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CCND1 Antibody (C-term T288)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS: 1
- PROTOCOLS
- BACKGROUND
Application 
| WB, E |
|---|---|
| Primary Accession | P24385 |
| Other Accession | NP_444284.1 |
| Reactivity | Human |
| Host | Rabbit |
| Clonality | Polyclonal |
| Isotype | Rabbit IgG |
| Calculated MW | 33729 Da |
| Antigen Region | 267-294 aa |
| Gene ID | 595 |
|---|---|
| Other Names | G1/S-specific cyclin-D1, B-cell lymphoma 1 protein, BCL-1, BCL-1 oncogene, PRAD1 oncogene, CCND1, BCL1, PRAD1 |
| Target/Specificity | This CCND1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 267-294 amino acids from the C-terminal region of human CCND1. |
| Dilution | WB~~1:1000 |
| Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
| Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
| Precautions | CCND1 Antibody (C-term T288) is for research use only and not for use in diagnostic or therapeutic procedures. |
| Name | CCND1 {ECO:0000303|PubMed:8204893, ECO:0000312|HGNC:HGNC:1582} |
|---|---|
| Function | Regulatory component of the cyclin D1-CDK4 (DC) complex that phosphorylates and inhibits members of the retinoblastoma (RB) protein family including RB1 and regulates the cell-cycle during G(1)/S transition (PubMed:1827756, PubMed:1833066, PubMed:19412162, PubMed:33854235, PubMed:8114739, PubMed:8302605). Phosphorylation of RB1 allows dissociation of the transcription factor E2F from the RB/E2F complex and the subsequent transcription of E2F target genes which are responsible for the progression through the G(1) phase (PubMed:1827756, PubMed:1833066, PubMed:19412162, PubMed:8114739, PubMed:8302605). Hypophosphorylates RB1 in early G(1) phase (PubMed:1827756, PubMed:1833066, PubMed:19412162, PubMed:8114739, PubMed:8302605). Cyclin D-CDK4 complexes are major integrators of various mitogenenic and antimitogenic signals (PubMed:1827756, PubMed:1833066, PubMed:19412162, PubMed:8302605). Also a substrate for SMAD3, phosphorylating SMAD3 in a cell-cycle-dependent manner and repressing its transcriptional activity (PubMed:15241418). Component of the ternary complex, cyclin D1/CDK4/CDKN1B, required for nuclear translocation and activity of the cyclin D-CDK4 complex (PubMed:9106657). Exhibits transcriptional corepressor activity with INSM1 on the NEUROD1 and INS promoters in a cell cycle-independent manner (PubMed:16569215, PubMed:18417529). |
| Cellular Location | Nucleus. Cytoplasm Nucleus membrane. Note=Cyclin D-CDK4 complexes accumulate at the nuclear membrane and are then translocated to the nucleus through interaction with KIP/CIP family members |
Provided below are standard protocols that you may find useful for product applications.
Background
The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance throughout the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition. This protein has been shown to interact with tumor suppressor protein Rb and the expression of this gene is regulated positively by Rb. Mutations, amplification and overexpression of this gene, which alters cell cycle progression, are observed frequently in a variety of tumors and may contribute to tumorigenesis.
References
Aggarwal, P., et al. Cancer Cell 18(4):329-340(2010) Iwatani, K., et al. Biochem. Biophys. Res. Commun. 400(3):426-431(2010) Halilovic, E., et al. Cancer Res. 70(17):6804-6814(2010) Zheng, W., et al. Anal. Quant. Cytol. Histol. 32(3):155-160(2010) Satiroglu-Tufan, N.L., et al. Genet. Mol. Res. 9(3):1557-1567(2010)
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