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首頁>>免疫學>>一抗>>磷酸化細胞信號轉(zhuǎn)導分子SMAD3抗體
磷酸化細胞信號轉(zhuǎn)導分子SMAD3抗體
  • 產(chǎn)品貨號:
    BN40559R
  • 中文名稱:
    磷酸化細胞信號轉(zhuǎn)導分子SMAD3抗體
  • 英文名稱:
    Rabbit anti-phospho-Smad3 (Thr179) Polyclonal antibody
  • 品牌:
    Biorigin
  • 貨號

    產(chǎn)品規(guī)格

    售價

    備注

  • BN40559R-100ul

    100ul

    ¥2470.00

    交叉反應(yīng):Human,Mouse,Rat(predicted:Dog,Pig,Cow,Horse,Sheep) 推薦應(yīng)用:WB,IHC-P,IHC-F,ICC,IF,Flow-Cyt,ELISA

產(chǎn)品描述

英文名稱phospho-Smad3 (Thr179)
中文名稱磷酸化細胞信號轉(zhuǎn)導分子SMAD3抗體
別    名Smad3 (phospho T179); p-Smad3 (phospho T179); DKFZP586N0721; DKFZp686J10186; hMAD 3; hMAD-3; hSMAD3; HSPC193; HST17436; JV15 2; JV15-2; JV152; LDS1C; LDS3; MAD (mothers against decapentaplegic Drosophila) homolog 3; MAD homolog 3; Mad homolog JV15 2; Mad protein homolog; MAD, mothers against decapentaplegic homolog 3; Mad3; MADH 3; MADH3; MGC60396; Mothers against decapentaplegic homolog 3; Mothers against DPP homolog 3; SMA and MAD related protein 3; SMAD 3; SMAD; SMAD family member 3; SMAD, mothers against DPP homolog 3; Smad3; SMAD3; SMAD3_HUMAN.  




產(chǎn)品類型磷酸化抗體 
研究領(lǐng)域腫瘤  細胞生物  染色質(zhì)和核信號  信號轉(zhuǎn)導  干細胞  
抗體來源Rabbit
克隆類型Polyclonal
交叉反應(yīng)Human, Mouse, Rat,  (predicted: Dog, Pig, Cow, Horse, Sheep, )
產(chǎn)品應(yīng)用WB=1:500-2000 ELISA=1:5000-10000 IHC-P=1:100-500 IHC-F=1:100-500 Flow-Cyt=1ug/Test ICC=1:100 IF=1:100-500 (石蠟切片需做抗原修復(fù))
not yet tested in other applications.
optimal dilutions/concentrations should be determined by the end user.
分 子 量48kDa
細胞定位細胞核 細胞漿 
性    狀Liquid
濃    度1mg/ml
免 疫 原KLH conjugated synthesised phosphopeptide derived from human Smad3 around the phosphorylation site of Thr179.:PE(p-T)PP 
亞    型IgG
純化方法affinity purified by Protein A
儲 存 液0.01M TBS(pH7.4) with 1% BSA, 0.03% Proclin300 and 50% Glycerol.
保存條件Shipped at 4℃. Store at -20 °C for one year. Avoid repeated freeze/thaw cycles.
PubMedPubMed
產(chǎn)品介紹The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein functions as a transcriptional modulator activated by transforming growth factor-beta and is thought to play a role in the regulation of carcinogenesis. [provided by RefSeq, Apr 2009]

Function:
Receptor-regulated SMAD (R-SMAD) that is an intracellular signal transducer and transcriptional modulator activated by TGF-beta (transforming growth factor) and activin type 1 receptor kinases. Binds the TRE element in the promoter region of many genes that are regulated by TGF-beta and, on formation of the SMAD3/SMAD4 complex, activates transcription. Also can form a SMAD3/SMAD4/JUN/FOS complex at the AP-1/SMAD site to regulate TGF-beta-mediated transcription. Has an inhibitory effect on wound healing probably by modulating both growth and migration of primary keratinocytes and by altering the TGF-mediated chemotaxis of monocytes. This effect on wound healing appears to be hormone-sensitive. Regulator of chondrogenesis and osteogenesis and inhibits early healing of bone fractures. Positively regulates PDPK1 kinase activity by stimulating its dissociation from the 14-3-3 protein YWHAQ which acts as a negative regulator.

Subcellular Location:
Cytoplasm. Nucleus. Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4. Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1. Co-localizes with LEMD3 at the nucleus inner membrane. MAPK-mediated phosphorylation appears to have no effect on nuclear import. PDPK1 prevents its nuclear translocation in response to TGF-beta.

Post-translational modifications:
Phosphorylated on serine and threonine residues. Enhanced phosphorylation in the linker region on Thr-179, Ser-204 and Ser-208 on EGF and TGF-beta treatment. Ser-208 is the main site of MAPK-mediated phosphorylation. CDK-mediated phosphorylation occurs in a cell-cycle dependent manner and inhibits both the transcriptional activity and antiproliferative functions of SMAD3. This phosphorylation is inhibited by flavopiridol. Maximum phosphorylation at the G(1)/S junction. Also phosphorylated on serine residues in the C-terminal SXS motif by TGFBR1 and ACVR1. TGFBR1-mediated phosphorylation at these C-terminal sites is required for interaction with SMAD4, nuclear location and transactivational activity, and appears to be a prerequisite for the TGF-beta mediated phosphorylation in the linker region. Dephosphorylated in the C-terminal SXS motif by PPM1A. This dephosphorylation disrupts the interaction with SMAD4, promotes nuclear export and terminates TGF-beta-mediated signaling. Phosphorylation at Ser-418 by CSNK1G2/CK1 promotes ligand-dependent ubiquitination and subsequent proteasome degradation, thus inhibiting SMAD3-mediated TGF-beta responses. Phosphorylated by PDPK1.
Acetylation in the nucleus by EP300 in the MH2 domain regulates positively its transcriptional activity and is enhanced by TGF-beta.
Ubiquitinated. Monoubiquitinated, leading to prevent DNA-binding. Deubiquitination by USP15 alleviates inhibition and promotes activation of TGF-beta target genes.
Poly-ADP-ribosylated by PARP1 and PARP2. ADP-ribosylation negatively regulates SMAD3 transcriptional responses during the course of TGF-beta signaling.

DISEASE:
Colorectal cancer
Loeys-Dietz syndrome 3

Similarity:
Belongs to the dwarfin/SMAD family.
Contains 1 MH1 (MAD homology 1) domain.
Contains 1 MH2 (MAD homology 2) domain.

SWISS:
P84022

Gene ID:
4088

Database links:

Entrez Gene: 4088 Human

Entrez Gene: 17127 Mouse

Entrez Gene: 25631 Rat

Omim: 603109 Human

SwissProt: P84022 Human

SwissProt: Q8BUN5 Mouse

SwissProt: P84025 Rat

Unigene: 727986 Human

Unigene: 742270 Human

Unigene: 7320 Mouse

Unigene: 10636 Rat



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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