Summary
Basic Information
Immunogen
Purified recombinant fragment of human CDKN1A (AA: 1-164) expressed in E. Coli.
Clonality
Monoclonal Antibody
Application Notes
Application | Note |
WB | 1:500-1:2,000 |
ICC | 1:25-1:200 |
FC | 1:200-1:400 |
ELISA | 1:10,000 |
Formulations & Storage [For reference only, actual COA shall prevail!]
Concentration
Batch dependent
Purity
> 95% Purity determined by SDS-PAGE.
Storage
Store at +4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freezethaw cycles.
Target
Function
May be involved in p53/TP53 mediated inhibition of cellular proliferation in response to DNA damage. Binds to and inhibits cyclin-dependent kinase activity, preventing phosphorylation of critical cyclin-dependent kinase substrates and blocking cell cycle progression. Functions in the nuclear localization and assembly of cyclin D-CDK4 complex and promotes its kinase activity towards RB1. At higher stoichiometric ratios, inhibits the kinase activity of the cyclin D-CDK4 complex. Inhibits DNA synthesis by DNA polymerase delta by competing with POLD3 for PCNA binding (PubMed:11595739).
Plays an important role in controlling cell cycle progression and DNA damage-induced G2 arrest (PubMed:9106657).
Biological Process
Animal organ regeneration Source: Ensembl
Cell cycle arrest Source: BHF-UCL
Cellular response to amino acid starvation Source: UniProtKB
Cellular response to DNA damage stimulus Source: BHF-UCL
Cellular response to extracellular stimulus Source: BHF-UCL
Cellular response to gamma radiation Source: Ensembl
Cellular response to heat Source: Ensembl
Cellular response to ionizing radiation Source: BHF-UCL
Cellular response to UV-B Source: UniProtKB
Cellular senescence Source: BHF-UCL
Cytokine-mediated signaling pathway Source: Reactome
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest Source: BHF-UCL
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator Source: Ensembl
G1/S transition of mitotic cell cycle Source: BHF-UCL
G2/M transition of mitotic cell cycle Source: BHF-UCL
Granulocyte differentiation Source: Reactome
Heart development Source: BHF-UCL
Intestinal epithelial cell maturation Source: Ensembl
Intrinsic apoptotic signaling pathway Source: ProtInc
Intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator Source: Ensembl
Mitotic cell cycle arrest Source: BHF-UCL
Mitotic G2 DNA damage checkpoint Source: UniProtKB
Negative regulation of apoptotic process Source: Ensembl
Negative regulation of cardiac muscle tissue regeneration Source: BHF-UCL
Negative regulation of cell growth Source: BHF-UCL
Negative regulation of cell population proliferation Source: BHF-UCL
Negative regulation of cyclin-dependent protein kinase activity Source: CAFA
Negative regulation of DNA biosynthetic process Source: UniProtKB
Negative regulation of G1/S transition of mitotic cell cycle Source: MGI
Negative regulation of gene expression Source: Ensembl
Negative regulation of phosphorylation Source: BHF-UCL
Negative regulation of protein binding Source: UniProtKB
Negative regulation of vascular associated smooth muscle cell proliferation Source: BHF-UCL
Positive regulation of B cell proliferation Source: Ensembl
Positive regulation of fibroblast proliferation Source: BHF-UCL
Positive regulation of programmed cell death Source: Ensembl
Positive regulation of protein kinase activity Source: MGI
Positive regulation of reactive oxygen species metabolic process Source: BHF-UCL
Protein import into nucleus Source: Ensembl
Protein stabilization Source: Reactome
Ras protein signal transduction Source: BHF-UCL
Regulation of cell cycle G1/S phase transition Source: UniProtKB
Regulation of cyclin-dependent protein serine/threonine kinase activity Source: ProtInc
Regulation of transcription by RNA polymerase II Source: Reactome
Regulation of transcription initiation from RNA polymerase II promoter Source: Reactome
Replicative senescence Source: Ensembl
Response to arsenic-containing substance Source: Ensembl
Response to corticosterone Source: Ensembl
Response to drug Source: Ensembl
Response to hyperoxia Source: Ensembl
Response to organonitrogen compound Source: Ensembl
Response to toxic substance Source: Ensembl
Response to X-ray Source: Ensembl
Stress-induced premature senescence Source: BHF-UCL
Tissue regeneration Source: Ensembl
Wound healing Source: Ensembl
Cellular Location
Nucleus; Cytoplasm
PTM
Phosphorylation of Thr-145 by Akt or of Ser-146 by PKC impairs binding to PCNA. Phosphorylation at Ser-114 by GSK3-beta enhances ubiquitination by the DCX(DTL) complex. Phosphorylation of Thr-145 by PIM2 enhances CDKN1A stability and inhibits cell proliferation. Phosphorylation of Thr-145 by PIM1 results in the relocation of CDKN1A to the cytoplasm and enhanced CDKN1A protein stability. UV radiation-induced phosphorylation at Thr-80 by LKB1 and at Ser-146 by NUAK1 leads to its degradation.
Ubiquitinated by MKRN1; leading to polyubiquitination and 26S proteasome-dependent degradation. Ubiquitinated by the DCX(DTL) complex, also named CRL4(CDT2) complex, leading to its degradation during S phase or following UV irradiation. Ubiquitination by the DCX(DTL) complex is essential to control replication licensing and is PCNA-dependent: interacts with PCNA via its PIP-box, while the presence of the containing the 'K+4' motif in the PIP box, recruit the DCX(DTL) complex, leading to its degradation. Ubiquitination at Ser-2 leads to degradation by the proteasome pathway. Ubiquitinated by RNF114; leading to proteasomal degradation.
Acetylation leads to protein stability. Acetylated in vitro on Lys-141, Lys-154, Lys-161 and Lys-163. Deacetylation by HDAC1 is prevented by competitive binding of C10orf90/FATS to HDAC1 (By similarity).