CHK2 Antibody (YA3581)
(Synonyms: CDS1; LFS2; CHEK2)CHK2 Antibody (YA3581) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to CHK2.
-
Host:
Mouse
-
Isotype:
IgG
-
Application:
WB, IHC-P, ICC/IF, ELISA
-
Reactivity :
Human
-
Formulation:
Supplied in PBS with 0.05% sodium azide.
-
Conjugation:
Non-conjugated
Applications
| Application |
WB
WB: Western Blot
|
IHC-P
IHC-P: Immunohistochemistry-Paraffin
|
ICC/IF
ICC/IF: Immunocytochemistry/
Immunofluorescence |
ELISA
ELISA: Enzyme Linked Immunosorbent Assay
|
|---|---|---|---|---|
| Dilution Ratio | 1:500-1:2000 | 1:200-1:1000 | 1:200-1:1000 | 1:10000 |
Product Details
CHK2 Antibody (YA3581) is a Mouse-derived and non-conjugated IgG2b monoclonal antibody, targeting to CHK2.
-
Host Mouse
-
Clonality Monoclonal
-
Species ReactivityHuman
-
Observed Molecular WeightObserved band size: 61 kDaNote: Due to possible protein modifications or aggregation, the molecular weight should be confirmed by actual measurement, and the predicted value is for reference only.
-
Calculated Molecular Weight Predicted band size: 61 kDa
Purified recombinant fragment of human CHK2 (aa481-531) expressed in E. Coli.
affinity purified.
Non-conjugated
Unmodified
IgG
Product Properties
-
Appearance
Solution
-
Formulation
Supplied in PBS with 0.05% sodium azide.
-
Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
-
Shipping
Shipping with blue ice.
Background
-
Function
Checkpoint kinase Chk2 (CHEK2) is a serine/threonine kinase and key DNA damage response component that coordinates checkpoint activation, DNA repair, apoptosis, senescence, or damage tolerance after genotoxic stress[1]. Mechanistically, ATM-mediated Thr68 phosphorylation triggers CHK2 dimerization through phospho-Thr68-FHA interactions, followed by activation-loop autophosphorylation and kinase activation[2]. Activated CHK2 connects DNA damage signaling to p53 stabilization, BRCA1 phosphorylation, and cell-cycle control, therefore supporting genome integrity research in cancer models[3][4]. In disease contexts, CHK2 functions as a tumor-suppressive kinase linked to cancer susceptibility, while experimental data also show context-dependent roles in DNA damage-induced apoptosis and checkpoint arrest[5][6]. Compared with Chk1, CHK2 is structurally distinct and is activated mainly by DNA damage, whereas Chk1 has a broader role in S-phase and G2 checkpoint control[6]. For experimental applications, the selective CHK2 inhibitor CCT241533 blocks CHK2 activity in tumor cell lines after DNA damage and potentiates cytotoxicity of PARP inhibitors, supporting pathway-dissection studies rather than unsupported monotherapy claims[7].- CHK2 links ATM-driven DNA damage signaling to p53, BRCA1, apoptosis, and checkpoint control. - CHK2 differs from Chk1 in activation pattern, checkpoint dependence, and experimental inhibitor utility.
-
Subcellular Localization
Nucleus; Nucleus; Nucleus; Nucleus; Nucleus; Nucleus, PML body; Nucleus, nucleoplasm
-
Expression
Tissue_specificity:This gene is highly expressed in the testes, spleen, colon, and peripheral blood leukocytes, but lowly expressed in other tissues. -
Isoforms & Post-Translational Modification
O96017 has 13 isomers: O96017-1: 60915 Da (predicted); O96017-2: 26084 Da (predicted); O96017-3: 17370 Da (predicted); O96017-4: 50203 Da (predicted); O96017-5: 22594 Da (predicted); O96017-6: 18706 Da (predicted); O96017-7: 38125 Da (predicted); O96017-8: 32142 Da (predicted); O96017-9: 65419 Da (predicted); O96017-10: 15420 Da (predicted); O96017-11: 24396 Da (predicted); O96017-12: 57526 Da (predicted); O96017-13: 36157 Da (predicted).
Phosphorylated. Phosphorylated at Ser-73 by PLK3 in response to DNA damage, promoting phosphorylation at Thr-68 by ATM and the G2/M transition checkpoint. Phosphorylation at Thr-68 induces homodimerization. Autophosphorylates at Thr-383 and Thr-387 in the T-loop/activation segment upon dimerization to become fully active and phosphorylate its substrates like for instance CDC25C. DNA damage-induced autophosphorylation at Ser-379 induces CUL1-mediated ubiquitination and regulates the pro-apoptotic function. Phosphorylation at Ser-456 also regulates ubiquitination. Phosphorylated by PLK4;Ubiquitinated. CUL1-mediated ubiquitination regulates the pro-apoptotic function. Ubiquitination may also regulate protein stability. Ubiquitinated by RNF8 via 'Lys-48'-linked ubiquitination -
Subunit
Homodimer. Homodimerization is part of the activation process but the dimer may dissociate following activation. Interacts with PML. Interacts with TP53. Interacts with RB1; phosphorylates RB1. Interacts with BRCA1. Interacts (phosphorylated at Thr-68) with MDC1; requires ATM-mediated phosphorylation of CHEK2. Interacts with TP53BP1; modulates CHEK2 phosphorylation at Thr-68 in response to ionizing radiation. Interacts with CDC25A; phosphorylates CDC25A and mediates its degradation in response to ionizing radiation. Interacts with CUL1; mediates CHEK2 ubiquitination and regulation. Interacts with CDKN2AIP. Interacts (via protein kinase domain) with CCAR2 (via N-terminus). Interacts with SIRT1
-
SwissProt ID
-
Synonyms
CDS1; LFS2; CHEK2
Documentation
References
[1]. Zannini L, et al. CHK2 kinase in the DNA damage response and beyond. J Mol Cell Biol. 2014 Dec;6(6):442-57. [Content Brief]
[2]. Cai Z, et al. Structure and activation mechanism of the CHK2 DNA damage checkpoint kinase. Mol Cell. 2009 Sep 24;35(6):818-29. [Content Brief]
[3]. Hirao A, et al. DNA damage-induced activation of p53 by the checkpoint kinase Chk2. Science. 2000 Mar 10;287(5459):1824-7. [Content Brief]
[4]. Lee JS, et al. hCds1-mediated phosphorylation of BRCA1 regulates the DNA damage response. Nature. 2000 Mar 9;404(6774):201-4. [Content Brief]
[5]. Antoni L, et al. CHK2 kinase: cancer susceptibility and cancer therapy - two sides of the same coin? Nat Rev Cancer. 2007 Dec;7(12):925-36. [Content Brief]
[6]. Bucher N, et al. G2 checkpoint abrogation and checkpoint kinase-1 targeting in the treatment of cancer. Br J Cancer. 2008 Feb 12;98(3):523-8. [Content Brief]
[7]. Anderson VE, et al. CCT241533 is a potent and selective inhibitor of CHK2 that potentiates the cytotoxicity of PARP inhibitors. Cancer Res. 2011 Jan 15;71(2):463-72. [Content Brief]