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Rabbit Anti-TRIB3/HRP Conjugated antibody (bs-7538R-HRP)
訂購熱線:400-901-9800
訂購郵箱:sales@bioss.com.cn
訂購QQ:  400-901-9800
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說 明 書: 100ul  
100ul/2980.00元
大包裝/詢價(jià)
產(chǎn)品編號(hào) bs-7538R-HRP
英文名稱 Rabbit Anti-TRIB3/HRP Conjugated antibody
中文名稱 辣根過氧化物酶標(biāo)記的神經(jīng)細(xì)胞死亡誘導(dǎo)蛋白激酶抗體
別    名 C20orf97; Neuronal cell death inducible putative kinase; Neuronal cell death-inducible putative kinase; NIPK; p65 interacting inhibitor of NF-kappaB; p65-interacting inhibitor of NF-kappa-B; SINK; SKIP 3; SKIP3; TRB 3; TRB-3; TRB3; TRIB 3; Trib3; TRIB3_HUMAN; Tribbles homolog 3; Tribbles3.  
規(guī)格價(jià)格 100ul/2980元 購買        大包裝/詢價(jià)
說 明 書 100ul  
研究領(lǐng)域 心血管  細(xì)胞生物  信號(hào)轉(zhuǎn)導(dǎo)  細(xì)胞凋亡  細(xì)胞周期蛋白  糖尿病  細(xì)胞分化  
抗體來源 Rabbit
克隆類型 Polyclonal
交叉反應(yīng) Human, Rat,  (predicted: Mouse, Chicken, Dog, Pig, Cow, Horse, Rabbit, )
產(chǎn)品應(yīng)用 WB=1:500-2000 ELISA=1:100-1000 IHC-P=1:50-200 IHC-F=1:50-200 
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量 40kDa
性    狀 Lyophilized or Liquid
濃    度 1mg/ml
免 疫 原 KLH conjugated synthetic peptide derived from human TRIB3/p65 interacting inhibitor of NF-kappaB
亞    型 IgG
純化方法 affinity purified by Protein A
儲(chǔ) 存 液 0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件 Store at -20 °C for one year. Avoid repeated freeze/thaw cycles. The lyophilized antibody is stable at room temperature for at least one month and for greater than a year when kept at -20°C. When reconstituted in sterile pH 7.4 0.01M PBS or diluent of antibody the antibody is stable for at least two weeks at 2-4 °C.
產(chǎn)品介紹 background:
Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. Binds to ATF4 and inhibits its transcriptional activation activity. Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. Interacts with MAPK kinases and regulates activation of MAP kinases. May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. Does not display kinase activity.
Tissue specificity: Highest expression in liver, pancreas, peripheral blood leukocytes and bone marrow. Also highly expressed in a number of primary lung, colon and breast tumors. Expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney.

Function:
Disrupts insulin signaling by binding directly to Akt kinases and blocking their activation. May bind directly to and mask the 'Thr-308' phosphorylation site in AKT1. Binds to ATF4 and inhibits its transcriptional activation activity. Interacts with the NF-kappa-B transactivator p65 RELA and inhibits its phosphorylation and thus its transcriptional activation activity. Interacts with MAPK kinases and regulates activation of MAP kinases. May play a role in programmed neuronal cell death but does not appear to affect non-neuronal cells. Does not display kinase activity.

Subunit:
Interacts with AKT1, AKT2, ATF4, MAP2K1 and MAP2K7.

Subcellular Location:
Nucleus.

Tissue Specificity:
Highest expression in liver, pancreas, peripheral blood leukocytes and bone marrow. Also highly expressed in a number of primary lung, colon and breast tumors. Expressed in spleen, thymus, and prostate and is undetectable in other examined tissues, including testis, ovary, small intestine, colon, leukocyte, heart, brain, placenta, lung, skeletal muscle, and kidney.

Similarity:
Belongs to the protein kinase superfamily. CAMK Ser/Thr protein kinase family. Tribbles subfamily.
Contains 1 protein kinase domain.

Database links:

Entrez Gene: 57761 Human

Omim: 607898 Human

SwissProt: Q96RU7 Human

Unigene: 516826 Human

 



Important Note:
This product as supplied is intended for research use only, not for use in human, therapeutic or diagnostic applications.
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