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Browse our CDKN1A Proteins (CDKN1A)

Full name:
Cyclin-Dependent Kinase Inhibitor 1A Proteins (CDKN1A)
On are 2 Cyclin-Dependent Kinase Inhibitor 1A (CDKN1A) Proteins from 2 different suppliers available. Additionally we are shipping CDKN1A Kits (5) and CDKN1A Antibodies (4) and many more products for this protein. A total of 11 CDKN1A products are currently listed.
CAP20, CDKI, Cdkn1, CIP1, MDA-6, mda6, P21, p21Cip1, p21WAF, SDI1, Waf1
list all proteins Gene Name GeneID UniProt
CDKN1A 1026 P38936
Mouse CDKN1A CDKN1A 12575 P39689

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CDKN1A Proteins (CDKN1A) by Origin

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Human Cyclin-Dependent Kinase Inhibitor 1A (CDKN1A) interaction partners

  1. the combination of a proteasomal inhibitor and dimethylfumarate superinduces p21 expression in human dermal lymphendothelial cells

  2. By upregulating p53 (show TP53 Proteins) and p21 expression and inhibiting Akt (show AKT1 Proteins) (Ser473) phosphorylation, SEMA3B (show SEMA3B Proteins) could induce cell cycle arrest at G1/S phase.

  3. p21 expression is observed in half of the cases.

  4. Our findings suggest a possible association between p21 Ser31tabArg polymorphism and susceptibility to the development of cervical lesions in women from Pernambuco. Brazil.

  5. The results demonstrated that the -402, -20, and +182 CDKN1A regions showed a significantly increased acetylation level in at least one of the two histones evaluated (H3 and H4) in patients with gastric adenocarcinomas.

  6. p21 C70T polymorphism does not associate with Uterine leiomyoma (UL). However, CA genotype of C98A polymorphism may contribute to the susceptibility to UL.

  7. miR (show MLXIP Proteins)-639 upregulation was associated with development of thyroid carcinoma, promoting cell proliferation and cell cycle by targeting CDKN1A.

  8. The low p21 level is necessary for the suppressive effect of miR (show MLXIP Proteins)-31.

  9. via gain-of-function analyses, DCN (show DCN Proteins) overexpression could inhibit renal cell carcinoma (show MOK Proteins) (RCC (show XRCC1 Proteins)) cell proliferation and metastasis in vitro and vivo. At the mechanism level, we found that an ectopic expression of DCN (show DCN Proteins) significantly upregulated P21 and E-cadherin (show CDH1 Proteins) expression. Altogether, these results revealed that DCN (show DCN Proteins) is a tumor suppressor in RCC (show XRCC1 Proteins), and it could serve as a potential therapeutic target in patients with RCC (show XRCC1 Proteins).

  10. Low CIP1 expression is associated with colorectal cancer.

Mouse (Murine) Cyclin-Dependent Kinase Inhibitor 1A (CDKN1A) interaction partners

  1. lincRNA-p21 overexpression dramatically inhibited acetylation of H3 and H4 at the Thy-1 (show THY1 Proteins) promoter and Thy-1 (show THY1 Proteins) expression levels in HLF1 (show HLF Proteins) cells. Finally, lincRNA-p21 interference rescued LPS (show TLR4 Proteins)-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 Proteins).

  2. p21 upregulation in hair follicle stem cells is associated with telogen retention in aged mice

  3. 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.

  4. we observed that miR (show MLXIP Proteins)-378 modulates the oscillation amplitudes of Cdkn1a in the control of cell cycle and Por (show POR Proteins) in the regulation of oxidation reduction by forming partnership with different circadian transcription factors

  5. The findings define PRMT7 (show PRMT7 Proteins) as a regulator of the DNMT3b (show DNMT3B Proteins)/p21 axis required to maintain muscle stem cell regenerative capacity.

  6. Dynamics of CDKN1A in single cells has been defined defined by an endogenous fluorescent tagging.

  7. Ablation of p21Cip1 in the Cdk4 (show CDK4 Proteins) R24C background accelerates mesenchymal tumor development in mice.

  8. The lack of functional Waf1 is indispensable for maintaining self-renewal and pluripotency of embryonic stem cells.

  9. p27(Kip1 (show CDKN1B Proteins)) and p21(Cip1) are insufficient for the proliferative inhibition of smooth muscle cells cultured in type 1 collagen.

  10. Foxo3 (show FOXO3 Proteins) circular RNA retards cell cycle progression via forming ternary complexes with p21 and CDK2 (show CDK2 Proteins).

CDKN1A Protein Profile

Protein Summary

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.

Alternative names and synonyms associated with CDKN1A

  • cyclin-dependent kinase inhibitor 1A (p21, Cip1) (CDKN1A)
  • cyclin-dependent kinase inhibitor 1A (P21) (Cdkn1a)
  • CAP20 protein
  • CDKI protein
  • Cdkn1 protein
  • CIP1 protein
  • MDA-6 protein
  • mda6 protein
  • P21 protein
  • p21Cip1 protein
  • p21WAF protein
  • SDI1 protein
  • Waf1 protein

Protein level used designations for CDKN1A

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 , p21

1026 Homo sapiens
12575 Mus musculus
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