PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16406622-8 2006 Pretreatment with ATRA, cells expressing antisense cyclinD1 or antisense CDK4 showed a lesser decrease of B(a)P-induced overexpression of E2F-1 compared with similarly treated HELF. Tretinoin 18-22 cyclin dependent kinase 4 Homo sapiens 73-77 21437295-10 2011 The ensemble of models also correctly predicted Rb and p47phox regulation and the correlation between p21-CDK4-cyclin D formation and G1/0-arrest following exposure to RA. Tretinoin 168-170 cyclin dependent kinase 4 Homo sapiens 106-110 18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 46-59 cyclin dependent kinase 4 Homo sapiens 91-95 18539384-3 2008 In addition, LMP1 abolished the potentials of retinoic acid (RA) to down-regulate Cdk2 and Cdk4 and to up-regulate p16, p21, and p27, resulting in activation of E2F1 in the presence of RA. Tretinoin 61-63 cyclin dependent kinase 4 Homo sapiens 91-95 15715961-6 2005 RA treatment caused cell cycle arrest at G(1) and decreased the expressions and activities of CDK2 or CDK4 in RA-sensitive HepG2 and SNU354 cells. Tretinoin 0-2 cyclin dependent kinase 4 Homo sapiens 102-106 15715961-7 2005 On the other hand, RA-resistant Hep3B and SNU449 cells progressed into the S/G(2)+M phase and showed increased CDK2 and CDK4 expression and activity. Tretinoin 19-21 cyclin dependent kinase 4 Homo sapiens 120-124 15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 cyclin dependent kinase 4 Homo sapiens 133-158 15040006-9 2004 We have also shown that the ATRA dependent increase in p27/kip1 protein in CAOV3 cells leads to a decrease in the kinase activity of cyclin dependent kinase 4 (CDK4) following ATRA treatment. Tretinoin 28-32 cyclin dependent kinase 4 Homo sapiens 160-164 15040006-10 2004 Finally, we found that CAOV3 cells stably transfected with a p27/kip1antisense construct, which express lower levels of p27/kip1 following ATRA treatment, and have a higher CDK4 kinase activity are less sensitive to ATRA induced growth suppression. Tretinoin 139-143 cyclin dependent kinase 4 Homo sapiens 173-177 12955881-5 2003 In fetal cells, however, the induction of apoptosis and differentiation by RA was obtained via inhibition of cyclin D1-cdk4 activity, as result of an increased binding to the p16 inhibitor. Tretinoin 75-77 cyclin dependent kinase 4 Homo sapiens 119-123 15587392-7 2004 ATRA inhibited the mRNA expression of CDK6, CDK4, cyclinD3 and cyclinD1. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 44-48 15587392-9 2004 ATRA and sodium butyrate inhibited the mRNA expression of CDK6, CDK4, CDK2, cyclinD1, cyclinD2 and cyclinD3. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 64-68 12915404-8 2003 Obligate CDK4 phosphorylation sites seemed most important to the stability of the protein and are among the candidate sites that are dephosphorylated by PP2A following ATRA treatment. Tretinoin 168-172 cyclin dependent kinase 4 Homo sapiens 9-13 11030153-8 2000 We also showed that an increase in CDK2-bound p27 and CDK4-bound p18 are caused by treatment with ATRA and a decrease in CDK6-bound cyclin D3 is induced synergistically by treatment with both reagents. Tretinoin 98-102 cyclin dependent kinase 4 Homo sapiens 54-58 11753676-6 2001 Also, RA treatment increased expression of the cdk inhibitor p27 and decreased activity of cdk 2, cdk 4 and cdk 6. Tretinoin 6-8 cyclin dependent kinase 4 Homo sapiens 98-103 10896783-6 2000 Evaluation of the kinase activity of cyclin-Cdk complexes showed that RA increases p27(Kip1) expression in CH27 cells leading to markedly reduced cyclin A/Cdk2 kinase activity and slightly reduced cyclin E/Cdk2 kinase activity, with no effect on cyclin D/Cdk4 and cyclin D/Cdk6 activities. Tretinoin 70-72 cyclin dependent kinase 4 Homo sapiens 255-259 10447003-8 1999 These findings provide the first evidence that t-RA activates degradation of CDK-4 through the ubiquitin-proteasome pathway, a novel mechanism by which t-RA causes HBE cells to exit the cell cycle, and blockade of these signaling events may contribute to the development of retinoid resistance in NSCLC cells. Tretinoin 47-51 cyclin dependent kinase 4 Homo sapiens 77-82 10447003-8 1999 These findings provide the first evidence that t-RA activates degradation of CDK-4 through the ubiquitin-proteasome pathway, a novel mechanism by which t-RA causes HBE cells to exit the cell cycle, and blockade of these signaling events may contribute to the development of retinoid resistance in NSCLC cells. Tretinoin 152-156 cyclin dependent kinase 4 Homo sapiens 77-82 11601206-6 1999 The activities of cyclin E/CDK2 and the amounts of cyclin D1/CDK4 complexes were decreased in ATRA- or AE-treated HL-60 cells. Tretinoin 94-98 cyclin dependent kinase 4 Homo sapiens 61-65 10094816-4 1999 In addition, RA had no effect on the levels of Bcl-XL; Bcl-XS; cyclins A, B, D1, D3, or E; or Rb1 expression but markedly down-modulated Cdk2 kinase activity and reduced Cdk4 expression. Tretinoin 13-15 cyclin dependent kinase 4 Homo sapiens 170-174 9778049-3 1998 Herein we show that RA-induced LCL accumulation in the G0/G1 phases correlated with the loss of the catalytic activity of all three G1-associated CDKs (CDK2, CDK4 and CDK6) and with increased levels of underphosphorylated pRb and, in some LCLs, p130. Tretinoin 20-22 cyclin dependent kinase 4 Homo sapiens 158-162 9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase 4 Homo sapiens 50-54 9778049-6 1998 p27Kip-1 may also contribute to the inhibition of CDK4 kinase activity, as the amount of CDK4-associated p27Kip-1 was increased by 50% after RA exposure. Tretinoin 141-143 cyclin dependent kinase 4 Homo sapiens 89-93 9778049-9 1998 Overall, these results demonstrate that RA treatment of EBV-immortalized B lymphocytes is associated with multiple effects on G1 regulatory proteins, including p27Kip1 up-regulation, decreased levels of cyclins D2, D3 and A, and inhibition of CDK2, CDK4 and CDK6 activity, which ultimately result in reduced pRb phosphorylation and G0/G1 growth arrest. Tretinoin 40-42 cyclin dependent kinase 4 Homo sapiens 249-253 9259311-6 1997 While cdk4 activity was similar in control and RA-treated cells, cdk2 activity began to decrease within 48 h of exposure to RA and was profoundly reduced after 72 h. This reduced activity was associated with decreased phosphorylation of cdk2. Tretinoin 47-49 cyclin dependent kinase 4 Homo sapiens 6-10 9260897-2 1997 RA did not affect cyclins D1, A, and E and cyclin-dependent kinase 2 (CDK2) expression, but significantly reduced cyclin D3 and CDK4 expression after 24 h. RA also inhibited cyclin B1 and CDC2 expression, possibly responsible for the reduction of the proportion of cells in G2 + M and S phases. Tretinoin 0-2 cyclin dependent kinase 4 Homo sapiens 128-132 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 cyclin dependent kinase 4 Homo sapiens 146-150 9185997-7 1997 Expression of cyclin D1, cyclin-dependent kinase 4, and cyclin E proteins, however, decreased in association with RA-mediated G1 arrest. Tretinoin 114-116 cyclin dependent kinase 4 Homo sapiens 25-50 30216786-2 2018 With retinoic acid (RA) induction, a high percentage of cells were found to be arrested at the G0/G1 phase, with decreased levels of cyclinD1, CDK4, phosphorylation status of pRb and E2F1, in addition to an elevated level of p27. Tretinoin 5-18 cyclin dependent kinase 4 Homo sapiens 143-147 24563337-8 2014 ATRA treated with C-PC could induce more cell cycle arrests than the single drug used by decrease in cyclin D1 and CDK4 expression. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 115-119 24635079-8 2014 ATRA also induced G1 cell-cycle arrest, inhibited the expression of cyclin D1/cyclin-dependent kinase (CDK)4 and cyclinE/CDK2, and increased the expression of the cyclin-dependent kinase inhibitors p21 and p27. Tretinoin 0-4 cyclin dependent kinase 4 Homo sapiens 103-108