Product Name: CCND1 Antibody
Species Reactivity: Human
Tested Applications: WB
Applications: For WB starting dilution is: 1:1000
User Note: Optimal dilutions for each application to be determined by the researcher.
Predicted Molecular Weight: 34 kDa
Immunogen: 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.
Host Species: Rabbit
Purification: This antibody is purified through a protein A column, followed by peptide affinity purification.
Physical State: Liquid
CAS NO.: 1439934-41-4
Product: CTX-0294885
Buffer: Supplied in PBS with 0.09% (W/V) sodium azide.
Concentration: 0.5 mg/ml
Storage Conditions: Store at 4˚C for three months and -20˚C, stable for up to one year. As with all antibodies care should be taken to avoid repeated freeze thaw cycles. Antibodies should not be exposed to prolonged high temperatures.
Clonality: Polyclonal
Conjugate: Unconjugated
Alternate Names: G1/S-specific cyclin-D1, B-cell lymphoma 1 protein, BCL-1, BCL-1 oncogene, PRAD1 oncogene, CCND1, BCL1, PRAD1
Accession NO.: P24385
Protein Ino: 116152
Official Symbol: CCND1
Geneid: 595
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.
PubMed ID:http://aac.asm.org/content/43/9/2138.abstract
