SAB1400160
Monoclonal Anti-SMAD3 antibody produced in mouse
clone 7F3, purified immunoglobulin, buffered aqueous solution
别名:
Anti-DKFZP586N0721, Anti-DKFZp686J10186, Anti-HSPC193, Anti-HsT17436, Anti-JV152, Anti-MADH3, Anti-MGC60396, Anti-Smad 3
产品名称
Monoclonal Anti-SMAD3 antibody produced in mouse, clone 7F3, purified immunoglobulin, buffered aqueous solution
biological source
mouse
conjugate
unconjugated
antibody form
purified immunoglobulin
antibody product type
primary antibodies
clone
7F3, monoclonal
form
buffered aqueous solution
species reactivity
human, rat
technique(s)
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
indirect ELISA: suitable
proximity ligation assay: suitable
western blot: 1-5 μg/mL
isotype
IgG1κ
UniProt accession no.
application(s)
research pathology
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Quality Level
Gene Information
human ... SMAD3(4088)
Application
Monoclonal Anti-SMAD3 antibody produced in mouse has been used in immunohistochemistry (1:200).
Biochem/physiol Actions
Mothers against decapentaplegic homolog 3 (SMAD3) protein possesses tumor-suppressive actions. It is involved in epithelial to mesenchymal transition (EMT). SMAD3 also possesses tumor-promoting actions of transforming growth factor-beta (TGF-β). The N-terminal domain Mad homology 1 (MH1) of SMAD3 plays a role in DNA binding. The SMAD3 gene mutation is linked to an increased incidence of knee osteoarthritis. DNA methylation change in the SMAD3 gene promoter is associated with atopic asthma. SMAD3 protein plays a regulatory role in immune responses. It also modulates fibrosis in the airways.
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.
General description
Mothers against decapentaplegic homolog 3 (SMAD3) protein is an important constituent of the transforming growth factor-beta (TGF-β) signaling pathway. Mad homology 1 (MH1) and Mad homology 2 (MH2) are the two functional domains of the SMAD3. The SMAD3 gene is located on human chromosome 15q22.33.
Immunogen
SMAD3 (NP_005893, 120 a.a. ~ 221 a.a) partial recombinant protein with GST tag. MW of the GST tag alone is 26 KDa.
Sequence
VCVNPYHYQRVETPVLPPVLVPRHTEIPAEFPPLDDYSHSIPENTNFPAGIEPQSNIPETPPPGYLSEDGETSDHQMNHSMDAGSPNLSPNPMSPAHNNLDL
Sequence
VCVNPYHYQRVETPVLPPVLVPRHTEIPAEFPPLDDYSHSIPENTNFPAGIEPQSNIPETPPPGYLSEDGETSDHQMNHSMDAGSPNLSPNPMSPAHNNLDL
Physical form
Solution in phosphate buffered saline, pH 7.4
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存储类别
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Amanda C Daly et al.
The Journal of biological chemistry, 285(9), 6489-6497 (2009-12-29)
Transforming growth factor beta (TGF-beta) regulates many biological processes, and aberrant TGF-beta signaling is implicated in tumor development. Smad3 is a central component of the TGF-beta signaling pathway, and once activated, Smad3 forms complexes with Smad4 or other receptor-regulated Smads
Chao Lu et al.
Molecular biology reports, 46(4), 4501-4505 (2019-06-12)
The mechanism of knee osteoarthritis (OA) is still not clearly elucidated. SMAD3 gene polymorphisms are considered to play a vital role in OA pathogenesis. We thus investigated the relationship of SMAD3 rs1065080 gene polymorphism and susceptibility to knee osteoarthritis in
R J Lund et al.
Allergy, 73(8), 1735-1740 (2018-05-08)
Children with rhinovirus-induced severe early wheezing have an increased risk of developing asthma later in life. The exact molecular mechanisms for this association are still mostly unknown. To identify potential changes in the transcriptional and epigenetic regulation in rhinovirus-associated atopic
Astrid Jeibmann et al.
Journal of neuro-oncology, 131(3), 477-484 (2017-01-22)
Atypical teratoid/rhabdoid tumors (ATRT) are highly malignant brain tumors arising in young children. The majority of ATRT is characterized by inactivation of the chromatin remodeling complex member SMARCB1 (INI1/hSNF5). Little is known, however, on downstream pathways involved in the detrimental
Bertrand Chesneau et al.
Molecular genetics & genomic medicine, 8(5), e1132-e1132 (2020-03-11)
Pathogenic SMAD3 variants are responsible for a cardiovascular phenotype, mainly thoracic aortic aneurysms and dissections. Precocious identification of the vascular risk such as aortic dilatation in mutated patients has a major impact in terms of management, particularly to avoid dissection
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