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Merck

SAB1400160

Sigma-Aldrich

Monoclonal Anti-SMAD3 antibody produced in mouse

clone 7F3, purified immunoglobulin, buffered aqueous solution

Synonym(e):

Anti-DKFZP586N0721, Anti-DKFZp686J10186, Anti-HSPC193, Anti-HsT17436, Anti-JV152, Anti-MADH3, Anti-MGC60396, Anti-Smad 3

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About This Item

MDL-Nummer:
UNSPSC-Code:
12352203
NACRES:
NA.43

Biologische Quelle

mouse

Qualitätsniveau

Konjugat

unconjugated

Antikörperform

purified immunoglobulin

Antikörper-Produkttyp

primary antibodies

Klon

7F3, monoclonal

Form

buffered aqueous solution

Speziesreaktivität

human, rat

Methode(n)

immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
indirect ELISA: suitable
proximity ligation assay: suitable
western blot: 1-5 μg/mL

Isotyp

IgG1κ

UniProt-Hinterlegungsnummer

Anwendung(en)

research pathology

Versandbedingung

dry ice

Lagertemp.

−20°C

Posttranslationale Modifikation Target

unmodified

Angaben zum Gen

human ... SMAD3(4088)

Allgemeine Beschreibung

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

Anwendung

Monoclonal Anti-SMAD3 antibody produced in mouse has been used in immunohistochemistry (1:200).

Biochem./physiol. Wirkung

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.

Physikalische Form

Solution in phosphate buffered saline, pH 7.4

Haftungsausschluss

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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Empfehlung

Lagerklassenschlüssel

10 - Combustible liquids

Flammpunkt (°F)

Not applicable

Flammpunkt (°C)

Not applicable


Analysenzertifikate (COA)

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Die Dokumentenbibliothek aufrufen

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
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
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
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
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

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