SAB4504169
Anti-phospho-DNA-PK (pSer2056) antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-DNA-PKC, Anti-DNA-PKcs, Anti-DNAPK, Anti-DNAPKc, Anti-DNPK1, Anti-HYRC, Anti-HYRC1, Anti-IMD26, Anti-XRCC7
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All Photos(8)
About This Item
UNSPSC Code:
12352203
NACRES:
NA.43
Recommended Products
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 469 kDa
species reactivity
human, mouse, rat
concentration
~1 mg/mL
technique(s)
ELISA: 1:10000
immunohistochemistry: 1:50-1:100
NCBI accession no.
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
phosphorylation (pSer2056)
Gene Information
human ... PRKDC(5591)
Related Categories
General description
Protein kinase, DNA-activated, catalytic polypeptide (PRKDC), also known as DNAPK, is encoded by the gene mapped to human chromosome 8q11. PRKDC is characterized by a large catalytic polypeptide and DNA-binding component comprised of the Ku70 and Ku80 heterodimer, that targets DNA-PKc, to DNA.
Immunogen
The antiserum was produced against synthesized peptide derived from human DNA-PK around the phosphorylation site of Ser2056.
Immunogen Range: 2022-2071
Immunogen Range: 2022-2071
Application
Anti-phospho-DNA-PK (pSer2056) antibody produced in rabbit has been used in immunofluorescence analysis.
Biochem/physiol Actions
Protein kinase, DNA-activated, catalytic polypeptide (PRKDC), also known as DNAPK, plays an essential role in the colorectal cancer (CRC) cell proliferation/survival. Therefore, it can be used as a potential prognostic biomarker and a therapeutic target for CRC. Decreased expression of PRKDC influences apoptosis partially by inhibiting AKT activation. Overexpression of activated DNAPK elevates the expression of rearranged during transfection (RET), which is a proto-oncogene involved in the development of medullary thyroid cancer (MTC). DNAPK plays a crucial role in non-homology end joining (NHEJ) pathway. Downregulation of DNAPK enhances anticancer drug induced DNA damage repair in osteosarcoma cell line MG63.
Features and Benefits
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Physical form
Rabbit IgG in phosphate buffered saline (without Mg2+ and Ca2+), pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol.
Disclaimer
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
10 - Combustible liquids
WGK
WGK 1
Certificates of Analysis (COA)
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Shangfeng Sun et al.
Gene, 584(1), 90-96 (2016-03-20)
Oncogene and non-oncogene addictions describe the phenomenon that tumor cells become reliant on certain genes for maintenance of malignancy. Reversal of these mutations profoundly affects tumor growth and survival, providing a fundamental rationale for development of targeted cancer therapy. However
J D Sipley et al.
Proceedings of the National Academy of Sciences of the United States of America, 92(16), 7515-7519 (1995-08-01)
The DNA-activated serine/threonine protein kinase (DNA-PK) is composed of a large (approximately 460 kDa) catalytic polypeptide (DNA-PKcs) and Ku, a heterodimeric DNA-binding component (p70/p80) that targets DNA-PKcs to DNA. A 41-kbp segment of the DNA-PKcs gene was isolated, and a
Weiwei Li et al.
Mutation research, 779, 112-123 (2015-07-24)
Although studies have shown that cadmium (Cd) interfered with DNA damage repair (DDR), whether Cd could affect non-homologous end joining (NHEJ) repair remains elusive. To further understand the effect of Cd on DDR, we used X-ray irradiation of Hela cells
Xin Li et al.
Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 36(12), 9365-9372 (2015-06-26)
Many chemotherapy drugs exert anticancer effects through causing DNA damage, such as DNA topoisomerase inhibitor and platinum-containing drugs. DNA damage repair is an important mechanism of drug resistance which is responsible for metastasis and recurrence after chemotherapy. DNA-dependent protein kinase
Giovanna Bellusci et al.
Cell death & disease, 10(10), 726-726 (2019-09-29)
Premature ovarian failure and infertility are adverse effects of cancer therapies. The mechanism underlying chemotherapy-mediated depletion of the ovarian reserve remains unclear. Here, we aim to identify the signaling pathways involved in the loss of the ovarian reserve to prevent
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