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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
23 2 and microRNAs, and represses expression of Cdkn1a, a cyclin-dependent kinase inhibitor that negativ
25 g, alone or in combination with silencing of CDKN1A, a well-described KLF4 target, did not fully reve
30 ription factor E2a and its downstream target Cdkn1a also distinguished Ssbp2(-/-) HSPCs from wild-typ
32 t gene cyclin-dependent kinase inhibitor 1A (CDKN1A, also known as p21(WAF1/CIP1)) increases apoptosi
34 ibition of reporter constructs driven by the CDKN1A and CDH1 promoters in PC-3 prostate carcinoma cel
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.
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
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
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
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
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
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.
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
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
87 nd miR-132-3p and genes including NFKBIZ and CDKN1A, but DE did not significantly modify this allerge
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
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
98 (Timp3, Adamts9) and cell cycle progression (Cdkn1a, Cdkn2b, Cenpj, Tubb4a), which are critical for l
102 vity to taxanes (ABCB1, ABCC1, ABCC2, ABCG2, CDKN1A, CYP1B1, CYP2C8, CYP3A4, CYP3A5, MAPT, and TP53)
104 ong induction of DNA damage responsive genes CDKN1A, DDIT3, GADD45A/G, and PPM1D, and repression of g
108 utations or MDM2 amplification, showing that CDKN1A dysfunction is not simply an alternative mechanis
110 trols GC B cell proliferation by suppressing CDKN1A, enabling cell cycle progression with a concomita
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
120 he islet progenitor cells failed to activate Cdkn1a expression and continued to proliferate, showing
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
127 ter-bound KLF6 inhibits transcription of the CDKN1A gene and other genes as well by tethering a trans
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
140 ted hypoxic induction of HIF-1 target genes (CDKN1A, GLUT-1, and VEGF), tumor angiogenesis in vitro,
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
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
151 f activated TP53, the tumour-suppressor gene CDKN1A is responsible for cell-cycle arrest following DN
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
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
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.
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.
168 ons were identified between BRAF mutation or CDKN1A or RUNX2 amplification and sex, age, histologic c
170 n p53 or its target gene, p21 (also known as Cdkn1a), or by antagonizing reprogramming-induced apopto
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
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
182 while wt- and S15A-p53 are detectable on the CDKN1A (p21) promoter (as a representative p53-responsiv
185 d that the cyclin-dependent kinase inhibitor CDKN1A (p21) was overexpressed in LCs and that Cdkn1a(-/
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
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
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
205 le-dependent kinase inhibitors CDKN2C/p18 or CDKN1A/p21 facilitates cell cycle entry of quiescent adu
208 0b, including BCL2L11/Bim, TFAP2C/AP-2gamma, CDKN1A/p21, and CDKN2A/p16, which normally protect cells
210 the combined effects of cytokinesis failure, CDKN1A/p21-mediated RB1 inhibition, and the onset of sen
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
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.
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
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
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
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
243 proteins hyper-transactivate p53-target gene CDKN1A upon glutamine deprivation, thus triggering cell
245 d that induction of the cell cycle inhibitor Cdkn1a was responsible for the decreased proliferation i
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
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)
256 nd clock-controlled genes (c-Myc, NR1D1, and CDKN1A), with Period1 expression being hair cycle depend
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