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these findings indicated that HMGB1 (show HMGB1 ELISA Kits) promoted hepatocellular carcinoma progression partly by enhancing the ERK1/2 (show MAPK1/3 ELISA Kits) and NF-kappaB (show NFKB1 ELISA Kits) pathways, upregulating MMP-2 (show MMP2 ELISA Kits), and downregulating p21 via an ERK (show EPHB2 ELISA Kits)/c-Myc (show MYC ELISA Kits) pathway
High CIP1 expression is associated with metastasis occurrence in Prostate Cancer.
Results indicated that p21 was responsible for the downregulation of G2/M transition regulatory proteins and the bypass of mitosis induced by irradiation.
JMJD5 (show JMJD5 ELISA Kits) is a tumor suppressor gene in HCC (show FAM126A ELISA Kits) pathogenesis, and the epigenetic silencing of JMJD5 (show JMJD5 ELISA Kits) promotes HCC (show FAM126A ELISA Kits) cell proliferation by directly down-regulating CDKN1A transcription.
Nested multiplex polymerase chain reactions to detect the presence of the HPV types, as well as immunohistochemical reactions were performed for the detection of cell cycle-related proteins p16, p27 (show PAK2 ELISA Kits), p53 (show TP53 ELISA Kits) and Ki-67 (show MKI67 ELISA Kits). The expression of all analyzed cell cycle-related proteins was increased in HPV-infected papillomas
High expression of CIP1 is associated with recurrence in oral squamous cell carcinoma.
Urolithin A incubation caused the up-regulation of CDKN1A and down-regulation of FN-1 (show FN1 ELISA Kits) in prostate cancer cells.
Results show that while HOXB13 (show HOXB13 ELISA Kits) suppressed p21 expression via regulation of JNK (show MAPK8 ELISA Kits) signals, alteration of p21 expression also affected c-Jun (show JUN ELISA Kits) and AP-1 (show FOSB ELISA Kits) activity in prostate cancer cells.
HIF-alpha promotes chronic CML (show BCR ELISA Kits) cell proliferation by up-regulating p21 expression
Alterations in p53 (show TP53 ELISA Kits) and p21 expression suggest that these proteins are involved in lower lip carcinogenesis. Moreover, p53 (show TP53 ELISA Kits) and hMSH2 (show MSH2 ELISA Kits) seem to be interrelated in early events of this process.
lincRNA-p21 overexpression dramatically inhibited acetylation of H3 and H4 at the Thy-1 (show THY1 ELISA Kits) promoter and Thy-1 (show THY1 ELISA Kits) expression levels in HLF1 (show HLF ELISA Kits) cells. Finally, lincRNA-p21 interference rescued LPS (show TLR4 ELISA Kits)-induced increase of lung and BAL collagen contents. LincRNA-p21 could lead to pulmonary fibrosis in ARDS by inhibition of the expression of Thy-1 (show THY1 ELISA Kits).
p21 upregulation in hair follicle stem cells is associated with telogen retention in aged mice
MiR-17-92 functions as a hepatocyte proliferation stimulator and acts in an estrogen-dependent manner. The loss of this miRNA results in increases in p21 and Pten expression and therefore impairs liver regeneration in female mice.
we observed that miR (show MLXIP ELISA Kits)-378 modulates the oscillation amplitudes of Cdkn1a in the control of cell cycle and Por (show POR ELISA Kits) in the regulation of oxidation reduction by forming partnership with different circadian transcription factors
The findings define PRMT7 (show PRMT7 ELISA Kits) as a regulator of the DNMT3b (show DNMT3B ELISA Kits)/p21 axis required to maintain muscle stem cell regenerative capacity.
Dynamics of CDKN1A in single cells has been defined defined by an endogenous fluorescent tagging.
Ablation of p21Cip1 in the Cdk4 (show CDK4 ELISA Kits) R24C background accelerates mesenchymal tumor development in mice.
The lack of functional Waf1 is indispensable for maintaining self-renewal and pluripotency of embryonic stem cells.
p27(Kip1 (show CDKN1B ELISA Kits)) and p21(Cip1) are insufficient for the proliferative inhibition of smooth muscle cells cultured in type 1 collagen.
Foxo3 (show FOXO3 ELISA Kits) circular RNA retards cell cycle progression via forming ternary complexes with p21 and CDK2 (show CDK2 ELISA Kits).
This gene encodes a potent cyclin-dependent kinase inhibitor. The encoded protein binds to and inhibits the activity of cyclin-CDK2 or -CDK4 complexes, and thus functions as a regulator of cell cycle progression at G1. The expression of this gene is tightly controlled by the tumor suppressor protein p53, through which this protein mediates the p53-dependent cell cycle G1 phase arrest in response to a variety of stress stimuli. This protein can interact with proliferating cell nuclear antigen (PCNA), a DNA polymerase accessory factor, and plays a regulatory role in S phase DNA replication and DNA damage repair. This protein was reported to be specifically cleaved by CASP3-like caspases, which thus leads to a dramatic activation of CDK2, and may be instrumental in the execution of apoptosis following caspase activation. Multiple alternatively spliced variants have been found for this gene.
CDK-interacting protein 1
, CDK-interaction protein 1
, DNA synthesis inhibitor
, cyclin-dependent kinase inhibitor 1
, melanoma differentiation associated protein 6
, wild-type p53-activated fragment 1
, melanoma differentiation-associated protein