181a mimics repressed foam cell formation, TC and TG levels induced by ox-LDL dramatically.	Thioguanine	64-66	microRNA 181a-2	Mus musculus	10-18
30170081-1	2018	We have previously reported that the miR-181a/Prox1/Notch1 pathway mediates the effect of morphine on modulating lineage-specific differentiation of adult neural stem/progenitor cells (NSPCs) via a PKCepsilon-dependent pathway, whereas fentanyl shows no such effect.	Morphine	90-98	microRNA 181a-2	Mus musculus	37-45
30170081-1	2018	We have previously reported that the miR-181a/Prox1/Notch1 pathway mediates the effect of morphine on modulating lineage-specific differentiation of adult neural stem/progenitor cells (NSPCs) via a PKCepsilon-dependent pathway, whereas fentanyl shows no such effect.	Fentanyl	236-244	microRNA 181a-2	Mus musculus	37-45
31949789-11	2018	Overexpression of miR-181a promoted extracellular matrix under high glucose by measuring related indexes such as collagen I, collagen IV, and fibronectin, which could be reversed by miR-181a inhibitors (P<0.05).	Glucose	68-75	microRNA 181a-2	Mus musculus	18-26
29535629-6	2018	Moreover, miR-181a inhibits NF-kappaB activation and accumulation of reactive oxygen species (ROS) by targeting TLR4 expression.	Reactive Oxygen Species	69-92	microRNA 181a-2	Mus musculus	10-18
29535629-6	2018	Moreover, miR-181a inhibits NF-kappaB activation and accumulation of reactive oxygen species (ROS) by targeting TLR4 expression.	Reactive Oxygen Species	94-97	microRNA 181a-2	Mus musculus	10-18
29535629-8	2018	Therefore, we provide the first evidence for the negative regulation of miR-181a in LPS-induced inflammation via the suppression of ROS generation and TLR4-NF-kappaB pathway.	Reactive Oxygen Species	132-135	microRNA 181a-2	Mus musculus	72-80
31189717-4	2019	Here, we show that tryptophan-derived metabolites produced by the gut microbiota controlled the expression of the miR-181 family in white adipocytes in mice to regulate energy expenditure and insulin sensitivity.	Tryptophan	19-29	microRNA 181a-2	Mus musculus	114-121
31189717-7	2019	As we also found that MIR-181 expression in WAT and the plasma abundance of tryptophan-derived metabolites were dysregulated in a cohort of obese human children, the MIR-181 family may represent a potential therapeutic target to modulate WAT function in the context of obesity.	Tryptophan	76-86	microRNA 181a-2	Mus musculus	166-173
30949956-0	2019	The Neuroprotective Effect of miR-181a After Oxygen-Glucose Deprivation/Reperfusion and the Associated Mechanism.	oxygen-glucose	45-59	microRNA 181a-2	Mus musculus	30-38
30949956-1	2019	The level of miR-181a decreases rapidly in N2a cells following oxygen-glucose deprivation/reperfusion, but its role in this process is unclear.	oxygen-glucose	63-77	microRNA 181a-2	Mus musculus	13-21
30949956-9	2019	Pre-treatment with miR-181a mimicked the increase in the miR-181a level in N2a cells after oxygen-glucose deprivation/reperfusion, resulting in a significant decrease in the apoptosis rate.	oxygen-glucose	91-105	microRNA 181a-2	Mus musculus	19-27
30949956-9	2019	Pre-treatment with miR-181a mimicked the increase in the miR-181a level in N2a cells after oxygen-glucose deprivation/reperfusion, resulting in a significant decrease in the apoptosis rate.	oxygen-glucose	91-105	microRNA 181a-2	Mus musculus	57-65
30949956-13	2019	These findings suggest that miR-181a protects neurons from apoptosis by inhibiting reelin expression and regulating the Smac/IAP signaling pathway after oxygen-glucose deprivation/reperfusion injury.	Oxygen	153-159	microRNA 181a-2	Mus musculus	28-36
30949956-13	2019	These findings suggest that miR-181a protects neurons from apoptosis by inhibiting reelin expression and regulating the Smac/IAP signaling pathway after oxygen-glucose deprivation/reperfusion injury.	Glucose	160-167	microRNA 181a-2	Mus musculus	28-36
29608244-11	2018	The strong anti-angiogenic effect of miR-181a was also displayed on the retinal neovascularization of the in vivo mouse model of oxygen-induced retinopathy.	Oxygen	129-135	microRNA 181a-2	Mus musculus	37-45
29207650-7	2017	Conversely, silencing of miR-181a over-activates the sirtuin1-peroxisome proliferator-activated receptor-gamma coactivator-1alpha pathway, increases insulin sensitivity and glycogen content, and decreases gluconeogenesis and lipid synthesis in hepatocytes, even under non-esterified fatty acids treatment conditions.	Glycogen	173-181	microRNA 181a-2	Mus musculus	25-33
28245171-9	2017	Low expression of miR-181a was closely related to cervical cancer growth and oxaliplatin resistance.	Oxaliplatin	77-88	microRNA 181a-2	Mus musculus	18-26
29207650-7	2017	Conversely, silencing of miR-181a over-activates the sirtuin1-peroxisome proliferator-activated receptor-gamma coactivator-1alpha pathway, increases insulin sensitivity and glycogen content, and decreases gluconeogenesis and lipid synthesis in hepatocytes, even under non-esterified fatty acids treatment conditions.	Fatty Acids	283-294	microRNA 181a-2	Mus musculus	25-33
29207650-8	2017	Furthermore, miR-181a overexpression or sirtuin1 knockdown in mice increases lipid accumulation and decreases insulin sensitivity and glycogen content in the liver.	Glycogen	134-142	microRNA 181a-2	Mus musculus	13-21
29207650-9	2017	Taken together, these findings indicate that increased hepatic miR-181a impairs glucose and lipid homeostasis by silencing sirtuin1 in non-alcoholic fatty liver disease.	Glucose	80-87	microRNA 181a-2	Mus musculus	63-71
25652854-1	2015	OBJECTIVE: To study the effect of Bacilli Calmette-Guerin (BCG) on miRNAs (miR-21, miR-181a, miR-155 and miR-144) in RAW264.7 cells, and with miR-144 as an example, to verify the relationship of miR-144 and Atg4a, an autophagy-related gene, and study the mechanism underlying the regulatory effect of miR-144 on autophagy in the process of Mycobacterium tuberculosis infection.	bcg	59-62	microRNA 181a-2	Mus musculus	83-91
26012717-1	2015	Previously we have shown that morphine regulates adult neurogenesis by modulating miR-181a maturation and subsequent hippocampal neural progenitor cell (NPC) lineages.	Morphine	30-38	microRNA 181a-2	Mus musculus	82-90
26012717-2	2015	Using NPCs cultured from PKCepsilon or beta-arrestin2 knockout mice and the MAPK/ERK kinase inhibitor U0126, we demonstrate that regulation of NPC differentiation via the miR-181a/Prox1/Notch1 pathway exhibits ligand-dependent selectivity.	U 0126	102-107	microRNA 181a-2	Mus musculus	171-179
26012717-8	2015	Thus, morphine modulates the lineage-specific differentiation of NPCs by PKCepsilon-dependent ERK activation with subsequent TRBP phosphorylation and miR-181a maturation.	Morphine	6-14	microRNA 181a-2	Mus musculus	150-158
26041820-3	2015	In this study, we report downregulation of the miR-181a/b gene cluster in APL blasts and NB4 leukemia cells upon ATRA treatment as a key event in the drug response.	Tretinoin	113-117	microRNA 181a-2	Mus musculus	47-55
25739786-5	2015	MiR-181a is able to target isocitrate dehydrogenase 1 (IDH1), a metabolic enzyme in TCA cycle.	Trichloroacetic Acid	84-87	microRNA 181a-2	Mus musculus	0-8
25652854-7	2015	RESULTS: After BCG stimulated RAW264.7 cells, the expression levels of miR-21, miR-155 and miR-144 were up-regulated, and miR-181a expression was down-regulated.	bcg	15-18	microRNA 181a-2	Mus musculus	122-130
24966929-0	2014	Reduced miR-9 and miR-181a expression down-regulates Bim concentration and promote osteoclasts survival.	bim	53-56	microRNA 181a-2	Mus musculus	18-26
24964978-0	2014	Morphine modulates mouse hippocampal progenitor cell lineages by upregulating miR-181a level.	Morphine	0-8	microRNA 181a-2	Mus musculus	78-86
24964978-2	2014	We now demonstrate that morphine can regulate neurogenesis by control of miR-181a and subsequent hippocampal neural progenitor cell (hNPC) lineages.	Morphine	24-32	microRNA 181a-2	Mus musculus	73-81
24964978-7	2014	In vitro and in vivo treatment with morphine resulted in an increase in miR-181a level in hNPCs and mouse hippocampi, respectively.	Morphine	36-44	microRNA 181a-2	Mus musculus	72-80
24964978-9	2014	Meanwhile, overexpression of the miR-181a inhibitor raised Prox1 levels, decreased Notch1 levels, and subsequently blocked the morphine-induced lineage changes.	Morphine	127-135	microRNA 181a-2	Mus musculus	33-41
24964978-10	2014	Thus, by modulating Prox1/Notch1 activities via miR-181a, morphine influences the fate of differentiating hNPCs differentiation and therefore the ultimate quantities of mature neurons and astrocytes.	Morphine	58-66	microRNA 181a-2	Mus musculus	48-56
25547709-0	2014	[Effects of propofol on miR-181a and Bcl-2 expression in glucose deprivation cultured astrocytes].	Propofol	12-20	microRNA 181a-2	Mus musculus	24-32
25547709-1	2014	OBJECTIVE: To explore the propofol regulation of Bcl-2 protein expression through miR-181a in glucose deprivation (GD) cultured astrocytes.	Propofol	26-34	microRNA 181a-2	Mus musculus	82-90
25547709-9	2014	And Bcl-2 protein expression was up-regulated while miR-181a expression inhibited by 10 micromol/L propofol.	Propofol	99-107	microRNA 181a-2	Mus musculus	52-60
25547709-10	2014	CONCLUSION: The protection of 10 micromol/L propofol against GD stress in astrocytes is correlated with inhibiting miR-181a and up-regulating Bcl-2 protein expression.	Propofol	44-52	microRNA 181a-2	Mus musculus	115-123
25187843-3	2014	The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells.	monooxyethylene trimethylolpropane tristearate	24-27	microRNA 181a-2	Mus musculus	106-113
25187843-3	2014	The results of in vitro MTT and BrdU incorporation assays, as well as cell-cycle analysis, indicated that miR-181 overexpression markedly promoted the proliferation of LNCaP cells.	Bromodeoxyuridine	32-36	microRNA 181a-2	Mus musculus	106-113
24792245-12	2014	In conclusion, our data analysis provides evidence that the anti-angiogenic effects of polyphenols from Chilean propolis can be modulated by miRNAs, in particular miR-181a, miR-106a and miR-20b.	Polyphenols	87-98	microRNA 181a-2	Mus musculus	163-171
23408835-6	2013	The microRNA miR-181a, which enhances activation-induced calcium flux in murine thymocytes, was expressed at significantly higher levels in CB naive CD4(+) T cells compared with adult cells.	Calcium	57-64	microRNA 181a-2	Mus musculus	13-21
23780685-0	2013	MiR-181a enhances drug sensitivity in mitoxantone-resistant breast cancer cells by targeting breast cancer resistance protein (BCRP/ABCG2).	mitoxantone	38-49	microRNA 181a-2	Mus musculus	0-8
24183997-5	2014	Enforced expression of miR-181a enhanced chemoresistance to cisplatin in cervical cancer cells through apoptosis reversion.	Cisplatin	60-69	microRNA 181a-2	Mus musculus	23-31
24183997-6	2014	In a nude mouse xenograft model, the overexpression of miR-181a markedly inhibited the therapeutic response to cisplatin.	Cisplatin	111-120	microRNA 181a-2	Mus musculus	55-63
24183997-10	2014	Our findings suggest that miR-181a may function as an oncogene and induce chemoresistance in cervical squamous cell carcinoma cells at least in part by down-regulating PRKCD, thus may provide a biomarker for predicting chemosensitivity to cisplatin in patients with cervical squamous cancer.	Cisplatin	239-248	microRNA 181a-2	Mus musculus	26-34
23408835-7	2013	Overexpression of miR-181a in adult naive CD4(+) T cells increased activation-induced calcium flux, implying that the increased miR-181a levels of CB naive CD4(+) T cells contributed to their enhanced signaling.	Calcium	86-93	microRNA 181a-2	Mus musculus	18-26
23262291-3	2013	Overexpression of miR-181a led to upregulation of key markers of osteoblastic differentiation as well as enhanced ALP levels and Alizarin red staining, indicating the importance of this miRNA for osteoblastic differentiation.	alizarin	129-141	microRNA 181a-2	Mus musculus	18-26
23256998-9	2012	RESULTS: Compared with those in the control group, the expression of miR-181a in 100 and 200 micromol/L t-BHP exposure groups was significantly decreased, with expression ratios of 0.744 and 0.766 (P < 0.01), while the expression of miR-181d in 50 micromol/L t-BHP exposure group was significantly increased, with an expression ratio of 1.29 (P < 0.01).	tert-Butylhydroperoxide	104-109	microRNA 181a-2	Mus musculus	69-77
23100311-6	2013	Furthermore, we show that lenalidomide, a drug approved for myelodysplastic syndromes and multiple myeloma, enhances translation of the C/EBPalpha-p30 isoform, resulting in higher miR-181a levels.	Lenalidomide	26-38	microRNA 181a-2	Mus musculus	180-188
23100311-8	2013	Similarly, lenalidomide exhibits antitumorigenic activity paralleled by increased miR-181a expression.	Lenalidomide	11-23	microRNA 181a-2	Mus musculus	82-90
23100311-10	2013	Altogether, our data provide a potential explanation for the improved clinical outcomes observed in CEBPA-mutated CN-AML patients, and suggest that lenalidomide treatment enhancing the C/EBPalpha-p30 protein levels and in turn miR-181a may sensitize AML blasts to chemotherapy.	Lenalidomide	148-160	microRNA 181a-2	Mus musculus	227-235
23256998-9	2012	RESULTS: Compared with those in the control group, the expression of miR-181a in 100 and 200 micromol/L t-BHP exposure groups was significantly decreased, with expression ratios of 0.744 and 0.766 (P < 0.01), while the expression of miR-181d in 50 micromol/L t-BHP exposure group was significantly increased, with an expression ratio of 1.29 (P < 0.01).	tert-Butylhydroperoxide	262-267	microRNA 181a-2	Mus musculus	69-77
22476949-11	2012	Inhibition of miR-181a by antisense oligonucleotides increases SIRT1 protein levels and activity, and improves insulin sensitivity in hepatocytes.	Oligonucleotides	36-52	microRNA 181a-2	Mus musculus	14-22
22476949-13	2012	In addition, overexpression of miR-181a by adenovirus impairs hepatic insulin signalling, and intraperitoneal injection of locked nucleic acid antisense oligonucleotides for miR-181a improves glucose homeostasis in diet-induced obesity mice.	Glucose	192-199	microRNA 181a-2	Mus musculus	174-182
22144581-0	2012	Dopamine-regulated microRNA MiR-181a controls GluA2 surface expression in hippocampal neurons.	Dopamine	0-8	microRNA 181a-2	Mus musculus	28-36
22476949-13	2012	In addition, overexpression of miR-181a by adenovirus impairs hepatic insulin signalling, and intraperitoneal injection of locked nucleic acid antisense oligonucleotides for miR-181a improves glucose homeostasis in diet-induced obesity mice.	Glucose	192-199	microRNA 181a-2	Mus musculus	31-39
25048087-6	2012	MicroRNA181a (miR181a) expression was also reduced after exposure to CA/1-D2.	1-d2	72-76	microRNA 181a-2	Mus musculus	14-21
25048087-8	2012	We found that transfection of antisense miR181a potentiated CA/1-D2-induced cell differentiation, while the transfection of precursor of miR181a partially inhibited the effect of CA/1-D2 on the differentiation.	1-d2	63-67	microRNA 181a-2	Mus musculus	40-47
25048087-8	2012	We found that transfection of antisense miR181a potentiated CA/1-D2-induced cell differentiation, while the transfection of precursor of miR181a partially inhibited the effect of CA/1-D2 on the differentiation.	1-d2	182-186	microRNA 181a-2	Mus musculus	137-144
22144581-8	2012	Moreover, miR-181a expression was induced by dopamine signaling in primary neurons, as well as by cocaine and amphetamines, in a mouse model of chronic drug treatment.	Dopamine	45-53	microRNA 181a-2	Mus musculus	10-18
22144581-8	2012	Moreover, miR-181a expression was induced by dopamine signaling in primary neurons, as well as by cocaine and amphetamines, in a mouse model of chronic drug treatment.	Cocaine	98-105	microRNA 181a-2	Mus musculus	10-18
22144581-8	2012	Moreover, miR-181a expression was induced by dopamine signaling in primary neurons, as well as by cocaine and amphetamines, in a mouse model of chronic drug treatment.	Amphetamines	110-122	microRNA 181a-2	Mus musculus	10-18
20023698-3	2010	The expression of tissue inhibitor of metalloprotease 3 (TIMP3), a tumor suppressor and a validated miR-181 target, was markedly suppressed in the livers of mice fed CDAA diet.	CDAA	166-170	microRNA 181a-2	Mus musculus	100-107