Phospho-Chk1 (Ser296) Antibody (YA216)
(Synonyms: CHK1, CHEK1, Serine/threonine-protein kinase Chk1, CHK1 checkpoint homolog, Cell cycle checkpoint kinase, Checkpoint kinase-1)Based on 1 publication(s) in Google Scholar
Phospho-Chk1 (Ser296) Antibody (YA216) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-Chk1 (Ser296).
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Host:
Rabbit
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Isotype:
IgG
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Application:
WB, IHC-P
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Reactivity :
Human
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Formulation:
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Conjugation:
Non-conjugated
Publications Citing Use of MedChemExpress (MCE) Phospho-Chk1 (Ser296) Antibody (YA216)
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Applications
| Application |
WB
WB: Western Blot
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IHC-P
IHC-P: Immunohistochemistry-Paraffin
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| Dilution Ratio | 1:500 | 1:50-1:200 |
Product Details
Phospho-Chk1 (Ser296) Antibody (YA216) is a Rabbit-derived and non-conjugated IgG monoclonal antibody, targeting to Phospho-Chk1 (Ser296).
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Host Rabbit
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Clonality Recombinant,Monoclonal
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Species ReactivityHuman
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Observed Molecular WeightObserved band size: 54 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.
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Calculated Molecular Weight Predicted band size: 54 kDa
Synthetic phosphopeptide corresponding to residues surrounding Ser296 of Human Chk1.The exact sequence is proprietary to MCE.
Endogenous
Protein A affinity purified.
Non-conjugated
Phosphorylated
IgG
Product Properties
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Appearance
Solution
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Formulation
Supplied in 1*TBS (pH7.4), 0.05% BSA and 40% Glycerol. Preservative: 0.05% Sodium Azide.
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Concentration
Batch-dependent, Please check the COA for the concentration of each lot. Check Lot Concentration
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Storage & Stability
Stored at -20°C for 1 year. Avoid repeated freeze / thaw cycles.
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Shipping
Shipping with blue ice.
Publications (1)
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Journal Impact Factor
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Most Recent
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Sci Bull
Dynamic R-loops at centromeres ensure chromosome alignment during oocyte meiotic divisions in mice. [Abstract]2025 Apr 30;70(8):1311-1327. PMID: 39984387
Background
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Function
Chk1 (checkpoint kinase 1) mediates the DNA damage response and normal cell-cycle regulation through checkpoint activation, cell-cycle arrest, DNA repair, and cell death control[1]. Mechanistically, Chk1 functions as a key transducer in genome-integrity checkpoints, especially within ATR-linked responses to stalled replication and genotoxic stress[2][3]. In cancer research, this role makes Chk1 relevant to replication stress, BRCA wild-type ovarian cancer models, and studies combining checkpoint inhibition with DNA-damaging therapy[4][5]. Compared with Chk2, Chk1 shows distinct activation biology and experimentally separable checkpoint functions, while Chk1-S acts as an endogenous splice-variant inhibitor that regulates Chk1-dependent checkpoints[2][6]. For experimental applications, Chk1 inhibitors such as prexasertib/LY2606368 induce replication catastrophe and have been tested in tumor models and recurrent high-grade serous ovarian cancer[7][8].
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Subcellular Localization
Nucleus; Chromosome; Cytoplasm; Cytoplasm, cytoskeleton, microtubule organizing center, centrosome
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Expression
Tissue_specificity:This gene is widely expressed in various tissues, with the highest expression in the thymus, testes, small intestine, and colon. -
Isoforms & Post-Translational Modification
O14757 has 3 isomers: O14757-1: 54434 Da (predicted); O14757-2: 43703 Da (predicted); O14757-3: 50415 Da (predicted).
Phosphorylated by ATR in a RAD17-dependent manner in response to ultraviolet irradiation and inhibition of DNA replication (PubMed:10859164, PubMed:11390642, PubMed:12446774, PubMed:12588868, PubMed:12676583, PubMed:12676925, PubMed:12676962, PubMed:14681223, PubMed:14988723, PubMed:15650047, PubMed:15707391, PubMed:15870257, PubMed:25083873, PubMed:31316063). Phosphorylated by ATM in response to ionizing irradiation (PubMed:12588868, PubMed:12676583). ATM and ATR can both phosphorylate Ser-317 and Ser-345 and this results in enhanced kinase activity (PubMed:11390642, PubMed:12446774, PubMed:12588868, PubMed:12660173, PubMed:12676583, PubMed:12676962, PubMed:14657349, PubMed:15665856, PubMed:15707391, PubMed:15870257, PubMed:25083873). Phosphorylation at Ser-345 induces a change in the conformation of the protein, activates the kinase activity and is a prerequisite for interaction with FBXO6 and subsequent ubiquitination at Lys-436 (PubMed:19716789). Phosphorylation at Ser-345 also increases binding to 14-3-3 proteins and promotes nuclear retention (PubMed:12676962). Conversely, dephosphorylation at Ser-345 by PPM1D may contribute to exit from checkpoint mediated cell cycle arrest (PubMed:15870257). Phosphorylation at Ser-280 by AKT1/PKB, may promote mono and/or diubiquitination. Also phosphorylated at undefined residues during mitotic arrest, resulting in decreased activity (By similarity);Ubiquitinated. Mono or diubiquitination promotes nuclear exclusion (By similarity). The activated form (phosphorylated on Ser-345) is polyubiquitinated at Lys-436 by some SCF-type E3 ubiquitin ligase complex containing FBXO6 promoting its degradation. Ubiquitination and degradation are required to terminate the checkpoint and ensure that activated CHEK1 does not accumulate as cells progress through S phase, when replication forks encounter transient impediments during normal DNA replication. 'Lys-63'-mediated ubiquitination by TRAF4 at Lys-132 activates cell cycle arrest and activation of DNA repair (PubMed:32357935);Proteolytically cleaved at the C-terminus by SPRTN during normal DNA replication, thereby promoting CHEK1 removal from chromatin and activating the protein kinase activity -
Subunit
Interacts (phosphorylated by ATR) with RAD51 (PubMed:15665856). Interacts with and phosphorylates CLSPN, an adapter protein that regulates the ATR-dependent phosphorylation of CHEK1 (PubMed:16963448). Interacts with BRCA1 (PubMed:11836499). Interacts with and phosphorylates CDC25A, CDC25B and CDC25C (PubMed:9278511). Interacts with FBXO6, which regulates CHEK1 (PubMed:19716789). Interacts with PPM1D, which regulates CHEK1 through dephosphorylation (PubMed:15870257). Interacts with TIMELESS; DNA damage-dependent (PubMed:15798197). Interacts with FEM1B; activates CHEK1 in response to stress (PubMed:19330022). Interacts with TLK1 (PubMed:12660173). Interacts with XPO1 and YWHAZ (PubMed:12676962). Interacts with CDK5RAP3; antagonizes CHEK1 (PubMed:19223857)
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SwissProt ID
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Synonyms
CHK1, CHEK1, Serine/threonine-protein kinase Chk1, CHK1 checkpoint homolog, Cell cycle checkpoint kinase, Checkpoint kinase-1
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Research Field
Epigenetics and Nuclear Signaling
Documentation
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Data Sheet (262 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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User Guide for Antibodies (1077 KB)
[1]. Patil M, et al. Checkpoint kinase 1 in DNA damage response and cell cycle regulation. Cell Mol Life Sci. 2013 Nov;70(21):4009-21. [Content Brief]
[2]. Bartek J, et al. Chk1 and Chk2 kinases in checkpoint control and cancer. Cancer Cell. 2003 May;3(5):421-9. [Content Brief]
[3]. Dai Y, et al. New insights into checkpoint kinase 1 in the DNA damage response signaling network. Clin Cancer Res. 2010 Jan 15;16(2):376-83. [Content Brief]
[4]. Rabezanahary H, et al. Live virus neutralizing antibodies against pre and post Omicron strains in food and retail workers in Québec, Canada. Heliyon. 2024 May 21;10(10):e31026. [Content Brief]
[5]. Nair J, et al. Resistance to the CHK1 inhibitor prexasertib involves functionally distinct CHK1 activities in BRCA wild-type ovarian cancer. Oncogene. 2020 Aug;39(33):5520-5535. [Content Brief]
[6]. Pabla N, et al. Checkpoint kinase 1 (Chk1)-short is a splice variant and endogenous inhibitor of Chk1 that regulates cell cycle and DNA damage checkpoints. Proc Natl Acad Sci U S A. 2012 Jan 3;109(1):197-202. [Content Brief]
[7]. King C, et al. LY2606368 Causes Replication Catastrophe and Antitumor Effects through CHK1-Dependent Mechanisms. Mol Cancer Ther. 2015 Sep;14(9):2004-13. [Content Brief]
[8]. Lee JM, et al. Prexasertib, a cell cycle checkpoint kinase 1 and 2 inhibitor, in BRCA wild-type recurrent high-grade serous ovarian cancer: a first-in-class proof-of-concept phase 2 study. Lancet Oncol. 2018 Feb;19(2):207-215. [Content Brief]