Anti-Cdk4 antibody [EPR4513] (ab108355)
- Product nameAnti-Cdk4 antibody [EPR4513]See all Cdk4 primary antibodies ...
- DescriptionRabbit monoclonal [EPR4513] to Cdk4
- Tested applicationsWB, ICC/IF more details
- Species reactivityReacts with: Human
Does not react withMouse, Rat
A synthetic peptide corresponding to residues on the C terminus of Human Cdk4.
- Positive controlWB: HeLa, MCF7 and K562 cell lysates ICC/IF: HeLa cells
- General notesProduced under U.S. Patent No. 5,675,063.
- Storage instructionsStore at -20°C. Stable for 12 months at -20°C
- Storage bufferPBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%
- PurityTissue culture supernatant
- Clonality Monoclonal
- Clone numberEPR4513
- Research Areas
Our Abpromise guarantee covers the use of ab108355 in the following tested applications.
The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
|WB||WB: 1/1000 - 1/10000. Detects a band of approximately 34 kDa (predicted molecular weight: 34 kDa).|
|ICC/IF||ICC/IF: 1/100 - 1/250.|
- FunctionSer/Thr-kinase component of cyclin D-CDK4 (DC) complexes that phosphorylate and inhibit members of the retinoblastoma (RB) protein family including RB1 and regulate the cell-cycle during G(1)/S transition. Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complexes and the subsequent transcription of E2F target genes which are responsible for the progression through the G(1) phase. Hypophosphorylates RB1 in early G(1) phase. Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals. Also phosphorylates SMAD3 in a cell-cycle-dependent manner and represses its transcriptional activity. Component of the ternary complex, cyclin D/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex.
- Involvement in diseaseDefects in CDK4 are a cause of susceptibility to cutaneous malignant melanoma type 3 (CMM3) [MIM:609048]. Malignant melanoma is a malignant neoplasm of melanocytes, arising de novo or from a pre-existing benign nevus, which occurs most often in the skin but also may involve other sites.
- Sequence similaritiesBelongs to the protein kinase superfamily. CMGC Ser/Thr protein kinase family. CDC2/CDKX subfamily.
Contains 1 protein kinase domain.
modificationsPhosphorylation at Thr-172 is required for enzymatic activity. Phosphorylated, in vitro, at this site by CCNH-CDK7, but, in vivo, appears to be phosphorylated by a proline-directed kinase. In the cyclin D-CDK4-CDKN1B complex, this phosphorylation and consequent CDK4 enzyme activity, is dependent on the tyrosine phosphorylation state of CDKN1B. Thus, in proliferating cells, CDK4 within the complex is phosphorylated on Thr-172 in the T-loop. In resting cells, phosphorylation on Thr-172 is prevented by the non-tyrosine-phosphorylated form of CDKN1B.
- Cellular localizationCytoplasm. Nucleus. Membrane. Cytoplasmic when non-complexed. Forms a cyclin D-CDK4 complex in the cytoplasm as cells progress through G(1) phase. The complex accumulates on the nuclear membrane and enters the nucleus on transition from G(1) to S phase. Also present in nucleoli and heterochromatin lumps. Colocalizes with RB1 after release into the nucleus.
- Cdk 4 antibodycdk4 antibodyCDK4 protein antibody
- CDK4_HUMAN antibodyCell division kinase 4 antibodyCell division protein kinase 4 antibodyCMM 3 antibodyCMM3 antibodyCrk3 antibodyCyclin dependent kinase 4 antibodyCyclin-dependent kinase 4 antibodyMelanoma cutaneous malignant 3 antibodyMGC14458 antibodyp34 cdk4 antibodyPSK J3 antibodyPSK-J3 antibody
Anti-Cdk4 antibody [EPR4513] images
All lanes : Anti-Cdk4 antibody [EPR4513] (ab108355) at 1/1000 dilution
Lane 1 : Hela cell lysate
Lane 2 : MCF7 cell lysate
Lane 3 : K562 cell lysate
Lysates/proteins at 10 µg per lane.
Predicted band size : 34 kDa
ab108355, at a 1/100 dilution, staining Cdk4 in HeLa cells by Immunofluorescence.
References for Anti-Cdk4 antibody [EPR4513] (ab108355)
ab108355 has not yet been referenced specifically in any publications.