ライフサイエンスコーパス: CDKN1A

1 a damage-inducible cell-cycle inhibitor p21 (CDKN1A).

2 the universal cell cycle inhibitor p21(cip) (CDKN1A).

3 e gene encoding the cell cycle inhibitor p21(CDKN1A).

4 coding cyclin-dependent kinase inhibitor 1a (Cdkn1a).

5 of the cyclin-dependent kinase inhibitor p21(CDKN1A).

6 inhibitors, p15Ink4b (Cdkn2b) and p21Cdkn1a (Cdkn1a).

7 which activates transcription of p21(Waf1) (CDKN1A).

8 wnregulation by TP53 generally requires p21 (CDKN1A).

9 s, inducing senescence via activation of p21/CDKN1A.

10 on loss of cyclin-dependent kinase inhibitor CDKN1A.

11 a phenotype that was rescued by depletion of Cdkn1a.

12 er, and function in collaboration to repress CDKN1A.

13 ion of transcription of target genes such as CDKN1a.

14 he cyclin-dependent kinase inhibitor, p21cip/CDKN1A.

15 ng the cyclin-dependent kinase inhibitor p21/CDKN1A.

16 rve head variation) alters the expression of cdkn1a.

17 transcription of the cell cycle arrest gene CDKN1A.

18 ecrease levels of p53 and the p53 target p21/CDKN1A.

19 tor coordinately upregulated GADD45alpha and CDKN1A.

20 transcription of a number of genes including CDKN1A.

21 n-dependent kinase inhibitor p21(Waf1/Cip1) (Cdkn1a), a factor associated with reduced proliferative

22 by upregulation of the cell cycle inhibitor, cdkn1a, a Copeb transcriptional target.

23 2 and microRNAs, and represses expression of Cdkn1a, a cyclin-dependent kinase inhibitor that negativ

24 However, our data reveal that Cdkn1a, a NOTCH target, was upregulated in Nle1 mutants,

25 g, alone or in combination with silencing of CDKN1A, a well-described KLF4 target, did not fully reve

26 Both CDKN1A accumulation and apoptosis were partially depende

27 Transient p53-p21 (also known as CDKN1A) activation and cell-cycle arrest promoted cell s

28 cyclin-dependent kinase inhibitor p21(Cip1) (Cdkn1a) activity.

29 ed expression of its downstream target gene, Cdkn1a (alias p21 or p21(Waf1/Cip1)).

30 ription factor E2a and its downstream target Cdkn1a also distinguished Ssbp2(-/-) HSPCs from wild-typ

31 Haploinsufficiency for p21 (Cdkn1a) also synergizes with KrasG12D to drive PDAC in t

32 t gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21(WAF1/CIP1)) increases apoptosi

33 or CtBP1 in PC-3 cells induced expression of CDKN1A and CDH1 and additional KLF6 target genes.

34 ibition of reporter constructs driven by the CDKN1A and CDH1 promoters in PC-3 prostate carcinoma cel

35 ether on the promoters of the genes encoding CDKN1A and CDH1.

36 gest that in a European-American population, CDKN1A and CDKN1B variants are associated with advanced

37 on of the cyclin-dependent kinase inhibitors CDKN1A and CDKN1B, G(1) cell cycle arrest and apoptosis.

38 5% CI, 1.05-4.22) for high-risk genotypes of CDKN1A and CDKN1B, respectively].

39 2 and Tbx3 repress the cell-cycle inhibitors Cdkn1a and Cdkn1b, we conclude that Tbx2 and Tbx3 mainta

40 suppressor gene TP53, cell cycle inhibitors CDKN1A and CDKN2A, and MAOA-downstream genes that promot

41 , and the cyclin-dependent kinase inhibitors CDKN1A and CDKN2B.

42 gh upregulation of the cell cycle inhibitors Cdkn1a and Cdkn2c.

43 c-Myc-targeted cell cycle regulators CCND1, CDKN1A and CDKN2D in a time-dependent manner.

44 uble-strand break response pathway (Atm, p21/Cdkn1a and Chk2/Chek2) had decreased tumor latency and/o

45 sion of p53 transcriptional targets, such as CDKN1A and DDB2, and enhanced expression of proliferatio

46 d levels of the cell cycle regulator p21/WAF/CDKN1A and disrupts TGF-beta-driven differentiation of s

47 recurrent protein-inactivating mutations in CDKN1A and FAT1.

48 We observed a significant upregulation of CDKN1A and FOXO3A in decitabine- versus control-treated

49 ted by the re-expression of a subset of TSs (CDKN1A and FOXO3A) that are epigenetically silenced via

50 cells decreases cellular levels of TP53 and CDKN1A and increases CDC2 and proliferating cell nuclear

51 r, we identified a novel association between CDKN1A and POAG.

52 tumour suppressors including Lrig1, Bmpr1a, Cdkn1a and Pten.

53 C) formation through epigenetic silencing of CDKN1A and release of cell cycle checkpoints.

54 CDKN1A and RUNX2 (both 6p21.2) were amplified in 11 and

55 owever, further investigation of the role of CDKN1A and RUNX2 in CoMs development and that of MLH1, T

56 essor that collaborates with p53 to regulate CDKN1A and SMAD3 transcription and tumor growth in gynec

57 veral downstream targets of ARID1A including CDKN1A and SMAD3, which are well-known p53 target genes.

58 ncer regions of the key cell cycle regulator Cdkn1a and the stem cell regulator Bmp4 in NSPCs and alt

59 ncreasing the expression of its target genes CDKN1A and ZNF652.

60 ivo by downregulating miR17 and upregulating CDKN1A and ZNF652.

61 Analysis of CDKN1A and/or CDKN1B genotypes may prove useful in deter

62 rylation, together with the induction of p21(CDKN1A) and apoptosis of normal breast epithelium.

63 easured by induction of p21/WAF1 (encoded by Cdkn1a) and apoptosis, while irradiated early- and mid-p

64 n-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A) and B-cell CLL/lymphoma 2 binding component 3 (B

65 vealed the CIP/KIP family members p21(cip1) (Cdkn1a) and p27(kip1) (Cdkn1b) to be expressed at higher

66 We report that defects of p21(CDKN1A) and p53 enhance camptothecin-induced histone H2A

67 the expression of cell-cycle inhibitor p21 (CDKN1A) and that the inhibitory effects of DANCR loss on

68 -dependent kinase (CDK) inhibitor p21(Cip1) (CDKN1A) and the proapoptotic Bcl-2 family member p53 up-

69 This occurs through the induction of p21 (CDKN1A) and the recruitment of the repressive DREAM comp

70 al KLF6 target genes notably p21(WAF1/CIP1) (CDKN1A) and to a lesser extent E-cadherin (CDH1), indica

71 ramming, down-regulation of CDK 1A mRNA (p21/CDKN1A), and up-regulation of antiapoptotic Bcl-2 mRNA.

72 Nr4a1, Cdkn1a, and c-fos transcripts were evaluated in WT and E

73 gets have been characterized so far: m-numb, CDKN1A, and c-mos.

74 cellular senescence markers such as CDKN2A, CDKN1A, and CAV1 was elevated in the peripheral lung tis

75 ction in expression of mRNA for MAPK9, TP53, CDKN1A, and CDKN1B was greater in patients not receiving

76 fied DNA regulatory regions within the Cd44, Cdkn1a, and Cdkn2b genes, indicating they are direct FOX

77 activate transcription of the reporter gene CDKN1A, and in situ subcellular fractionation experiment

78 e and microRNA networks, containing miR-150, CDKN1A, and MYC, and provide mechanistic support for the

79 Csf1R, Mpo, Cebpd, the cell cycle inhibitor Cdkn1a, and myeloid markers Cebpa and Gfi1.

80 The other loci were in NFIA, near CDKN1A, and near C6orf204.

81 ession of the cell-cycle regulators Rb1, p21/Cdkn1a, and p16/Ink4a, resulting in a loss of cell-cycle

82 ases in ROS along with decreases in TP53 and CDKN1A, and that these cellular responses are mechanisti

83 aches, we further identified p21 (encoded by CDKN1A) as a functionally important megakaryopoietic reg

84 lation of p21(CIP1/WAF1/Sdi1) (also known as Cdkn1a) as a major contributor to the interference with

85 of the p53 pathway, gadd45 (Gadd45a) or p21 (Cdkn1a), as well as MEFs lacking both gadd45 and p21 gen

86 Among p53-regulated genes, p21 (Cdkn1a), but not Puma (Bbc3) played a partial role in iP

87 nd miR-132-3p and genes including NFKBIZ and CDKN1A, but DE did not significantly modify this allerge

88 Repression of CDKN1A by allergen-induced miR-132-3p may contribute to

89 ses that occur along with the decreased TP53/CDKN1A bystander effect also would expectedly favor enha

90 n the CCNB1, CCND1, CCNE1, CDK2, CDK4, CDK6, CDKN1A, CDKN1B, and CDKN2A genes were genotyped and eval

91 ich has been implicated in human malignancy: CDKN1A, CDKN1B, and CDKN2C.

92 Down-regulation of the genes encoding Cdkn1a, Cdkn1b, and Mcl1 occurs after acute Apc excision

93 yclin-dependent kinase inhibitors, including Cdkn1a, Cdkn1b, Cdkn1c, Cdkn2b, and Cdkn2c.

94 CND1, CCND2, CCND3, CCNE1, CDK2, CDK4, CDK6, CDKN1A, CDKN1B, CDKN2A, CDKN2B, CDKN2C, and CDKN2D-and r

95 ssed reduced baseline levels of MAPK9, TP53, CDKN1A, CDKN1B, CHEK2, and RANGAP1 messenger RNA (mRNA)

96 or suppressor genes (CDKN2B, CDKN2A, CDKN2D, CDKN1A, CDKN1B, TP53, BRCA1, TIMP3, APC, RASSF1, CDH1, M

97 Bmi-1 and hence inhibits the TP53, PTEN and CDKN1A/CDKN2A pathway.

98 (Timp3, Adamts9) and cell cycle progression (Cdkn1a, Cdkn2b, Cenpj, Tubb4a), which are critical for l

99 Human BCCIPalpha (Tok-1alpha) is a BRCA2 and CDKN1A (Cip1, p21) interacting protein.

100 ting partner, and through Miz-1 binds to the CDKN1A core promoter.

101 n Mitf-mediated activation of the p21(Cip1) (CDKN1A) cyclin-dependent kinase inhibitor gene.

102 vity to taxanes (ABCB1, ABCC1, ABCC2, ABCG2, CDKN1A, CYP1B1, CYP2C8, CYP3A4, CYP3A5, MAPT, and TP53)

103 Three genes - CDKN1A, DDB2 and ADRB2 - exhibited a trend towards loss

104 ong induction of DNA damage responsive genes CDKN1A, DDIT3, GADD45A/G, and PPM1D, and repression of g

105 G1 to S phase transition of GC B cells in a Cdkn1a-dependent manner.

106 /Waf1)) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect.

107 tly down-regulating the cell cycle inhibitor Cdkn1a during heart development.

108 utations or MDM2 amplification, showing that CDKN1A dysfunction is not simply an alternative mechanis

109 evels of phospho-Rb, indicating that loss of Cdkn1a enables progression of cell cycle.

110 trols GC B cell proliferation by suppressing CDKN1A, enabling cell cycle progression with a concomita

111 cell cycle arrest through targets including CDKN1A (encodes p21((waf1/cip1))).

112 CDKN1A encoding p21(Cip1) has been identified as a Gfi-1

113 y eIF2alpha-P involved induced expression of CDKN1A encoding the p21 (CIP1/WAF1) protein.

114 Furthermore, we showed that CDKN1A (encoding p21) acted in part to mediate growth su

115 LED knockdown reduces CDKN1A enhancer induction and activity, and cell cycle a

116 literature mining revealed that seven genes (CDKN1A, ESR1, MAX, MYC, PPARGC1A, SP1, and STK11) and on

117 idence interval (CI), 0.46-0.82] but not for CDKN1A-expressed (RR, 1.32; 95% CI, 0.76-2.31) tumors.

118 wer risk for CDKN1A-nonexpressed but not for CDKN1A-expressed cancers was also present among current

119 use and colorectal cancer risk according to CDKN1A expression (P(heterogeneity) = 0.01).

120 he islet progenitor cells failed to activate Cdkn1a expression and continued to proliferate, showing

121 he endogenous promoter and full induction of CDKN1A expression.

122 GC B cells of Cdkn1a (-/-) Ezh2 (-/-) mice have high levels of phospho

123 Three genes of this panel (CDKN1A, FDXR and BBC3) were also highly sensitive to LPS

124 between unirradiated and irradiated samples (CDKN1A, FDXR, BBC3, PCNA, GADD45a, XPC, POLH and DDB2).

125 provides evidence for the importance of p21(CDKN1A) for the repair of replication-mediated DNA doubl

126 more, low dose-rate radiation did not induce Cdkn1a, Gadd45a, Mdm2, Atm, or Dbd2.

127 ter-bound KLF6 inhibits transcription of the CDKN1A gene and other genes as well by tethering a trans

128 The deletion of the Cdkn1a gene in Tsg101 conditional knock-out cells result

129 ol of the endogenous p21 promoter within the Cdkn1a gene locus were generated.

130 G-2 can directly repress the activity of the Cdkn1a gene promoter, suggesting a model by which FOG-2/

131 BRG1's association with the human CDKN2A and CDKN1A gene promoters was enhanced during senescence ind

132 LED was located at an enhancer region within CDKN1A gene, a potent p53-responsive cell cycle inhibito

133 ndent kinase (CDK)-inhibitor p21(Waf1/Cip1) (CDKN1A) gene, a prototypic transcriptional target of p53

134 of the cyclin-dependent kinase inhibitor 1A (CDKN1A) gene, with a focus on its dual role in promoting

135 involves stimulation of the p21(Waf1/Cip1) (Cdkn1a) gene.

136 bax gene, but not cell cycle-associated p21 (CDKN1A) gene.

137 at the regulatory region of the p53 and p21 (Cdkn1a) genes.

138 CDKN1A genotype was scored as CC, CT, and TT on the basi

139 The CDKN1A genotypes CT and TT were associated with an incre

140 ted hypoxic induction of HIF-1 target genes (CDKN1A, GLUT-1, and VEGF), tumor angiogenesis in vitro,

141 We show here that Gfi-1 represses CDKN1A in a manner that is independent of its DNA bindin

142 cell cycle control genes Cdkn2a, Cdkn2b and Cdkn1a in cultured cells, there is no evidence that loss

143 pression, caspase inhibition, or knockout of Cdkn1a in Emicro-Myc lymphoma, and depletion of Hdac3 in

144 nt with this notion, the genetic ablation of Cdkn1a in FOG-2(R3K5A) mice leads to an improvement in l

145 sed expression of p21 (also known as Waf1 or CDKN1a) in Atm-/- cells serves as a cellular defense mec

146 -dependent kinase (CDK) inhibitor encoded by CDKN1A, in HCC.

147 Nr4a1 increased 24.5- and 14.7-fold, Cdkn1a increased 14.2- and 12.3-fold, and c-fos increase

148 K) inhibitors p16INK4A (CDKN2A) and p21CIP1 (CDKN1A), increased secretion of many bio-active factors

149 this report, we show that BCCIP, a BRCA2 and CDKN1A-interacting protein, is required for the transact

150 of POAG and showed that genetic variation in CDKN1A is important in POAG risk.

151 f activated TP53, the tumour-suppressor gene CDKN1A is responsible for cell-cycle arrest following DN

152 p21 (WAF1/CIP1; CDKN1a) is a universal cell-cycle inhibitor directly con

153 e cyclin-dependent kinase inhibitor 1A gene (CDKN1A), is significantly greater (P<.001) among twin pa

154 ely regulates AFP and MYB but transactivates CDKN1A, is a good candidate for the 16q22 tumor-suppress

155 n Treg cell numbers upon exposure to IR, but Cdkn1a(-/-) LCs did not.

156 KN1A (p21) was overexpressed in LCs and that Cdkn1a(-/-) LCs underwent apoptosis and accumulated DNA

157 dly decreased their proliferation, increased Cdkn1a levels, and eventually caused profound hyperglyce

158 n of an active chromatin conformation at the CDKN1A locus and increased gene expression.

159 ngs suggest that TGM2-mediated autophagy and CDKN1A-mediated cell cycle arrest are two important barr

160 e(+)Trp53(Delta2-10/Delta2-10) mice, but not Cdkn1a(-/-) mice, formed tumors with bilineal differenti

161 reased beta-galactosidase activity, elevated CDKN1A mRNA expression, and induction of nuclear p21.

162 We further show that human CDKN1A mRNA splice variant 4 is preferentially translate

163 y upstream ORFs situated in the 5'-leader of CDKN1A mRNA.

164 x SNP associations in or near SCN5A, SCN10A, CDKN1A, NFIA, HAND1, TBX5 and SETBP1 replicated in Afric

165 y use was associated with a reduced risk for CDKN1A-nonexpressed [multivariate relative risk (RR), 0.

166 The lower risk for CDKN1A-nonexpressed but not for CDKN1A-expressed cancers

167 In contrast, in Cdkn1a null mice, proliferation was incompletely suppres

168 ons were identified between BRAF mutation or CDKN1A or RUNX2 amplification and sex, age, histologic c

169 increase expression of the p53 target genes CDKN1A or TNFRSF10B/DR5.

170 n p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apopto

171 o the role of the cell cycle checkpoint gene CDKN1a, or p21(cip1/waf1).

172 P = 3.0 x 10(-10)) and an upstream region of CDKN1A (P = 2 x 10(-52)), suggesting roles for cell cycl

173 e new CRC risk loci at 6p21 (rs1321311, near CDKN1A; P = 1.14 x 10(-10)), 11q13.4 (rs3824999, introni

174 ic variants in the 3'-untranslated region of CDKN1A (p21(cip1)) and in codon 109 of CDKN1B (p27(kip1)

175 ysis indicated that the cell cycle inhibitor Cdkn1a (p21(cip1)) is up-regulated 2.0+/-0.2-fold in FOG

176 ression of cyclin-dependent kinase inhibitor CDKN1A (p21(Cip1)).

177 Notably, the known KLF7 target Cdkn1a (p21(Cip1/Waf1)) was not induced by KLF7, and los

178 ion of the cyclin-dependent kinase inhibitor CDKN1A (p21(CIP1/WAF1)).

179 Steady-state expression and Induction of CDKN1a (p21) and Arf were impaired in HSCs from Dmtf1(-/

180 artment by directly inhibiting expression of Cdkn1a (p21) and Cdkn1c (p57), and in the primitive endo

181 In contrast, the expression levels of CDKN1A (p21) and CDKN2A (p16) were unchanged.

182 while wt- and S15A-p53 are detectable on the CDKN1A (p21) promoter (as a representative p53-responsiv

183 Our results identify endothelial Cdkn1a (p21) upregulation in a mouse model of early-onse

184 esulted in cyclin-dependent kinase inhibitor Cdkn1a (p21) upregulation.

185 d that the cyclin-dependent kinase inhibitor CDKN1A (p21) was overexpressed in LCs and that Cdkn1a(-/

186 er of tumor-suppressor genes including Rhoh, Cdkn1a (p21), and Blnk (SLP65).

187 RG, and four involving non-ETS genes such as CDKN1A (p21), CD9, and IKBKB (IKK-beta), genes known to

188 associated with significant derepression of Cdkn1a (p21), Cdkn1c (P27), Lats1, Lats2, Rb1, Rbl, Bim,

189 pregulation of senescence-associated targets Cdkn1a (p21), Serpine1 (PAI-1), Tagln (Sm22), Fn1 and Cl

190 sion of two additional genes, TP53 (p53) and CDKN1A (p21), which are considered functionally unrelate

191 n, including NFKBIA (IKBalpha), GADD45B, and CDKN1A (p21); transcription-related genes such as CEBP,

192 ll-cycle-related tumor biomarkers, including CDKN1A (p21, CIP1), CDKN1B (p27, KIP1), and TP53 (p53) b

193 F6 (CD95/FAS), the DNA-damage response genes CDKN1A (p21/Cip1), p53-induced gene-3, and DNA binding p

194 optosis is associated with overexpression of CDKN1A (p21/Waf1)and down-regulation of survivin at both

195 nhibition reduced median time to moribund in Cdkn1a(p21(CIP/WAF1))-/- mice after TBI.

196 inhibition decreased cell death in crypts in Cdkn1a(p21(CIP/WAF1))-/- mice at 4 h after TBI.

197 S phase cells in crypts in wild-type but not Cdkn1a(p21(CIP/WAF1))-/- mice.

198 lso increased cell death in crypts at 4 h in Cdkn1a(p21(CIP/WAF1))-/-, earlier than at 24 h in wild-t

199 germ-line p53(R283H) could transactivate the CDKN1A((p21, WAF1, cip1, SDI1)) but not the BAX gene and

200 T116 cells deficient for p53 (p53-/-) or p21(CDKN1A) (p21-/-) as the cells reach the late-S and G2 ph

201 RNA of cyclin-dependent kinase inhibitor 1A (Cdkn1a, p21) as a direct target of FXR1P.

202 -galactosidase activity, higher abundance of CDKN1A/P21 and TP53, and reduced cell proliferation.

203 /Cbfb deletion, PAR-1 overexpression induced CDKN1A/p21 expression and attenuated proliferation in ML

204 s hepatocarcinogenesis by directly targeting CDKN1A/p21 expression.

205 le-dependent kinase inhibitors CDKN2C/p18 or CDKN1A/p21 facilitates cell cycle entry of quiescent adu

206 Furthermore, expression of CDKN1a/p21 in bone increased 3.31 fold (p<0.01), and was

207 ch the cyclin-dependent kinase inhibitor 1A (CDKN1A/p21) gene was the most prominent.

208 0b, including BCL2L11/Bim, TFAP2C/AP-2gamma, CDKN1A/p21, and CDKN2A/p16, which normally protect cells

209 rogravity-induced osteocytic osteolysis, and CDKN1a/p21-mediated osteogenic cell cycle arrest.

210 the combined effects of cytokinesis failure, CDKN1A/p21-mediated RB1 inhibition, and the onset of sen

211 the quiescent survival-promoting function of CDKN1a/p21.

212 3 targets including the cell cycle regulator CDKN1A (p21CIP), the WNT pathway regulator DKK1 (dickkop

213 We further discovered that knocking down Cdkn1a (p21cip1), a Usp16 target and regulated gene, res

214 elevated levels of the cell cycle regulators Cdkn1a (p21Cip1), Ccnd2 (CyclinD2), and Trp63 (p63) that

215 ecreasing expression of TGF-beta targets p21(CDKN1A), p27 (CDKN1B), and E-cadherin.

216 p53 lysine 120 with the BAX gene but not the CDKN1A p53-responsive elements.

217 d p21 (cyclin-dependent kinase inhibitor 1a, Cdkn1a), p57, and p15 up-regulated at quiescence onset.

218 tial novel functions for NLE1 in the WNT and CDKN1A pathways during embryonic development in mammals.

219 We propose that p21(CDKN1A) prevents the collapse of replication forks damag

220 cent protein DsRed2 under the control of the CDKN1A promoter (HepG2CDKN1A-DsRed cells).

221 at while TFAP2C and Myc can downregulate the CDKN1A promoter independently, KDM5B acts as a corepress

222 through Miz-1, form a ternary complex on the CDKN1A promoter, and function in collaboration to repres

223 DNA damage induces five lncRNAs from the CDKN1A promoter, and one such lncRNA, named PANDA, is in

224 at three VDR binding sites (R1, 2, 3) on the CDKN1A promoter.

225 TATA binding protein (TBP) and POLR2E to the CDKN1A promoter.

226 , functional interaction by AP-2gamma at the CDKN1A proximal promoter.

227 RS duration), CAV1-CAV2 locus (PR interval), CDKN1A (QRS duration), NOS1AP, KCNH2, and KCNQ1 (QTc int

228 x promotes cell cycle progression via direct CDKN1A repression, thereby contributing to tumorigenesis

229 All three factors collaborate for optimal CDKN1A repression, which requires the AP-2 binding site

230 Deletion of Cdkn1a rescues the GC reaction in Ezh2 (-/-) mice.

231 r ROS bystander effect, this "decreased TP53/CDKN1A response" can be mimicked in otherwise untreated

232 ication of the central cell-cycle regulators CDKN1A, retinoblastoma protein, and cyclin D1 (CCND1), b

233 s1800054), ADH1B 3' UTR A --> G (rs1042026), CDKN1A S31R (rs1801270), ICAM5 V301I (rs1056538) and NUM

234 ing of ABL2, SEMA4D, ITGAL, and C1QA, TIMP1, CDKN1A) separated patients with castration-resistant pro

235 K11) and one novel MYC-centered pathway with CDKN1A, SP1, and STK11 might play important roles in met

236 l regulation of apoptosis, and genes such as Cdkn1a, suggesting a mechanism for how signaling centers

237 translation of a specific splice variant of CDKN1A that facilitates G1 arrest and subsequent DNA rep

238 in the MRL mouse, we show that the unrelated Cdkn1a(tmi/Tyj)/J p21(-/-) mouse (unlike the B6129SF2/J

239 Stabilized p53 binds CDKN1A to establish a G(1) phase of cell cycle without a

240 s evidence that miR-302 may silence p21Cip1 (CDKN1A) to promote cell proliferation, whereas studies i

241 Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently

242 These results thus implicate the E2A-CDKN1A transcriptional axis in the control of megakaryop

243 proteins hyper-transactivate p53-target gene CDKN1A upon glutamine deprivation, thus triggering cell

244 mation and inhibits camptothecin-induced p21(CDKN1A) upregulation in HCT116 wt cells.

245 d that induction of the cell cycle inhibitor Cdkn1a was responsible for the decreased proliferation i

246 D1, and Mmp2 were up-regulated whereas p21 (Cdkn1a) was down-regulated.

247 expression of the cell cycle inhibitor p21 (CDKN1A) was regulated by LRH-1 in HCT116 cells.

248 alidated previously implicated genes such as CDKN1A We developed an innovative approach that integrat

249 increased expression of ACTG2, TGFB1I1, and CDKN1A were mediated by up-regulation of the smooth musc

250 part, through direct regulation of Rbl2 and Cdkn1a, whereas apical-basal polarity is controlled by r

251 the expression of p53 target genes, such as CDKN1A (which encodes p21).

252 independent up-regulation of p21(WAF1/cip1) (CDKN1A), which is abrogated in several tumor-derived mut

253 d a 15-bp repressor element at the 3'-UTR of CDKN1A, which contains a binding site for miR-95-3p.

254 3 acetylation and to increased expression of CDKN1A, which encodes the cell cycle regulator p21(WAF1)

255 Reduced expression of both CDKN1A, which regulates the cell cycle downstream of TP5

256 nd clock-controlled genes (c-Myc, NR1D1, and CDKN1A), with Period1 expression being hair cycle depend