Rabbit anti-Human CHEK2-S33/35 Polyclonal Antibody | anti-CHEK2 antibody

Phospho-CHEK2-S33/35 Polyclonal Antibody

Cat. Num. AAA9128865

• Gene Names: CHEK2; CDS1; CHK2; LFS2; RAD53; hCds1; HuCds1; PP1425
• Reactivity: Human
• Applications: Western Blot
• Purity: Affinity Purification
• Synonyms: CHEK2-S33/35; Polyclonal Antibody; Phospho-CHEK2-S33/35 Polyclonal Antibody; anti-CHEK2 antibody

• Host: Rabbit
• Reactivity: Human
• Clonality: Polyclonal
• Isotype: IgG
• Purity/Purification: Affinity Purification
• Sequence Length: 586

• Applicable Applications for anti-CHEK2 antibody: Western Blot (WB)
• Application Notes: WB 1:500 - 1:2000
• Route: Synthetic Peptide
• Immunogen: A phospho specific peptide corresponding to residues surrounding S33/35 of human CHEK2
• Preparation and Storage: Store at -20 degree C. Avoid freeze / thaw cycles.; Buffer: PBS with 0.02% sodium azide, 50% glycerol, pH7.3.

Western Blot (WB)

(Western blot analysis of extracts of HeLa and 293 cells, using Phospho-CHEK2-S33/35 antibody at 1:1000 dilution. HeLa cells were treated by UV for 15-30 minutes. 293 cells were treated by UV for 15-30 minutes.Secondary antibody: HRP Goat Anti-Rabbit IgG (H+L) (MBS128200) at 1:10000 dilution.Lysates/proteins: 25ug per lane.Blocking buffer: 3% BSA.)

Related Product Information for anti-CHEK2 antibody

In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene.

NCBI and Uniprot Product Information

• NCBI GI #: 54112407
• NCBI GeneID: 11200
• NCBI Accession #: NP_001005735.1
• NCBI GenBank Nucleotide #: NM_001005735.1
• UniProt Accession #: O96017; Q6QA03; Q6QA04; Q6QA05; Q6QA06; Q6QA07; Q6QA08; Q6QA10; A8K3Y9; B7ZBF3; B7ZBF4; B7ZBF5
• Molecular Weight: 61kDa
• NCBI Official Full Name: serine/threonine-protein kinase Chk2 isoform c
• NCBI Official Synonym Full Names: checkpoint kinase 2
• NCBI Official Symbol: CHEK2
• NCBI Official Synonym Symbols: CDS1; CHK2; LFS2; RAD53; hCds1; HuCds1; PP1425
• NCBI Protein Information: serine/threonine-protein kinase Chk2
• UniProt Protein Name: Serine/threonine-protein kinase Chk2
• Protein Family: Serine/threonine-protein kinase
• UniProt Gene Name: CHEK2
• UniProt Synonym Gene Names: CDS1; CHK2; RAD53; Hucds1; hCds1
• UniProt Entry Name: CHK2_HUMAN

NCBI Description

In response to DNA damage and replication blocks, cell cycle progression is halted through the control of critical cell cycle regulators. The protein encoded by this gene is a cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. When activated, the encoded protein is known to inhibit CDC25C phosphatase, preventing entry into mitosis, and has been shown to stabilize the tumor suppressor protein p53, leading to cell cycle arrest in G1. In addition, this protein interacts with and phosphorylates BRCA1, allowing BRCA1 to restore survival after DNA damage. Mutations in this gene have been linked with Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype usually associated with inherited mutations in TP53. Also, mutations in this gene are thought to confer a predisposition to sarcomas, breast cancer, and brain tumors. This nuclear protein is a member of the CDS1 subfamily of serine/threonine protein kinases. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Apr 2012]

Uniprot Description

Chk2: a CAMK protein kinase of the Rad53 family. A cell cycle checkpoint regulator and putative tumor suppressor. It contains a forkhead-associated protein interaction domain essential for activation in response to DNA damage and is rapidly phosphorylated in response to replication blocks and DNA damage. Phosphorylates and inhibits CDC25C, preventing entry into mitosis, p53, leading to cell cycle arrest in G1, and BRCA1, restoring survival after DNA damage. Twelve splice variant isoforms have been described for human Chk2. LOF mutants cause Li-Fraumeni syndrome, a highly penetrant familial cancer phenotype also caused by p53 mutations. Familial mutations also associated with prostate and breast cancer, and mutations also seen in a variety of sporadic cancers and cell lines.

Protein type: Protein kinase, CAMK; Protein kinase, Ser/Thr (non-receptor); EC 2.7.11.1; Kinase, protein; Tumor suppressor; CAMK group; RAD53 family

Chromosomal Location of Human Ortholog: 22q12.1

Cellular Component: nucleoplasm; Golgi apparatus; PML body; chromosome, telomeric region

Molecular Function: protein serine/threonine kinase activity; identical protein binding; protein binding; protein homodimerization activity; ubiquitin protein ligase binding; metal ion binding; protein kinase binding; ATP binding

Biological Process: DNA damage induced protein phosphorylation; transcription, DNA-dependent; protein stabilization; protein amino acid autophosphorylation; positive regulation of transcription, DNA-dependent; DNA damage response, signal transduction; protein amino acid phosphorylation; DNA damage response, signal transduction resulting in induction of apoptosis; regulation of transcription, DNA-dependent; cellular protein catabolic process; cell division; double-strand break repair; DNA damage checkpoint; response to gamma radiation; regulation of protein catabolic process; G2/M transition of mitotic cell cycle; response to DNA damage stimulus

Disease: Li-fraumeni Syndrome 2; Breast Cancer; Prostate Cancer; Osteogenic Sarcoma