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Anti-Smad3 (phospho-T179) Antibody

品牌：Antibodies

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規(guī)格：50μl

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Anti-Smad3 (phospho-T179) Antibody

商品詳情參考文獻相關(guān)資料

Overview

Name:	Anti-Smad3 (phospho-T179) Antibody See all Smad3 primary antibodies
Description:	Rabbit polyclonal antibody to Smad3 (phospho-T179)
Specificity:	p-Smad3 (T179) pAb detects endogenous levels of Smad3 protein only when phosphorylated at Thr179.
Applications:	WB
Reactivity:	Human, Mouse, Rat
Immunogen:	Synthetic phosphopeptide derived from human Smad3 around the phosphorylation site of Threonine 179.
Host:	Rabbit
Clonality:	Polyclonal
Conjugate:	Unconjugated
Molecular Weight:	~ 48, 55 kDa
Purity:	The antibody was affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogen and the purity is > 95% (by SDS-PAGE).
Product Form:	1 mg/ml in Phosphate buffered saline (PBS) with 15 mM sodium azide, approx. pH 7.2.

Target

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.
Involvement in Disease:	Colorectal cancer: A complex disease characterized by malignant lesions arising from the inner wall of the large intestine (the colon) and the rectum. Genetic alterations are often associated with progression from premalignant lesion (adenoma) to invasive adenocarcinoma. Risk factors for cancer of the colon and rectum include colon polyps, long-standing ulcerative colitis, and genetic family history. Loeys-Dietz syndrome 3: An aortic aneurysm syndrome with widespread systemic involvement. The disorder is characterized by the triad of arterial tortuosity and aneurysms, hypertelorism, and bifid uvula or cleft palate. Patients with LDS3 also manifest early-onset osteoarthritis. They lack craniosynostosis and mental retardation.
Sequence Similarities:	Belongs to the dwarfin/SMAD family.
Post-Translational Modification:	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.
Cellular Location:	Cytoplasm. Nucleus. Cytoplasmic and nuclear in the absence of TGF-beta. On TGF-beta stimulation, migrates to the nucleus when complexed with SMAD4 (PubMed:15799969). Through the action of the phosphatase PPM1A, released from the SMAD2/SMAD4 complex, and exported out of the nucleus by interaction with RANBP1 (PubMed:16751101, PubMed:19289081). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15601644). MAPK-mediated phosphorylation appears to have no effect on nuclear import (PubMed:19218245). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236).
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
Synonyms:	DKFZP586N0721 Antibody DKFZp686J10186 Antibody hMAD 3 Antibody hMAD-3 Antibody hSMAD3 Antibody HSPC193 Antibody HST17436 Antibody JV15 2 Antibody JV15-2 Antibody JV152 Antibody LDS1C Antibody LDS3 Antibody MAD (mothers against decapentaplegic Drosophila) homolog 3 Antibody MAD homolog 3 Antibody Mad homolog JV15 2 Antibody Mad protein homolog Antibody MAD, mothers against decapentaplegic homolog 3 Antibody Mad3 Antibody MADH 3 Antibody MADH3 Antibody MGC60396 Antibody Mothers against decapentaplegic homolog 3 Antibody Mothers against DPP homolog 3 Antibody SMA and MAD related protein 3 Antibody SMAD Antibody SMAD 3 Antibody SMAD family member 3 Antibody SMAD, mothers against DPP homolog 3 Antibody Smad3 Antibody SMAD3_HUMAN Antibody
Information:	Target information shown above is from the UniProt Consortium.