SAB4300121
Anti-phospho-CHEK2 (pSer516) antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-CDS1 antibody produced in rabbit, Anti-CHK2 antibody produced in rabbit, Anti-CHK2 checkpoint homolog (S. pombe) antibody produced in rabbit, Anti-HuCds1 antibody produced in rabbit, Anti-LFS2 antibody produced in rabbit
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About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
Pricing and availability is not currently available.
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
~62 kDa
species reactivity
human
concentration
1 mg/mL
technique(s)
western blot: 1:500-1:1000
isotype
IgG
immunogen sequence
(Q-P-SP-T-S)
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
phosphorylation (pSer516)
Gene Information
human ... CHEK2(11200)
Immunogen
Peptide sequence around phosphorylation site of serine 516 (Q-P-S(p)-T-S), according to the protein CHEK2.
Features and Benefits
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Target 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 Chk2 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. Three transcript variants encoding different isoforms have been found for this gene.
Physical form
Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
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Yuanxin Zhang et al.
Oncology letters, 18(2), 1881-1887 (2019-08-20)
Cervical cancer continues to be a threat to female health globally. In the present study, the potential anticancer activity of 2-[2-hydroxyl-1-(4-methoxy phenyl) ethyl]-3-(4-benzyloxy phenyl) isoindolin-1-one (CDS-1548), was evaluated in HeLa cells. CDS-1548 is an organic small-molecule compound characterized by two
Shiyuan Hong et al.
Oncogene, 38(17), 3274-3287 (2019-01-12)
High-risk human papillomaviruses (HPVs) constitutively activate ataxia telangiectasia mutated (ATM) and ataxia telangiectasia- and Rad3-related (ATR) DNA damage repair pathways for viral genome amplification. HPVs activate these pathways through the immune regulator STAT-5. For the ATR pathway, STAT-5 increases expression
Helga B Landsverk et al.
Nucleic acids research, 47(4), 1797-1813 (2018-12-13)
Ataxia telangiectasia mutated and Rad3-related (ATR) kinase is a key factor activated by DNA damage and replication stress. An alternative pathway for ATR activation has been proposed to occur via stalled RNA polymerase II (RNAPII). However, how RNAPII might signal
Bo Liu et al.
The international journal of biochemistry & cell biology, 109, 40-58 (2019-02-03)
The role of protein phosphatase 2ACα (PP2ACα) in brain development is poorly understood. To understand the function of PP2ACα in neurogenesis, we inactivated Pp2acα gene in the central nervous system (CNS) of mice by Cre/LoxP system and generated the PP2ACα
Changhoon Choi et al.
PloS one, 14(6), e0218049-e0218049 (2019-06-14)
Recent studies have highlighted the implications of genetic variations in the relative biological effectiveness (RBE) of proton beam irradiation over conventional X-ray irradiation. Proton beam radiotherapy is a reasonable radiotherapy option for hepatocellular carcinoma (HCC), but the impact of genetic
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