PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 26459180-2 2016 We aim to improve ATRA therapy of AML by enhancing apoptosis through repression of the antiapoptotic proteins Bcl-2 and Mcl-1. Tretinoin 18-22 BCL2 apoptosis regulator Homo sapiens 110-115 26459180-5 2016 RESULTS: In differentiation-responsive AML cells, ATRA treatment induces long-lasting repression of Bcl-2 while first upmodulating and then reducing the Mcl-1 level. Tretinoin 50-54 BCL2 apoptosis regulator Homo sapiens 100-105 26459180-8 2016 Sorafenib blocks ATRA-induced Mcl-1 increase by reversing p90RSK activation and GSK3beta inactivation, maintains the repressed Bcl-2 level, and enhances ATRA induced apoptosis in non-APL AML cell lines and in primary AML cells. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 127-132 26459180-10 2016 ATRA and sorafenib can be developed as a novel drug combination therapy for AML patients because this drug combination augments apoptosis by inhibiting Bcl-2 and Mcl-1. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 152-157 27019266-6 2016 The retinoic acid differentiated SH-S cell line (10 muM) shows a clear apoptosis when treated with H2O2 150 muM, with a Bax/Bcl-2 ratio of 3.75 (SD 0.80) in contrast to the differentiated control cells subjected to H2O2 and with extract, which have the same ratio of 1.02 (SD 0.01-0.03). Tretinoin 4-17 BCL2 apoptosis regulator Homo sapiens 124-129 26064333-5 2015 RESULTS: Combined treatment with ATRA and Genistein was able to reduce the expressions of Bcl-2, MUC1 and ICAM-1 and exerted synergistic effects to inhibit the invasion of A549 cells. Tretinoin 33-37 BCL2 apoptosis regulator Homo sapiens 90-95 26064333-6 2015 CONCLUSION: ATRA and Genistein may synergistically inhibit MUC1 and ICAM-1 expressions and affect the expressions of cell cycle related proteins (CDK4, Rb and p-ERK1/2) and apoptosis related proteins (Bax and Bcl-2), inhibit the metastatic potential of lung cancer A549 cells. Tretinoin 12-16 BCL2 apoptosis regulator Homo sapiens 209-214 21357440-7 2011 TRA-8 combined with AT-101 or BH3I-2", inhibitors of antiapoptotic Bcl-2 proteins, produced synergistic cytotoxicity against ZR-75-1, BT-474, and T47D cells. Tretinoin 0-3 BCL2 apoptosis regulator Homo sapiens 67-72 25408532-4 2014 Here, using MTT assay and EB/AO staining as well as TUNEL assay we show that RA in a concentration-dependent manner induces apoptosis through upregulating Caspase expression and increasing Bax/Bcl2 ratio. Tretinoin 77-79 BCL2 apoptosis regulator Homo sapiens 193-197 25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 0-5 25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 79-105 25088254-4 2014 BCL-2 family proteins regulate apoptosis and over-expression of anti-apoptotic B-cell leukemia/lymphoma 2 (BCL-2) family proteins has been associated with chemotherapeutic resistance in APL including impairment of the ability of atRA to induce growth arrest and differentiation. Tretinoin 229-233 BCL2 apoptosis regulator Homo sapiens 107-112 25088254-5 2014 Here we investigated the novel BH3 domain mimetic, JY-1-106, which antagonizes the anti-apoptotic BCL-2 family members B-cell lymphoma-extra large (BCL-xL) and myeloid cell leukemia-1 (MCL-1) alone and in combination with retinoids including atRA, AM580 (RARalpha agonist), and SR11253 (RARgamma antagonist). Tretinoin 242-246 BCL2 apoptosis regulator Homo sapiens 98-103 23507259-4 2013 We have examined at the molecular level the crosstalk between these nuclear receptors from the point of view of their control of cell growth and show here that RA reverts estrogen-stimulated transcription of the pivotal anti-apoptotic bcl-2 gene by preventing demethylation of dimethyl lysine 9 in histone H3 (HeK9me2). Tretinoin 160-162 BCL2 apoptosis regulator Homo sapiens 235-240 23319320-4 2013 Western blotting showed a loss of NF-kappaB, Bcl-2 and p-Akt, and the accumulation of Bad and Akt in cytoplasm of ATRA-treated AML-I preadipocytes. Tretinoin 114-118 BCL2 apoptosis regulator Homo sapiens 45-50 22197812-12 2012 In H9 cells treated with RA for 29 days, GRP78/Bip, XBP-1 and Bcl2 were all upregulated. Tretinoin 25-27 BCL2 apoptosis regulator Homo sapiens 62-66 24592121-0 2013 Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells. Tretinoin 61-74 BCL2 apoptosis regulator Homo sapiens 37-42 24592121-6 2013 In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. Tretinoin 30-32 BCL2 apoptosis regulator Homo sapiens 65-70 21354561-6 2011 MAIN OUTCOME MEASURE(S): The effect of ATRA was examined on the expression and phosphorylation of relevant RA, PI3K/Akt, and Bcl2 proteins (immunochemical analysis), cell proliferation, cell cycle distribution, and apoptosis. Tretinoin 39-43 BCL2 apoptosis regulator Homo sapiens 125-129 21963974-4 2011 The Western blot assay indicated that the expression of Bcl-2 was decreased more in A549 cells treated with N-(3-trifluoromethylphenyl) retinamide than that in A549 cells treated with ATRA. Tretinoin 184-188 BCL2 apoptosis regulator Homo sapiens 56-61 20225234-8 2010 The effect of atRA was mediated by an increased expression of Bcl-2 whereas the Epo treatment upregulated not only Bcl-2 but also Bcl-xL. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 62-67 20067883-15 2009 beta-carotene, lycopene and all-trans retinoic acid alone and in combination with docetaxel were found to influence the expression of bcl-2 and p53 antigen in the cells examined. Tretinoin 38-51 BCL2 apoptosis regulator Homo sapiens 134-139 19115248-2 2009 The combined action of tamoxifen/all-trans retinoic acid was advantageous in MCF-7 cells, reducing cell proliferation, Bcl-2 and c-Myc protein levels and increasing E-Cadherin protein levels and Gap junctional Intercellular Communication. Tretinoin 43-56 BCL2 apoptosis regulator Homo sapiens 119-124 19115248-5 2009 The co-incubation of bradykinin-MCF-7 cells with tamoxifen/all-trans retinoic acid reduced cell proliferation, ERK1/2 activity, as well as Bcl-2, c-Myc, and bradykinin receptor-2 levels, without altering the enhanced E-cadherin levels induced by tamoxifen/all-trans retinoic acid. Tretinoin 69-82 BCL2 apoptosis regulator Homo sapiens 139-144 17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 85-98 BCL2 apoptosis regulator Homo sapiens 323-328 17941088-5 2008 RA improved mitochondrial function by inhibiting the stretch- and Ang II-induced reduction in mitochondrial membrane potential, cytochrome c release and by increasing the Bcl2/Bax ratio. Tretinoin 0-2 BCL2 apoptosis regulator Homo sapiens 171-175 18358086-9 2008 The ratio of Bax/Bcl-2 decreased in arterial duct VSMC after RA treatment due to the significant inhibition of Bax expression. Tretinoin 61-63 BCL2 apoptosis regulator Homo sapiens 17-22 17616812-8 2007 Combination of ATRA and IFN-gamma showed more efficacy than IFN-gamma alone in causing apoptosis that occurred due to increases in Bax:Bcl-2 ratio, mitochondrial release of cytochrome c, and caspase-3 activity. Tretinoin 15-19 BCL2 apoptosis regulator Homo sapiens 135-140 17436081-4 2007 In contrast, "alpha1,3FucT-VII" cells facilitated the apoptosis induced by all-trans retinoic acid (ATRA), which was verified by the greater sub-G1 (apoptotic cells) peak in flow cytometry analysis, more expressions of active caspase-3 and pro-apoptotic protein Bax, as well as less expressions of anti-apoptotic proteins, Bcl-2 and Bcl-X(L). Tretinoin 100-104 BCL2 apoptosis regulator Homo sapiens 323-328 16572199-4 2006 The level of Bcl-2 protein is decreased by ATRA treatment in NB4, HL-60 and HL-60/Res cells. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 13-18 17449938-7 2007 In addition, minoxidil plus ATRA elevated phosphorylated Erk, phosphorylated Akt and the ratio of Bcl-2/Bax, but decreased the expressions of P53 and P21 more effectively than by minoxidil alone. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 98-103 17449938-8 2007 Our results suggest that minoxidil plus ATRA would additively enhance hair growth by mediating dual functions: 1) the prolongation of cell survival by activating the Erk and Akt signaling pathways, and 2) the prevention of apoptosis of DPCs and epithelial cells by increasing the ratio of Bcl-2/Bax and downregulating the expressions of P53 and P21. Tretinoin 40-44 BCL2 apoptosis regulator Homo sapiens 289-294 16568081-10 2006 This may provide a new therapeutic strategy against the ATRA-resistant and aggressive neuroblastomas by combining treatment with ATRA and a Bcl-2 inhibitor. Tretinoin 56-60 BCL2 apoptosis regulator Homo sapiens 140-145 16568081-0 2006 Bcl-2 is a key regulator for the retinoic acid-induced apoptotic cell death in neuroblastoma. Tretinoin 33-46 BCL2 apoptosis regulator Homo sapiens 0-5 16568081-6 2006 Enforced expression of Bcl-2 significantly inhibited ATRA-mediated apoptosis in CHP134 cells. Tretinoin 53-57 BCL2 apoptosis regulator Homo sapiens 23-28 16568081-7 2006 In addition, treatment of RTBM1 cells with a Bcl-2 inhibitor, HA14-1, enhanced apoptotic response induced by ATRA. Tretinoin 109-113 BCL2 apoptosis regulator Homo sapiens 45-50 16109552-1 2005 OBJECTIVE: To investigate the effects of all-trans retinoic acid (ATRA), acitretin and tazarotene on apoptosis and Bax/Bcl-2 protein expressions of human melanoma A375 cells. Tretinoin 66-70 BCL2 apoptosis regulator Homo sapiens 119-124 15770638-2 2006 Microarray analysis by ATRA treatment for 48 hr in peripheral blood mononuclear cells (in vivo) and in cultured bone marrow mononuclear cells (in vitro) from a patient with APL revealed upregulation of CD11b, CD11c, CCAAT enhancer binding protein epsilon, Rb1, Mad, and tumor necrosis factor-related genes; and downregulation of hTERT, c-Myc, WT1, bcl-2, and eukaryotic translation elongation factor 1alpha2. Tretinoin 23-27 BCL2 apoptosis regulator Homo sapiens 348-353 16277846-6 2005 In ATRA and TPA group, the change of HSP70 had positive correlation with JWA, and negative correlation with Bcl-2. Tretinoin 3-7 BCL2 apoptosis regulator Homo sapiens 108-113 16242776-4 2006 Inhibition of ATRA-induced apoptosis by TGF-beta1 was associated with an increased level of Mcl-1 protein, an anti-apoptotic member of Bcl-2 family, but not with inhibition of mitochondrial membrane depolarization. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 135-140 15492114-2 2005 Studies were done to address the question whether ATRA-induced apoptosis is a consequence of destabilization of bcl-2 mRNA and decreased cellular levels of the anti-apoptotic protein, bcl-2. Tretinoin 50-54 BCL2 apoptosis regulator Homo sapiens 184-189 15492114-3 2005 ATRA induced differentiation of HL-60 cells along the granulocytic pathway within 48 h. The half-lives of bcl-2 mRNA in HL-60 cells incubated with ATRA for 48 or 72 h were reduced to 39 and 7% of the corresponding untreated control values, respectively. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 106-111 15492114-3 2005 ATRA induced differentiation of HL-60 cells along the granulocytic pathway within 48 h. The half-lives of bcl-2 mRNA in HL-60 cells incubated with ATRA for 48 or 72 h were reduced to 39 and 7% of the corresponding untreated control values, respectively. Tretinoin 147-151 BCL2 apoptosis regulator Homo sapiens 106-111 15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 13-18 15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 202-207 15492114-5 2005 Binding of a bcl-2 mRNA instability element (AU-rich element-1) to nucleolin in S100 extracts from ATRA-treated cells was decreased to 15% of control within 72 h. The decay of 5" capped, polyadenylated bcl-2 mRNA transcripts containing ARE-1 was more rapid in S100 extracts from ATRA-treated cells compared with untreated cells. Tretinoin 279-283 BCL2 apoptosis regulator Homo sapiens 13-18 15492114-6 2005 However, when recombinant nucleolin was added to extracts of ATRA-treated cells, the rate of bcl-2 mRNA decay was similar to the rate in extracts of untreated cells. Tretinoin 61-65 BCL2 apoptosis regulator Homo sapiens 93-98 15492114-7 2005 These results provide evidence that ATRA-induced apoptosis is a consequence of cellular differentiation, which leads to nucleolin down-regulation and bcl-2 mRNA instability. Tretinoin 36-40 BCL2 apoptosis regulator Homo sapiens 150-155 15254726-0 2004 Expression profiles of p53, p21, bax and bcl-2 proteins in all-trans-retinoic acid treated primary and metastatic melanoma cells. Tretinoin 69-82 BCL2 apoptosis regulator Homo sapiens 41-46 15254726-3 2004 In this study, we used a similar cell culture model system of matched primary and metastatic melanoma cells from the same patient to investigate whether p53 and bcl-2 family proteins were involved in atRA-induced apoptosis. Tretinoin 200-204 BCL2 apoptosis regulator Homo sapiens 161-166 15242250-4 2004 All-trans retinoic acid, taxol and okadiac acid induce downregulation or inactivation of nucleolin, which destabilizes bcl-2 mRNA and triggers apoptosis. Tretinoin 10-23 BCL2 apoptosis regulator Homo sapiens 119-124 15254726-5 2004 Expression of p53, p21 and bax was increased, and bcl-2 was decreased in melanoma cells after exposure to atRA at different concentrations for various periods of time. Tretinoin 106-110 BCL2 apoptosis regulator Homo sapiens 50-55 15254726-8 2004 These data indicate that p53, p21, bax and bcl-2 proteins were involved in atRA-induced apoptosis in melanoma cells. Tretinoin 75-79 BCL2 apoptosis regulator Homo sapiens 43-48 12955881-6 2003 Retinoic acid also modulates c-myc and Bcl-2 expression. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 39-44 14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 76-81 14587026-1 2003 All-trans retinoic acid (ATRA) can down regulate the anti-apoptotic protein Bcl-2 and the cell cycle proteins cyclin D1 and cdk2 in estrogen receptor-positive breast cancer cells. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 76-81 14686729-9 2003 In addition, apoptosis occurred in both cell lines treated with either PGZ or ATRA, which was associated with a downregulation of bcl-2 and an upregulation of bax proteins. Tretinoin 78-82 BCL2 apoptosis regulator Homo sapiens 130-135 14686729-11 2003 Furthermore, treatment of fresh glioblastoma tissue from patients with PGZ, either alone or in combination with ATRA, induced a significant level of tumor cell apoptosis together with a downregulation of bcl-2 protein level as compared with untreated control brain tissue. Tretinoin 112-116 BCL2 apoptosis regulator Homo sapiens 204-209 12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 57-62 12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 98-103 12644474-4 2003 We observed growth arrest and apoptosis, upon decreasing Bcl-2 protein and transcript in the high Bcl-2-expressing, androgen-independent prostate cancer cell line, by all-trans-retinoic acid treatment (ATRA), but this did not occur in the androgen-dependent cell line expressing low levels of Bcl-2. Tretinoin 177-190 BCL2 apoptosis regulator Homo sapiens 98-103 12644474-6 2003 In stable clones expressing ectopic Par-4 and in ATRA-treated cells, we observed decreased Bcl-2 protein and transcript. Tretinoin 49-53 BCL2 apoptosis regulator Homo sapiens 91-96 12531222-3 2003 All-trans retinoic acid (ATRA) down-regulates bcl-2 expression and heightens AML sensitivity to cytosine arabinoside (ara-C)-induced apoptosis in vitro. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 46-51 12531222-3 2003 All-trans retinoic acid (ATRA) down-regulates bcl-2 expression and heightens AML sensitivity to cytosine arabinoside (ara-C)-induced apoptosis in vitro. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 46-51 12820386-5 2003 When compared with undifferentiated controls, ATRA induced Bcl-2 expression, while loss of Bax expression was observed only in cells differentiated by ATRA + BMP-6. Tretinoin 46-50 BCL2 apoptosis regulator Homo sapiens 59-64 12736759-9 2003 CONCLUSIONS: The ATRA-induced increase in cytotoxicity of ara-C was, in part, the result of an increase in the functional expression of nucleoside transporters, and a role for bcl-2 was also indicated. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 176-181 12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 52-56 BCL2 apoptosis regulator Homo sapiens 9-14 12820386-6 2003 The high Bcl-2/Bax ratio in cells differentiated by ATRA and ATRA + BMP-6, respectively, correlated with the survival of these cells in serum-free media. Tretinoin 61-65 BCL2 apoptosis regulator Homo sapiens 9-14 12513735-0 2002 [Study on telomerase activity and expression of hTERT, c-myc and bcl-2 during terminal differentiation of HL-60 cells induced by retinoic acid]. Tretinoin 129-142 BCL2 apoptosis regulator Homo sapiens 65-70 12446691-10 2003 Interestingly, the cytosolic calcium chelator BAPTA-AM and K-201 protected RA-treated chondrocytes from undergoing apoptotic changes, as indicated by higher bcl-2 gene expression, reduced caspase-3 activity, and the percentage of TUNEL-positive cells. Tretinoin 75-77 BCL2 apoptosis regulator Homo sapiens 157-162 12431242-2 2002 ATRA induced apoptosis in all the B-CLL samples tested, and this was accompanied by a specific reduction in Bcl-2 and Mcl-1 protein expression in the apoptotic cells. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 108-113 12513735-4 2002 It is concluded that the telomerase activity is related to decrease expression of hTERT, c-myc and bcl-2 mRNA during HL-60 cell differentiation induced by ATRA. Tretinoin 155-159 BCL2 apoptosis regulator Homo sapiens 99-104 12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 15-38 BCL2 apoptosis regulator Homo sapiens 54-59 12139741-6 2002 Treatment with all-trans retinoic acid (ATRA) reduced Bcl-2 and Bcl-X(L) expression in the leukaemic Q cells, and enhanced their chemosensitivity to cytosine arabinoside (ara-C). Tretinoin 40-44 BCL2 apoptosis regulator Homo sapiens 54-59 12063559-13 2002 These data demonstrate that ATRA and 9cisRA may inhibit HER-2/neu induced aberrant proliferation in part by retarding cell cycle progression, down-regulating HER-2/neu-mediated signal transduction and inducing Bcl-2-dependent apoptosis through a retinoid receptor-mediated mechanism. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 210-215 12186376-5 2002 However, only MCF-7, MDA-MB-231, and ZR-75-1 cells, which expressed a high level of bcl-2 protein, underwent apoptosis when exposed to the combination of TGZ and either ATRA or 9-cis-RA. Tretinoin 169-173 BCL2 apoptosis regulator Homo sapiens 84-89 12186376-5 2002 However, only MCF-7, MDA-MB-231, and ZR-75-1 cells, which expressed a high level of bcl-2 protein, underwent apoptosis when exposed to the combination of TGZ and either ATRA or 9-cis-RA. Tretinoin 177-185 BCL2 apoptosis regulator Homo sapiens 84-89 11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 42-55 BCL2 apoptosis regulator Homo sapiens 293-298 12012012-5 2002 Bcl-2 over-expression inhibited both delay in S-phase exit and CDDP-induced apoptosis in ATRA-pretreated cells. Tretinoin 89-93 BCL2 apoptosis regulator Homo sapiens 0-5 11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 68-81 BCL2 apoptosis regulator Homo sapiens 219-224 11739380-7 2002 Interestingly, the survival of the neuroblastoma cells treated with retinoic acid was partly dependent on the expression of RAGE, and inhibition of RAGE function partially blocked the increase in anti-apoptotic protein Bcl-2 following retinoic acid treatment. Tretinoin 235-248 BCL2 apoptosis regulator Homo sapiens 219-224 11927016-6 2002 With YCU-N861 cells, ATRA also caused a decrease in Bcl-2 and Bcl-X(L) and an increase in Bax. Tretinoin 21-25 BCL2 apoptosis regulator Homo sapiens 52-57 11561905-9 2001 Furthermore, treating Bcl-2 cultures with ceramide (10 microM), a second messenger mediating the RA-initiated death signal in parental cells, no longer caused DNA laddering. Tretinoin 97-99 BCL2 apoptosis regulator Homo sapiens 22-27 11886382-1 2002 Recently, it was disclosed that all-trans retinoic acid (ATRA) inhibits myeloma cell growth by downregulating the interleukin 6 (IL-6)/IL-6 receptor (IL-6R) auto/paracrine loop, and upregulating p21/Cip1 cyclin-dependent kinase inhibitor (CDK-I), thereby inducing apoptosis with a decrease in Bcl-2 protein expression. Tretinoin 57-61 BCL2 apoptosis regulator Homo sapiens 293-298 12025892-2 2002 Because ATRA has effects (increase in apoptosis, suppression of bcl-2), it has also been used for the treatment of other French-American-British (FAB) subtypes of acute myelogenous leukemia (AML). Tretinoin 8-12 BCL2 apoptosis regulator Homo sapiens 64-69 12025892-10 2002 Logistic regression analysis revealed that ATRA administration was the important factor in CR, among other potential factors including age, white blood count, bcl-2 expression, and the uptake and efflux of Rh123 (p = 0.05). Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 159-164 11683923-8 2001 Western blot for Bcl-2 family also performed in neutrophilic differentiated HL-60 cells by all-trans-retinoic acid. Tretinoin 91-114 BCL2 apoptosis regulator Homo sapiens 17-22 11429697-8 2001 Retinoic acid markedly decreased the Bcl-2 levels in MCF-7 and ZR-75 cells. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 37-42 11429697-9 2001 Accordingly, coexpression of Bcl-2 and cyclin D1 rendered the cells resistant to retinoic acid-induced apoptosis. Tretinoin 81-94 BCL2 apoptosis regulator Homo sapiens 29-34 11384110-3 2001 ATRA enhanced docetaxel-induced apoptosis and combined treatment with ATRA and docetaxel resulted in down-regulation of Bcl-2. Tretinoin 70-74 BCL2 apoptosis regulator Homo sapiens 120-125 11426618-5 2000 Increased expression of the leukocyte integrins CD11b and CD18 as well as down-regulation of the anti-apoptotic gene bcl-2 are associated with late stage differentiation of the myeloid lineage and retinoic acid induced maturation of acute myeloid leukemic cells. Tretinoin 197-210 BCL2 apoptosis regulator Homo sapiens 117-122 11384110-7 2001 We conclude that ATRA synergistically enhances docetaxel toxicity by down-regulating Bcl-2 expression and partially reverses the docetaxel-induced G2/M arrest by inhibiting docetaxel-induced cdc2 phosphorylation in a pathway that is dependent on MAPK. Tretinoin 17-21 BCL2 apoptosis regulator Homo sapiens 85-90 11181829-0 2001 Antisense inhibition of BCL-2 expression induces retinoic acid-mediated cell death during differentiation of human NT2N neurons. Tretinoin 49-62 BCL2 apoptosis regulator Homo sapiens 24-29 11181829-5 2001 This concentration of retinoic acid was not toxic to undifferentiated NT2/D1 cells but was sufficient to up-regulate the BCL-2 protein in 6 days. Tretinoin 22-35 BCL2 apoptosis regulator Homo sapiens 121-126 11181829-7 2001 Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. Tretinoin 151-164 BCL2 apoptosis regulator Homo sapiens 45-50 11181829-7 2001 Inhibition of the accumulation of endogenous BCL-2 with vectors expressing the antisense mRNA of Bcl-2 caused extensive apoptosis after 3 weeks of the retinoic acid treatment. Tretinoin 151-164 BCL2 apoptosis regulator Homo sapiens 97-102 11181829-10 2001 The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Tretinoin 32-45 BCL2 apoptosis regulator Homo sapiens 15-20 11181829-10 2001 The ability of BCL-2 to prevent retinoic acid-induced cell death was also confirmed in undifferentiated NT2/D1 cells that were transfected with a vector containing Bcl-2 cDNA in sense orientation and exposed to toxic doses (40-80 microM) of retinoic acid. Tretinoin 241-254 BCL2 apoptosis regulator Homo sapiens 15-20 11181829-11 2001 Furthermore, down-regulation of BCL-2 levels by an antisense oligonucleotide in neuronally differentiated NT2/D1 cells increased their susceptibility to retinoic acid-induced apoptosis. Tretinoin 153-166 BCL2 apoptosis regulator Homo sapiens 32-37 11181829-12 2001 These results indicate that one function of the up-regulation of endogenous BCL-2 during neuronal differentiation is to regulate the sensitivity of young post-mitotic neurons to retinoic acid-mediated apoptosis. Tretinoin 178-191 BCL2 apoptosis regulator Homo sapiens 76-81 10816444-0 2000 Bcl-2 accelerates retinoic acid-induced growth arrest and recovery in human gastric cancer cells. Tretinoin 18-31 BCL2 apoptosis regulator Homo sapiens 0-5 10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 201-203 BCL2 apoptosis regulator Homo sapiens 39-44 10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 BCL2 apoptosis regulator Homo sapiens 43-47 10816444-6 2000 In this study, when treated with RA, SC-M1/Bcl2 cells, which were generated by transfecting SC-M1 cells with bcl-2 DNA, were growth-arrested two days earlier than SC-M1/neo cells, which were generated by transfecting SC-M1 cells with vector DNA. Tretinoin 33-35 BCL2 apoptosis regulator Homo sapiens 109-114 10816444-7 2000 This indicates that Bcl-2 accelerates RA-induced growth arrest. Tretinoin 38-40 BCL2 apoptosis regulator Homo sapiens 20-25 10816444-8 2000 In addition to the accelerated growth arrest, RA-treated SC-M1/Bcl2 cells also recovered from growth arrest two days faster than SC-M1/neo cells after the removal of RA. Tretinoin 46-48 BCL2 apoptosis regulator Homo sapiens 63-67 10816444-12 2000 In a search for the mechanism by which Bcl-2 affects growth regulation, we found that p21 gene expression was more prominent in SC-M1/Bcl2 cells than in SC-M1/neo cells in the presence of RA, but when RA was removed, p21 gene expression levels in SC-M1/Bcl2 cells were also reduced earlier than in SC-M1/neo cells. Tretinoin 188-190 BCL2 apoptosis regulator Homo sapiens 39-44 10766196-8 2000 Pretreatment of MCF-7 cells with either 1,25(OH)2D3 or ATRA increased the phosphorylation of Bcl-2 by variable concentrations of paclitaxel. Tretinoin 55-59 BCL2 apoptosis regulator Homo sapiens 93-98 10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 82-86 BCL2 apoptosis regulator Homo sapiens 235-240 10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 82-86 BCL2 apoptosis regulator Homo sapiens 19-24 10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 91-95 BCL2 apoptosis regulator Homo sapiens 19-24 10713328-7 2000 Down-regulation of Bcl-2 protein expression was evident in NB4 cells treated with ATRA and ATRA in combination with Iso-Q or 1,25 D(3), but not in cells treated with a classic chemotherapeutic agent, arabinosycytosine, suggesting that Bcl-2 down-regulation is neither necessary, nor specific for apoptosis in this model. Tretinoin 91-95 BCL2 apoptosis regulator Homo sapiens 235-240 10648421-1 2000 When bcl-2 is immunoprecipitated from (32)P-labeled cell extracts of all-trans retinoic acid (ATRA)-treated acute myeloblastic leukemia (AML) blasts, a phosphorylated protein of approximately 30 kd is coprecipitated. Tretinoin 79-92 BCL2 apoptosis regulator Homo sapiens 5-10 10648421-1 2000 When bcl-2 is immunoprecipitated from (32)P-labeled cell extracts of all-trans retinoic acid (ATRA)-treated acute myeloblastic leukemia (AML) blasts, a phosphorylated protein of approximately 30 kd is coprecipitated. Tretinoin 94-98 BCL2 apoptosis regulator Homo sapiens 5-10 11059564-6 2000 Moreover, proadifen weakened ATRA-induced downregulation of the Bcl-2 protein. Tretinoin 29-33 BCL2 apoptosis regulator Homo sapiens 64-69 10623473-6 2000 Employing bcl-2-overexpressing HL-60 cells permitted demonstration of nuclear lobulation, ELCS formation, and centrosome-MT movement concomitantly during RA-induced differentiation, implying independence between the cellular reorganization and apoptotic programs. Tretinoin 154-156 BCL2 apoptosis regulator Homo sapiens 10-15 10940651-8 2000 On the basis of these results, ATRA-induced apoptosis in these AML cell lines is independent of the p53 pathway, although it is associated with the down-regulation of bcl-2. Tretinoin 31-35 BCL2 apoptosis regulator Homo sapiens 167-172 10428509-10 1999 ATRA-induced apoptosis caused actin cleavage, which was not affected by G-CSF, and Bcl-2 downregulation. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 83-88 10518116-8 1999 The expression of the proteins of the protooncogene Bcl-2 and the tumor suppressor gene p53 following staurosporine or retinoic acid treatment was assessed by Western blot and immunocytochemistry. Tretinoin 119-132 BCL2 apoptosis regulator Homo sapiens 52-57 10518116-9 1999 Retinoic acid increased Bcl-2 and decreased p53 levels, whereas staurosporine decreased Bcl-2 and increased p53 levels. Tretinoin 0-13 BCL2 apoptosis regulator Homo sapiens 24-29 10557066-0 1999 Expression of Bcl-2-related genes in normal and AML progenitors: changes induced by chemotherapy and retinoic acid. Tretinoin 101-114 BCL2 apoptosis regulator Homo sapiens 14-19 10557066-10 1999 Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C. Tretinoin 57-61 BCL2 apoptosis regulator Homo sapiens 18-23 10557066-10 1999 Downregulation of Bcl-2 mRNA and protein was observed by ATRA and the combination of Ara-C, followed by ATRA, resulted in markedly increased cytotoxicity in HL-60 cells, as compared to Ara-C alone or ATRA followed by Ara-C. Tretinoin 104-108 BCL2 apoptosis regulator Homo sapiens 18-23 9779827-0 1998 Evidence of a direct role for Bcl-2 in the regulation of articular chondrocyte apoptosis under the conditions of serum withdrawal and retinoic acid treatment. Tretinoin 134-147 BCL2 apoptosis regulator Homo sapiens 30-35 10456672-0 1999 Effect of all-trans retinoic acid on chemotherapy induced apoptosis and down-regulation of Bcl-2 in human myeloid leukaemia CD34 positive cells. Tretinoin 20-33 BCL2 apoptosis regulator Homo sapiens 91-96 10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 10-33 BCL2 apoptosis regulator Homo sapiens 114-119 10456672-4 1999 Recently, all-trans retinoic acid (RA) has been reported to enhance cytarabine-induced apoptosis and downregulate Bcl-2 in several human myeloid leukaemia CD34 negative cells. Tretinoin 35-37 BCL2 apoptosis regulator Homo sapiens 114-119 10456672-11 1999 As single agents, RA, cytarabine and fludarabine reduced Bcl-2 expression in a dose dependent manner in both cell types. Tretinoin 18-20 BCL2 apoptosis regulator Homo sapiens 57-62 10456672-13 1999 The addition of RA to cytarabine enhanced its induced reduction of Bcl-2 in KG1 CD34+CD7- but not in KGla CD34+CD7+ human myeloid leukaemia cells. Tretinoin 16-18 BCL2 apoptosis regulator Homo sapiens 67-72 10194425-1 1999 Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Tretinoin 45-68 BCL2 apoptosis regulator Homo sapiens 132-137 10194425-1 1999 Preclinical data suggest that retinoids, eg, all-trans retinoic acid (ATRA), lower concentrations of antiapoptotic proteins such as bcl-2, possibly thereby improving the outcome of anti-acute myeloid leukemia (AML) chemotherapy. Tretinoin 70-74 BCL2 apoptosis regulator Homo sapiens 132-137 10518116-10 1999 The opposite alteration of Bcl-2 (anti-apoptotic) and p53 (apoptotic) contents in SH-SY5Y cells with retinoic acid and staurosporine are attributed to the changes in cell vulnerability. Tretinoin 101-114 BCL2 apoptosis regulator Homo sapiens 27-32 10233386-8 1999 However, both of the cell lines showed progressive down-regulation of bcl-2, which began after 12-24 h exposure of the cells to ATRA as determined by ELISA, Western blotting and flow cytometry. Tretinoin 128-132 BCL2 apoptosis regulator Homo sapiens 70-75 10233386-9 1999 The present results show that mitochondria have a role in ATRA-induced apoptosis in AML cells and down-regulation of bcl-2 is related to it. Tretinoin 58-62 BCL2 apoptosis regulator Homo sapiens 117-122 9779827-2 1998 Here we demonstrate the importance of Bcl-2 in regulating articular chondrocyte apoptosis in response to both serum withdrawal and retinoic acid treatment. Tretinoin 131-144 BCL2 apoptosis regulator Homo sapiens 38-43 9779827-8 1998 In contrast, chondrocytes overexpressing Bcl-2 were resistant to apoptosis induced by both serum withdrawal and retinoic acid treatment. Tretinoin 112-125 BCL2 apoptosis regulator Homo sapiens 41-46 9716607-0 1998 Phosphorylation of BCL-2 after exposure of human leukemic cells to retinoic acid. Tretinoin 67-80 BCL2 apoptosis regulator Homo sapiens 19-24 9716607-4 1998 Metabolic labeling experiments using 32Pi showed that, while control bcl-2 was labeled, incorporation was greatly increased when cells were treated with ATRA. Tretinoin 153-157 BCL2 apoptosis regulator Homo sapiens 69-74 9716607-5 1998 A comparison of bcl-2 from blasts treated with ATRA or taxol showed that bcl-2 was phosphorylated on serine in cells treated with either agent; however, both qualitative and quantitative differences were seen. Tretinoin 47-51 BCL2 apoptosis regulator Homo sapiens 16-21 9716607-5 1998 A comparison of bcl-2 from blasts treated with ATRA or taxol showed that bcl-2 was phosphorylated on serine in cells treated with either agent; however, both qualitative and quantitative differences were seen. Tretinoin 47-51 BCL2 apoptosis regulator Homo sapiens 73-78 9716607-7 1998 Quantitatively, all bcl-2 from ATRA-treated cells was in the phosphorylated isoform, while after taxol, both phosphorylated and native bcl-2 was present; incorporation of 32Pi into bcl-2 was stimulated to greater extent in ATRA-treated compared with taxol-treated cells. Tretinoin 31-35 BCL2 apoptosis regulator Homo sapiens 20-25 9716607-8 1998 We used immunoprecipitation experiments to ask if bcl-2 phosphorylated after ATRA or taxol had altered capacity to dimerize with bax. Tretinoin 77-81 BCL2 apoptosis regulator Homo sapiens 50-55 9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 87-91 BCL2 apoptosis regulator Homo sapiens 18-23 9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 18-23 9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 93-98 9716607-10 1998 We conclude that: bcl-2 is phosphorylated on serine after treatment of AML blasts with ATRA; bcl-2 phosphorylation after ATRA is different from that seen after taxol; bcl-2 phosphorylated after either agent retains capacity to dimerize with bax. Tretinoin 121-125 BCL2 apoptosis regulator Homo sapiens 93-98 9716607-11 1998 The ATRA or taxol-induced phosphorylation of bcl-2 can also be seen in blast cells obtained from AML patients. Tretinoin 4-8 BCL2 apoptosis regulator Homo sapiens 45-50 9716607-2 1998 We report here that bcl-2 is phosphorylated on serine in acute myeloblastic leukemia (AML) blasts exposed to all trans retinoic acid (ATRA). Tretinoin 119-132 BCL2 apoptosis regulator Homo sapiens 20-25 9716607-2 1998 We report here that bcl-2 is phosphorylated on serine in acute myeloblastic leukemia (AML) blasts exposed to all trans retinoic acid (ATRA). Tretinoin 134-138 BCL2 apoptosis regulator Homo sapiens 20-25 15624332-6 1997 9-cis RA was more potent than all-trans retinoic acid (ATRA) did in inducing terminal differentiation associated apoptosis and in downregulation of Bcl-2 expression. Tretinoin 40-53 BCL2 apoptosis regulator Homo sapiens 148-153 9642262-8 1998 In addition, RA-induced suppression of Bcl-2 expression was abrogated by overexpression of BAG-1. Tretinoin 13-15 BCL2 apoptosis regulator Homo sapiens 39-44 9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 98-103 9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 139-144 9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 181-185 BCL2 apoptosis regulator Homo sapiens 98-103 9671760-7 1998 The observed apoptosis mediated by TGZ and ATRA may be related to the striking down-regulation of bcl-2, because forced over-expression of bcl-2 in MCF7 cells cultured with TGZ and ATRA blocks their cell death. Tretinoin 181-185 BCL2 apoptosis regulator Homo sapiens 139-144 9649124-9 1998 This regimen of melatonin followed by atRA induced cytocidal effects on MCF-7 cells by activating pathways leading to apoptosis (programmed cell death) as evidenced by decreased ER and Bcl-2 and increased Bax and transforming growth factor beta 1 (TGF-beta1) expression. Tretinoin 38-42 BCL2 apoptosis regulator Homo sapiens 185-190 9620283-7 1998 Flow cytometry analysis revealed that the mean fluorescence intensity of bcl-2 protein was slightly decreased in cells treated with ATRA. Tretinoin 132-136 BCL2 apoptosis regulator Homo sapiens 73-78 9620283-8 1998 These results indicate that in U266B1 cells, combined treatment with anti-Fas mAb and ATRA enhances the induction of apoptosis by modulating the expression of Fas and bcl-2 by ATRA. Tretinoin 86-90 BCL2 apoptosis regulator Homo sapiens 167-172 9558392-6 1998 ATRA treatment also led to downregulation of bcl-2 and endogenous RARalpha in PML-RARalpha-expressing cells, but had little effect on the level of exogenously expressed PML-RARalpha. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 45-50 9558392-7 1998 We conclude that (1) subtle differences exist in the biologic activities of the L and S isoforms of PML-RARalpha, and (2) both isoforms are capable of transducing an ATRA-mediated signal that leads to downregulation of bcl-2 and induction of programmed cell death. Tretinoin 166-170 BCL2 apoptosis regulator Homo sapiens 219-224 9815594-7 1997 The expression of Bcl-2 relative to Bax decreased more after combined treatment with cisplatin and ATRA than after either drug alone. Tretinoin 99-103 BCL2 apoptosis regulator Homo sapiens 18-23 9402847-0 1997 In vitro down-regulation of bcl-2 expression by all-trans retinoic acid in AML blasts. Tretinoin 58-71 BCL2 apoptosis regulator Homo sapiens 28-33 9402847-1 1997 Using flow cytometry, we have investigated the effects of 0.5 microM all-trans-retinoic acid (ATRA) on bcl-2 expression in the blast cells of 25 acute myeloblastic leukemia (AML) patients and the HL-60 cell line after incubation for 6 days. Tretinoin 69-92 BCL2 apoptosis regulator Homo sapiens 103-108 9402847-1 1997 Using flow cytometry, we have investigated the effects of 0.5 microM all-trans-retinoic acid (ATRA) on bcl-2 expression in the blast cells of 25 acute myeloblastic leukemia (AML) patients and the HL-60 cell line after incubation for 6 days. Tretinoin 94-98 BCL2 apoptosis regulator Homo sapiens 103-108 9402847-2 1997 We observed a significant decrease of bcl-2 expression after treatment with ATRA in 12 of 25 AML samples and the HL-60 cells. Tretinoin 76-80 BCL2 apoptosis regulator Homo sapiens 38-43 9402847-3 1997 The mean fluorescence intensity (MFI) ratio for the bcl-2 levels of the ATRA responders (n = 12) was reduced to 7.9 +/- 4.8 following incubation with ATRA compared with 10.9 +/- 6.5 (mean +/- SD) for control samples incubated without ATRA (p = 0.011). Tretinoin 72-76 BCL2 apoptosis regulator Homo sapiens 52-57 9402847-9 1997 Because many chemotherapeutic agents also operate through the activation of programmed cell death and bcl-2 levels are positively associated with resistance to apoptosis, ATRA can be used in combination chemotherapy to increase the chemosensitivity of some patients with AML. Tretinoin 171-175 BCL2 apoptosis regulator Homo sapiens 102-107 15624332-6 1997 9-cis RA was more potent than all-trans retinoic acid (ATRA) did in inducing terminal differentiation associated apoptosis and in downregulation of Bcl-2 expression. Tretinoin 55-59 BCL2 apoptosis regulator Homo sapiens 148-153 9225073-0 1997 Modulation of p53, WAF1/p21 and BCL-2 expression during retinoic acid-induced differentiation of NB4 promyelocytic cells. Tretinoin 56-69 BCL2 apoptosis regulator Homo sapiens 32-37 8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 198-211 BCL2 apoptosis regulator Homo sapiens 96-101 10743138-2 1997 The results indicated that after treated with ST and RA, the cells became well-differentiated, the cell growth was suppressed, contact suppress was partially recovered, colony forming was decreased, protooncogenes (C-myc bcl-2) protein was decreased, tumor suppressor gene (p53) protein was increased. Tretinoin 53-55 BCL2 apoptosis regulator Homo sapiens 221-226 8830674-3 1996 We show here that bax protein also declined with a time course similar to the downregulation of bcl-2 following treatment of HL60 with phorbol myristate acetate (PMA), dimethyl sulphoxide (DMSO) or retinoic acid (RA). Tretinoin 213-215 BCL2 apoptosis regulator Homo sapiens 96-101 8790944-0 1996 Induction of mcl1/EAT, Bcl-2 related gene, by retinoic acid or heat shock in the human embryonal carcinoma cells, NCR-G3. Tretinoin 46-59 BCL2 apoptosis regulator Homo sapiens 23-28 8666983-2 1996 WHen the cells were treated with 12-O-tetradecanoylphorbol 13-acetate (TPA) or retinoic acid, the level of Bcl-2 protein was increased compared with the control. Tretinoin 79-92 BCL2 apoptosis regulator Homo sapiens 107-112 8826891-0 1996 Down-regulation of bcl-2 in AML blasts by all-trans retinoic acid and its relationship to CD34 antigen expression. Tretinoin 52-65 BCL2 apoptosis regulator Homo sapiens 19-24 8826891-3 1996 All-trans retinoic acid (ATRA) has been reported to increase the sensitivity of AML cell lines to Ara-C and to induce differentiation in the HL60 promyelocytic cell line, with both effects being accompanied by a decrease in bcl-2 expression. Tretinoin 0-23 BCL2 apoptosis regulator Homo sapiens 224-229 8826891-3 1996 All-trans retinoic acid (ATRA) has been reported to increase the sensitivity of AML cell lines to Ara-C and to induce differentiation in the HL60 promyelocytic cell line, with both effects being accompanied by a decrease in bcl-2 expression. Tretinoin 25-29 BCL2 apoptosis regulator Homo sapiens 224-229 8826891-4 1996 Using flow cytometry and a monoclonal antibody to bcl-2, we have investigated the effects of ATRA (1 microM) on bcl-2 expression in the blast cells of 25 AML patients and the K562 cell line after incubation for 72 or 24 h, respectively. Tretinoin 93-97 BCL2 apoptosis regulator Homo sapiens 112-117 8826891-5 1996 Using Kolmogorov-Smirnov statistical analysis where a D value of > 0.12 was statistically significant, we found that in 8/25 AML samples and the K562 cells there was a significant decrease in bcl-2 protein expression after incubation with ATRA (D value range 0.14-0.44). Tretinoin 242-246 BCL2 apoptosis regulator Homo sapiens 195-200 8826891-6 1996 The mean peak fluorescence (MPF) values for the bcl-2 levels of the ATRA responders (n = 8) was reduced to 35.5 +/- 6.9 following incubation with ATRA compared to 47.6 +/- 8.2 (mean +/- SEM) for control samples incubated in the absence of ATRA (P = 0.014). Tretinoin 68-72 BCL2 apoptosis regulator Homo sapiens 48-53 8826891-6 1996 The mean peak fluorescence (MPF) values for the bcl-2 levels of the ATRA responders (n = 8) was reduced to 35.5 +/- 6.9 following incubation with ATRA compared to 47.6 +/- 8.2 (mean +/- SEM) for control samples incubated in the absence of ATRA (P = 0.014). Tretinoin 146-150 BCL2 apoptosis regulator Homo sapiens 48-53 8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 43-47 BCL2 apoptosis regulator Homo sapiens 23-28 8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 154-158 BCL2 apoptosis regulator Homo sapiens 23-28 8826891-8 1996 The down-regulation of bcl-2 expression by ATRA was particularly associated with CD34-negative AML and of the eight AML patients" cells that responded to ATRA by down-regulating bcl-2, seven were CD34 negative (P < 0.05). Tretinoin 154-158 BCL2 apoptosis regulator Homo sapiens 178-183 8826891-9 1996 Our data suggest that the addition of ATRA to combination chemotherapy would increase the chemosensitivity of some patients with AML, particularly CD34-negative AML, due to down-regulation of bcl-2 expression. Tretinoin 38-42 BCL2 apoptosis regulator Homo sapiens 192-197 8713132-7 1996 Furthermore, RA induced bcl-2 but prevented the processing of actin, whereas 4-HPR had little effect on bcl-2 but increased the specific processing of actin. Tretinoin 13-15 BCL2 apoptosis regulator Homo sapiens 24-29 8713132-8 1996 These results suggest that RA promotes neutrophil differentiation and the establishment of a semi apoptosis-resistant state, possibly through the overexpression of the bcl-2 gene. Tretinoin 27-29 BCL2 apoptosis regulator Homo sapiens 168-173 8603522-7 1996 RA-mediated interruption of the IL-6 autocrine loop was associated with a decrease of bcl-2 oncoprotein expression and apoptosis of the myeloma cells which was RA concentration- and time-dependent. Tretinoin 0-2 BCL2 apoptosis regulator Homo sapiens 86-91 8790944-7 1996 The expression of mcl1/EAT, the Bcl-2 related gene, was increased at an early stage of the retinoic acid-induced differentiation and preceded the up-regulation of cytokeratin and hCG genes after ratinoic acid treatment. Tretinoin 91-104 BCL2 apoptosis regulator Homo sapiens 32-37 8642855-6 1996 We found that the half-life of bcl-2 protein is markedly shortened after treatment with ATRA. Tretinoin 88-92 BCL2 apoptosis regulator Homo sapiens 31-36 7553653-6 1995 Marked induction of bcl-2 in NB cells followed RA-induced differentiation, whereas in cell lines failing to differentiate, bcl-2 was not detected. Tretinoin 47-49 BCL2 apoptosis regulator Homo sapiens 20-25 8609716-7 1995 After incubation with ATRA, cell survival was not altered and was correlated with a concomitant absence of apoptosis, despite a significant decrease of the BcL-2 protein in APL differentiated cells. Tretinoin 22-26 BCL2 apoptosis regulator Homo sapiens 156-161 7564507-0 1995 Direct evidence for the participation of bcl-2 in the regulation by retinoic acid of the Ara-C sensitivity of leukemic stem cells. Tretinoin 68-81 BCL2 apoptosis regulator Homo sapiens 41-46 7564507-7 1995 The effect of ATRA on bcl-2 expression was compared in sense-transfected cells and their parents; by Northern blotting it was shown that the endogenous but not the transfected genes were down-regulated after ATRA exposure. Tretinoin 14-18 BCL2 apoptosis regulator Homo sapiens 22-27 7564507-7 1995 The effect of ATRA on bcl-2 expression was compared in sense-transfected cells and their parents; by Northern blotting it was shown that the endogenous but not the transfected genes were down-regulated after ATRA exposure. Tretinoin 208-212 BCL2 apoptosis regulator Homo sapiens 22-27 7564507-10 1995 We conclude that data from the transfectants provides evidence that expression of bcl-2 is a determinant of sensitivity to Ara-C and H2O2; and that the effect of ATRA on sensitivity requires the presence of bcl-2 genes in association with regulatory elements. Tretinoin 162-166 BCL2 apoptosis regulator Homo sapiens 207-212 7630193-10 1995 NB4 cells treated with either all-trans or 9-cis retinoic acid (1 microM) were induced to differentiate and the level of Bcl-2 protein decreased to undetectable levels during terminal maturation when only a few apoptotic cells were detected. Tretinoin 49-62 BCL2 apoptosis regulator Homo sapiens 121-126 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 44-57 BCL2 apoptosis regulator Homo sapiens 118-123 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 59-82 BCL2 apoptosis regulator Homo sapiens 118-123 7769841-16 1995 Left unexplained are the action of HC, which does not affect bcl-2 expression and the mechanism by which ara-C prevents down-regulation of bcl-2 by ATRA. Tretinoin 148-152 BCL2 apoptosis regulator Homo sapiens 139-144 7769841-4 1995 Exposure of OCI/AML-2 or OCI/AML-5 cells to retinoic acid (all-trans retinoic acid, ATRA) led to a down-regulation of bcl-2 expression that was first seen after 2 h of exposure and was complete after a day. Tretinoin 84-88 BCL2 apoptosis regulator Homo sapiens 118-123 7769841-5 1995 The down-regulation could be prevented by exposing the cells to ara-C either before or after ATRA; decrease in bcl-2 protein was moderate and only obvious after 36 h of ATRA treatment. Tretinoin 93-97 BCL2 apoptosis regulator Homo sapiens 111-116 7769841-5 1995 The down-regulation could be prevented by exposing the cells to ara-C either before or after ATRA; decrease in bcl-2 protein was moderate and only obvious after 36 h of ATRA treatment. Tretinoin 169-173 BCL2 apoptosis regulator Homo sapiens 111-116 7769841-15 1995 ATRA regulates ara-C toxicity by its action on bcl-2. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 47-52 8402688-10 1993 Conversely, stimulation of this I-type clone with retinoic acid resulted in an accumulation of N-type cells (which are thought to represent embryonic precursors of sympathetic neurons), decreased vimentin and beta-2-microglobulin, increased neurofilament-M, and a marked elevation in p26-Bcl-2. Tretinoin 50-63 BCL2 apoptosis regulator Homo sapiens 288-293 8161792-5 1994 After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Tretinoin 51-64 BCL2 apoptosis regulator Homo sapiens 25-29 8161792-5 1994 After treatment of HL-60/BCL2 cells with all-trans retinoic acid or phorbol myristic acid, Bcl2 levels did not decrease as in normal HL-60 cells but, rather, increased because of activation of the viral promoter. Tretinoin 51-64 BCL2 apoptosis regulator Homo sapiens 91-95 30806286-8 2019 ATRA inhibits Bcl-2, up-regulates Beclin-1 expression, and reduces induction of mTOR activation/phosphorylation in NB4 cells. Tretinoin 0-4 BCL2 apoptosis regulator Homo sapiens 14-19 34288263-8 2021 Moreover, all-trans-retinoic acid, which enhances CD38 expression and induces cell differentiation in myeloma cells, reduced B-cell marker expression and the BCL2/BCL2L1 ratio in myeloma cell lines, leading to reduced efficacy of venetoclax. Tretinoin 10-33 BCL2 apoptosis regulator Homo sapiens 158-162 33194073-10 2020 Additionally, we confirmed that Bcl-2 is associated with the induction of ATRA-induced autophagy instead of the PI3K/Akt/mTOR pathway. Tretinoin 74-78 BCL2 apoptosis regulator Homo sapiens 32-37 33194073-11 2020 These findings suggest that ATRA induces autophagy and autophagic cell death through the Bcl-2/Beclin1 pathway. Tretinoin 28-32 BCL2 apoptosis regulator Homo sapiens 89-94 27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 44-67 BCL2 apoptosis regulator Homo sapiens 190-212 30248940-6 2018 Combined treatment with melatonin and retinoic acid decreased the expression of the Bcl-2. Tretinoin 38-51 BCL2 apoptosis regulator Homo sapiens 84-89 30248940-12 2018 The changes in the activation of proliferation in HL-60 cells, the mitotic index, and Bcl-2 expression under combined effect of retinoic acid (10 nM) with melatonin (1 mM) are similar to changes that are induced by 1 muM retinoic acid. Tretinoin 128-141 BCL2 apoptosis regulator Homo sapiens 86-91 29417442-13 2018 Moreover, augmented caspase-3 up-regulation and bcl-2 down-regulation were found following combined application of DAPT and ATRA. Tretinoin 124-128 BCL2 apoptosis regulator Homo sapiens 48-53 27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 44-67 BCL2 apoptosis regulator Homo sapiens 214-218 27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 69-73 BCL2 apoptosis regulator Homo sapiens 190-212 27354299-3 2016 Our objective was to analyze treatment with all-trans-retinoic acid (ATRA) by suppression of the phosphoinositide 3-kinase (PI3K) pathway on growth, signaling pattern and interactions among PI3K/B-cell lymphoma 2 (Bcl2)/retinol leiomyoma proteins. Tretinoin 69-73 BCL2 apoptosis regulator Homo sapiens 214-218 27354299-11 2016 CONCLUSIONS: ATRA treatment on PI3K pathway suppression significantly affected growth, signaling pattern and interactions among PI3K/Bcl2/retinol proteins involved in the growth, survival and apoptosis of leiomyomas. Tretinoin 13-17 BCL2 apoptosis regulator Homo sapiens 133-137