Rabbit anti-Human, Mouse CHK1 Polyclonal Antibody | anti-CHEK1 antibody

CHK1 Antibody (C-term)

Cat. Num. AAA9216960

• Gene Names: CHEK1; CHK1
• Reactivity: Human, Mouse
• Applications: Western Blot
• Synonyms: CHK1; Polyclonal Antibody; CHK1 Antibody (C-term); Purified Rabbit Polyclonal Antibody (Pab); Serine/threonine-protein kinase Chk1; CHK1 checkpoint homolog; Cell cycle checkpoint kinase; Checkpoint kinase-1; CHEK1; anti-CHEK1 antibody

• Host: Rabbit
• Reactivity: Human, Mouse
• Clonality: Polyclonal
• Sequence Length: 476

• Applicable Applications for anti-CHEK1 antibody: Western Blot (WB)
• Application Notes: WB~~1:2000
• Antigen Type: Synthetic Peptide
• Preparation and Storage: Maintain refrigerated at 2-8 degree C for up to 6 months. For long term storage store at -20 degree C in small aliquots to prevent freeze-thaw cycles.

Western Blot (WB)

(All lanes : Anti-CHK1 Antibody (D440) at 1:2000 dilutionLane 1: CCRF-CEM whole cell lysateLane 2: Hela whole cell lysateLane 3: mouse colon lysateLysates/proteins at 20 ug per lane. SecondaryGoat Anti-Rabbit IgG, (H+L), Peroxidase conjugated at 1/10000 dilution. Predicted band size : 54 kDaBlocking/Dilution buffer: 5% NFDM/TBST.)

Related Product Information for anti-CHEK1 antibody

Checkpoint pathways control the order and timing of cell cycle transitions and ensure that critical events, such as DNA replication and chromosome segregation, are completed with high fidelity. Antibodies against CHK1 recognize a 54-kD protein on immunoblots of mammalian cell extracts, but the protein has altered mobility when isolated from cells treated with ionizing radiation (IR), indicating that CHK1 is modified in response to DNA damage. In vitro, CHK1 directly phosphorylates a regulator of CDC2 tyrosine phosphorylation, CDC25C. Evidence indicates that in response to DNA damage, CHK1 phosphorylates and inhibits CDC25C, thus preventing activation of the CDC2-cyclin B complex and mitotic entry. Proteolysis of activated CHK1 may promote checkpoint termination under normal conditions and may play a role in the cytotoxic effects of camptothecin and related anticancer drugs.

Product Categories/Family for anti-CHEK1 antibody

Cancer

References

Chen, M.S., et al., Mol. Cell. Biol. 23(21):7488-7497 (2003). Krause, D.R., et al., Oncogene 22(38):5927-5937 (2003). Wang, X., et al., J. Biol. Chem. 278(33):30869-30874 (2003). Goudelock, D.M., et al., J. Biol. Chem. 278(32):29940-29947 (2003). Xiao, Z., et al., J. Biol. Chem. 278(24):21767-21773 (2003).

NCBI and Uniprot Product Information

• NCBI GI #: 166295194
• NCBI GeneID: 1111
• NCBI Accession #: NP_001107593.1
• NCBI GenBank Nucleotide #: NM_001114121.2
• UniProt Accession #: O14757; A8K934; B4DDD0; B4DSK3; B5BTY6; F5H7S4; H2BI51
• Molecular Weight: 50,415 Da
• NCBI Official Full Name: serine/threonine-protein kinase Chk1 isoform 1
• NCBI Official Synonym Full Names: checkpoint kinase 1
• NCBI Official Symbol: CHEK1
• NCBI Official Synonym Symbols: CHK1
• NCBI Protein Information: serine/threonine-protein kinase Chk1
• UniProt Protein Name: Serine/threonine-protein kinase Chk1
• UniProt Gene Name: CHEK1
• UniProt Synonym Gene Names: CHK1
• UniProt Entry Name: CHK1_HUMAN

NCBI Description

The protein encoded by this gene belongs to the Ser/Thr protein kinase family. It is required for checkpoint mediated cell cycle arrest in response to DNA damage or the presence of unreplicated DNA. This protein acts to integrate signals from ATM and ATR, two cell cycle proteins involved in DNA damage responses, that also associate with chromatin in meiotic prophase I. Phosphorylation of CDC25A protein phosphatase by this protein is required for cells to delay cell cycle progression in response to double-strand DNA breaks. Several alternatively spliced transcript variants have been found for this gene. [provided by RefSeq, Oct 2011]

Uniprot Description

Serine/threonine-protein kinase which is required for checkpoint-mediated cell cycle arrest and activation of DNA repair in response to the presence of DNA damage or unreplicated DNA. May also negatively regulate cell cycle progression during unperturbed cell cycles. This regulation is achieved by a number of mechanisms that together help to preserve the integrity of the genome. Recognizes the substrate consensus sequence [R-X-X-S/T]. Binds to and phosphorylates CDC25A, CDC25B and CDC25C. Phosphorylation of CDC25A at 'Ser-178' and 'Thr-507' and phosphorylation of CDC25C at 'Ser-216' creates binding sites for 14-3-3 proteins which inhibit CDC25A and CDC25C. Phosphorylation of CDC25A at 'Ser-76', 'Ser-124', 'Ser-178', 'Ser-279' and 'Ser-293' promotes proteolysis of CDC25A. Phosphorylation of CDC25A at 'Ser-76' primes the protein for subsequent phosphorylation at 'Ser-79', 'Ser-82' and 'Ser-88' by NEK11, which is required for polyubiquitination and degradation of CDCD25A. Inhibition of CDC25 leads to increased inhibitory tyrosine phosphorylation of CDK-cyclin complexes and blocks cell cycle progression. Also phosphorylates NEK6. Binds to and phosphorylates RAD51 at 'Thr-309', which promotes the release of RAD51 from BRCA2 and enhances the association of RAD51 with chromatin, thereby promoting DNA repair by homologous recombination. Phosphorylates multiple sites within the C-terminus of TP53, which promotes activation of TP53 by acetylation and promotes cell cycle arrest and suppression of cellular proliferation. Also promotes repair of DNA cross-links through phosphorylation of FANCE. Binds to and phosphorylates TLK1 at 'Ser-743', which prevents the TLK1-dependent phosphorylation of the chromatin assembly factor ASF1A. This may enhance chromatin assembly both in the presence or absence of DNA damage. May also play a role in replication fork maintenance through regulation of PCNA. May regulate the transcription of genes that regulate cell-cycle progression through the phosphorylation of histones. Phosphorylates histone H3.1 (to form H3T11ph), which leads to epigenetic inhibition of a subset of genes. May also phosphorylate RB1 to promote its interaction with the E2F family of transcription factors and subsequent cell cycle arrest.