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phospho-ATM (Ser1981) Rabbit pAb (bs-2272R)  
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產(chǎn)品編號 bs-2272R
英文名稱 phospho-ATM (Ser1981) Rabbit pAb
中文名稱 磷酸化毛細(xì)血管擴(kuò)張性共濟(jì)失調(diào)癥突變蛋白抗體
別    名 ATM(phospho-Ser1981); ATM(phospho S1981); AT complementation group A; AT complementation group C; AT complementation group D; AT complementation group E; AT mutated; AT protein; AT1; ATA; Ataxia telangiectasia gene mutated in human beings; Ataxia telangiectasia mutated; ATC; ATDC; ATE; ATM; Human phosphatidylinositol 3 kinase homolog; Serine protein kinase ATM; T cell prolymphocytic leukemia; TEL1; TPLL.  
Specific References  (2)     |     bs-2272R has been referenced in 2 publications.
[IF=5.008] Yin, H., et al. "The molecular mechanism of G2M cell cycle arrest induced by AFB1 in the jejunum." Oncotarget (2016).  IHC-P ;  Chicken.  
[IF=5.008] Guo, Hongrui, et al. "Dietary NiCl2 causes cell cycle arrest in the broiler's kidney." Oncotarget. (2015) 6.34:35964-77.  IHC-P ;  Chicken.  
產(chǎn)品類型 磷酸化抗體 
研究領(lǐng)域 信號轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  細(xì)胞周期蛋白  激酶和磷酸酶  
抗體來源 Rabbit
克隆類型 Polyclonal
克 隆 號
交叉反應(yīng) Human (predicted: Mouse,Rat)
產(chǎn)品應(yīng)用 IHC-P=1:100-500,IHC-F=1:100-500,IF=1:100-500,Flow-Cyt=1μg /test
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
理論分子量 370 kDa
檢測分子量
細(xì)胞定位 細(xì)胞核 細(xì)胞漿 
性    狀 Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated Synthesised phosphopeptide derived from human ATM around the phosphorylation site of Ser1981: EG(p-S)QS 
亞    型 IgG
純化方法 affinity purified by Protein A
緩 沖 液 0.01M TBS (pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
保存條件 Shipped at 4℃. Store at -20℃ for one year. Avoid repeated freeze/thaw cycles.
注意事項(xiàng) This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
PubMed PubMed
產(chǎn)品介紹 ATM is a 370 kDa nuclear phosphoprotein involved in the autosomal recessive disease Ataxia Telangiectasia (AT). ATM belongs to a novel family of proteins associated with cell cycle regulation, apoptosis, and response to DNA damage repair (DNA damage caused by such things as ionizing irradiation activates ATM kinase). The C terminal region has extensive homology to the catalytic domains of Phosphatidylinositol 3 kinases (PI3 kinases).

Subcellular Location:
Nucleus. Cytoplasmic vesicle. Primarily nuclear. Found also in endocytic vesicles in association with beta-adaptin.

Tissue Specificity:
Found in pancreas, kidney, skeletal muscle, liver, lung, placenta, brain, heart, spleen, thymus, testis, ovary, small intestine, colon and leukocytes.

Post-translational modifications:
Phosphorylated by NUAK1/ARK5. Autophosphorylation on Ser-367, Ser-1893, Ser-1981 correlates with DNA damage-mediated activation of the kinase.
Acetylation, on DNA damage, is required for activation of the kinase activity, dimer-monomer transition, and subsequent autophosphorylation on Ser-1981. Acetylated in vitro by KAT5/TIP60.

DISEASE:
Defects in ATM are the cause of ataxia telangiectasia (AT) [MIM:208900]; also known as Louis-Bar syndrome, which includes four complementation groups: A, C, D and E. This rare recessive disorder is characterized by progressive cerebellar ataxia, dilation of the blood vessels in the conjunctiva and eyeballs, immunodeficiency, growth retardation and sexual immaturity. AT patients have a strong predisposition to cancer; about 30% of patients develop tumors, particularly lymphomas and leukemias. Cells from affected individuals are highly sensitive to damage by ionizing radiation and resistant to inhibition of DNA synthesis following irradiation.
Note=Defects in ATM contribute to T-cell acute lymphoblastic leukemia (TALL) and T-prolymphocytic leukemia (TPLL). TPLL is characterized by a high white blood cell count, with a predominance of prolymphocytes, marked splenomegaly, lymphadenopathy, skin lesions and serous effusion. The clinical course is highly aggressive, with poor response to chemotherapy and short survival time. TPLL occurs both in adults as a sporadic disease and in younger AT patients.
Note=Defects in ATM contribute to B-cell non-Hodgkin lymphomas (BNHL), including mantle cell lymphoma (MCL).
Note=Defects in ATM contribute to B-cell chronic lymphocytic leukemia (BCLL). BCLL is the commonest form of leukemia in the elderly. It is characterized by the accumulation of mature CD5+ B lymphocytes, lymphadenopathy, immunodeficiency and bone marrow failure.

Similarity:
Belongs to the PI3/PI4-kinase family. ATM subfamily.
Contains 1 FAT domain.
Contains 1 FATC domain.
Contains 1 PI3K/PI4K domain.

SWISS:
Q13315

Gene ID:
472

Database links:

Entrez Gene: 472 Human

Entrez Gene: 11920 Mouse

Entrez Gene: 300711 Rat

Omim: 607585 Human

SwissProt: Q13315 Human

SwissProt: Q62388 Mouse

SwissProt: P17764 Rat

Unigene: 367437 Human

Unigene: 5088 Mouse

Unigene: 214048 Rat



產(chǎn)品圖片
Tissue/cell: human lung carcinoma; 4% Paraformaldehyde-fixed and paraffin-embedded; Antigen retrieval: citrate buffer ( 0.01M, pH 6.0 ), Boiling bathing for 15min; Block endogenous peroxidase by 3% Hydrogen peroxide for 30min; Blocking buffer (normal goat serum,C-0005) at 37℃ for 20 min; Incubation: Anti-phospho-ATM(Ser1981) Polyclonal Antibody, Unconjugated(bs-2272R) 1:200, overnight at 4°C, followed by conjugation to the secondary antibody(SP-0023) and DAB(C-0010) staining
Blank control (blue line): Hela (fixed with 2% paraformaldehyde (10 min) , then permeabilized with 90% ice-cold methanol for 20 min on ice). Primary Antibody (green line): Rabbit Anti- phospho-ATM(Ser1981) antibody (bs-2272R),Dilution: 1μg /10^6 cells; Isotype Control Antibody (orange line): Rabbit IgG . Secondary Antibody (white blue line): Goat anti-rabbit IgG-FITC,Dilution: 1μg /test.
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