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
biological source
rabbit
Quality Level
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)
General 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.
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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Physical form
Solution in phosphate-buffered saline containing 0.02% sodium azide and 50% glycerol
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Storage Class
10 - Combustible liquids
wgk_germany
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
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Xiu-Feng Gong et al.
Experimental cell research, 362(2), 378-385 (2017-12-07)
MicroRNAs (miRNAs) play critical roles in breast cancer cell biological processes, including proliferation and apoptosis by inhibiting the expression of their target genes. Herein, we reported that miR-630 overexpression initiates apoptosis, blocks cell cycle progression and suppresses cell proliferation in
Qiu-Xia Liang et al.
Cell death & disease, 9(5), 508-508 (2018-05-05)
Premature ovarian failure (POF), a major cause of female infertility, is a complex disorder, but the molecular mechanisms underlying the disorder are only poorly understood. Here we report that protein kinase CK2 contributes to maintaining follicular survival through PI3K/AKT pathway
Yongzhu Lv et al.
The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 22(6), 617-625 (2018-11-08)
Neddylation is a post-translational protein modification process. MLN4924 is a newly discovered pharmaceutical neddylation inhibitor that suppresses cancer growth with several cancer types. In our study, we first investigated the effect of MLN4924 on colon cancer cells (HCT116 and HT29).
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
Darawalee Wangsa et al.
FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 32(7), 3502-3517 (2018-02-18)
A considerable proportion of tumors exhibit aneuploid karyotypes, likely resulting from the progressive loss of chromosomes after whole-genome duplication. Here, by using isogenic diploid and near-tetraploid (4N) single-cell-derived clones from the same parental cell lines, we aimed at exploring how
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