SAB4504208
Anti-phospho-Smad2/3 (pThr8) antibody produced in rabbit
affinity isolated antibody
Synonym(s):
Anti-HSPC193, Anti-HsT17436, Anti-JV15-2, Anti-LDS1C, Anti-LDS3, Anti-MADH3
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About This Item
NACRES:
NA.41
UNSPSC Code:
12352203
Conjugate:
unconjugated
Clone:
polyclonal
Application:
ELISA, WB
Citations:
15
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen 48 kDa
species reactivity
rat, mouse, human
concentration
~1 mg/mL
technique(s)
ELISA: 1:10000, western blot: 1:500-1:1000
UniProt accession no.
shipped in
wet ice
storage temp.
−20°C
target post-translational modification
phosphorylation (pThr8)
Quality Level
Gene Information
human ... SMAD2(4087), SMAD3(4088)
General description
SMAD3 (homologues of the Drosophila protein, mothers against decapentaplegic (Mad) and the Caenorhabditis elegans protein) is located on human chromosome 15q22. SMAD2 (SMAD family member 2) is also called as MADR2 (substrate of the TGFβ receptor). It is located on human chromosome 18q21. Smad2/3 belongs to the mothers against Dpp (MAD) related family of proteins. SMAD2 has two highly conserved amino and carboxyl-terminal domains (MH1 and MH2 domains) but has no known structural motifs.
Immunogen
The antiserum was produced against synthesized peptide derived from human Smad2/3 around the phosphorylation site of Thr8.
Immunogen Range: 1-50
Immunogen Range: 1-50
Application
Anti-phospho-Smad3 (pSer425) antibody has been used in western blotting.
Biochem/physiol Actions
SMAD (homologues of the Drosophila protein, mothers against decapentaplegic (Mad) and the Caenorhabditis elegans protein) proteins play an important role in the intracellular signalling of transforming growth factor β (TGFβ). Reduction in the phosphorylation level of Smad3 helps autophagy to control the endothelial-mesenchymal transition. In human arterial smooth muscle cells, suppressing siRNA of SMAD3 improves the viability of cells. Mutations in SMAD2 (SMAD family member 2) results in arterial aneurysms and dissections. Upregulation of Smad2 blocks the multiplication of gingival epithelial cells. It plays an important role in TGF-β (transforming growth factor β)/activin signaling pathways. Smad2 positively and negatively controls TGFβ-dependent transcription with the help of forkhead DNA-binding protein FAST2.
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
10 - Combustible liquids
wgk
WGK 1
flash_point_f
Not applicable
flash_point_c
Not applicable
Regulatory Information
低风险生物材料
常规特殊物品
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Smad2 and Smad3 Positively and Negatively Regulate TGF?-Dependent Transcription through the Forkhead DNA-Binding Protein FAST2
Labbe E, et al.
Molecular Cell (1998)
Jiaqiang An et al.
Oncology reports, 38(5), 3001-3010 (2017-10-20)
In the past decades, altered Follistatin‑like 1 (FSTL1) expression has been documented in a variety of cancers, while its functional roles are poorly understood. Particularly in breast cancer, the expression of FSTL1 and its signaling pathway remain to be determined. In the
Frequency of Smad Gene Mutations in Human Cancers'
Riggins G J, et al.
Cancer Research (1997)
Peng Feng et al.
iScience, 26(12), 108484-108484 (2023-12-14)
Fibrosis disrupts tissue balance and links to severe illnesses, impairing organ function and, in some cases, even fatality. The interaction between M2 macrophages and fibroblasts is vital for tissue equilibrium. Transforming growth factor β1 (TGF-β1) released by M2 macrophages plays
Absence of chloride intracellular channel 4 (CLIC4) predisposes to acute kidney injury but has minimal impact on recovery
Edwards JC, et al.
BMC Nephrology (2014)
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