CHEK2 Antikörper (N-Term)

Produktnummer ABIN1881196

Produktdetails anti-CHEK2 Antikörper

Target: CHEK2 (Checkpoint Kinase 2 (CHEK2))

Bindungsspezifität: AA 111-141, N-Term

Reaktivität: Human

Wirt: Kaninchen

Klonalität: Polyklonal

Konjugat: Dieser CHEK2 Antikörper ist unkonjugiert

Applikation: Western Blotting (WB), Immunofluorescence (IF), Immunohistochemistry (Paraffin-embedded Sections) (IHC (p)), Flow Cytometry (FACS)

Aufreinigung: This antibody is purified through a protein A column, followed by peptide affinity purification.

Immunogen: This CHEK2 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 111-141 amino acids from the N-terminal region of human CHEK2.

Klon: RB19067

Isotyp: Ig Fraction

Anwendungsinformationen

Applikationshinweise: IF: 1:10~50. WB: 1:1000. WB: 1:1000. IHC-P: 1:50~100. FC: 1:10~50

Beschränkungen: Nur für Forschungszwecke einsetzbar

Handhabung

Format: Liquid

Buffer: Purified polyclonal antibody supplied in PBS with 0.09 % (W/V) sodium azide.

Konservierungsmittel: Sodium azide

Vorsichtsmaßnahmen: This product contains Sodium azide: a POISONOUS AND HAZARDOUS SUBSTANCE which should be handled by trained staff only.

Lagerung: 4 °C,-20 °C

Haltbarkeit: 6 months

Referenzen für anti-CHEK2 Antikörper (ABIN1881196)

Xiao, Zheng, Huang, Liu, Zhang, Ma: "Deficiency of 53BP1 inhibits the radiosensitivity of colorectal cancer." in: International journal of oncology, Vol. 49, Issue 4, pp. 1600-8, (2017) (PubMed).

Yao, Huang, Zheng, Liu, Lin, Zhang, Yang, Zhang, Ma: "53BP1 loss induces chemoresistance of colorectal cancer cells to 5-fluorouracil by inhibiting the ATM-CHK2-P53 pathway." in: Journal of cancer research and clinical oncology, Vol. 143, Issue 3, pp. 419-431, (2017) (PubMed).

Yang, Wood, Hrushesky: "Mammalian TIMELESS is required for ATM-dependent CHK2 activation and G2/M checkpoint control." in: The Journal of biological chemistry, Vol. 285, Issue 5, pp. 3030-4, (2010) (PubMed).

Varmark, Kwak, Theurkauf: "A role for Chk2 in DNA damage induced mitotic delays in human colorectal cancer cells." in: Cell cycle (Georgetown, Tex.), Vol. 9, Issue 2, pp. 312-20, (2010) (PubMed).

Zhu, Miao, Huang, Feng, Zhang, Lu, Cai, Tong, Xu, Qian, Ding: "Naphthalimides induce G(2) arrest through the ATM-activated Chk2-executed pathway in HCT116 cells." in: Neoplasia (New York, N.Y.), Vol. 11, Issue 11, pp. 1226-34, (2009) (PubMed).

Details zu CHEK2

Target: CHEK2 (Checkpoint Kinase 2 (CHEK2))

Andere Bezeichnung: CHEK2 (CHEK2 Produkte)

Synonyme: CDS1 antikoerper, CHK2 antikoerper, HuCds1 antikoerper, LFS2 antikoerper, PP1425 antikoerper, RAD53 antikoerper, hCds1 antikoerper, fa66f08 antikoerper, wu:fa66f08 antikoerper, zgc:55865 antikoerper, Cds1 antikoerper, HUCDS1 antikoerper, Rad53 antikoerper, Chk2 antikoerper, cds1 antikoerper, chek2 antikoerper, chk2 antikoerper, hucds1 antikoerper, lfs2 antikoerper, pp1425 antikoerper, rad53 antikoerper, checkpoint kinase 2 antikoerper, serine/threonine-protein kinase chk2 antikoerper, checkpoint kinase 2 L homeolog antikoerper, CHEK2 antikoerper, chek2 antikoerper, Chek2 antikoerper, MCYG_07308 antikoerper, chek2.L antikoerper

Hintergrund: CHEK2 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.

Molekulargewicht: 60915

NCBI Accession: NP_001005735, NP_001244316, NP_009125, NP_665861

UniProt: O96017

Pathways: p53 Signalweg, Apoptose, Zellzyklus