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Mouse Monoclonal Smad4 antibody [4G1C6] (STJ98385)
Supplier: St John’s Laboratory Ltd.
Recommended applications: WB, IHC, IF, FC, ELISA
Recommended dilution: WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
Recommended protocols: check protocols
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Check alternative names for the antibodyExpand
SMAD4 antibody, DPC4 antibody, MADH4 antibody,|(Small) Mothers Against Decapentaplegic antibody|SMAD 4 antibody|SMAD family member 4 antibody|SMAD mothers against DPP homolog 4 antibody|SMAD4 antibody|SMAD4_HUMAN antibody|Anti-Smad4 antibody [EP618Y] (ab40759)
SCBT cat No: To be updated
Smad4 Monoclonal Antibody
|Catalogue No.|| |
Smad4 Monoclonal Antibody detects endogenous levels of Smad4 protein.
Purified recombinant fragment of human Smad4 expressed in E Coli
WB, IHC, IF, FC, ELISA
|Recommended dilution|| |
WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; FC 1:200-1:400; ELISA 1:10000
Smad4 Antibody was tube-contained. Ascitic fluid containing 0.03% sodium azide.
Smad4 Antibody was purified using affinity purification.
-20 Celsius degree. Avoid repeated freeze/thaw cycles.
|Alternative antibody names|| |
Mothers against decapentaplegic homolog 4 antibody, MAD homolog 4 antibody, Mothers against DPP homolog 4 antibody, Deletion target in pancreatic carcinoma 4 antibody, SMAD family member 4 antibody, SMAD 4 antibody, Smad4 antibody, hSMAD4 antibody
|Protein names|| |
Mothers against decapentaplegic homolog 4 , MAD homolog 4 , Mothers against DPP homolog 4 , Deletion target in pancreatic carcinoma 4 , SMAD family member 4 , SMAD 4 , Smad4 , hSMAD4
|Protein function|| |
In muscle physiology, plays a central role in the balance between atrophy and hypertrophy. When recruited by MSTN, promotes atrophy response via phosphorylated SMAD2/4. MSTN decrease causes SMAD4 release and subsequent recruitment by the BMP pathway to promote hypertrophy via phosphorylated SMAD1/5/8. Acts synergistically with SMAD1 and YY1 in bone morphogenetic protein (BMP)-mediated cardiac-specific gene expression. Binds to SMAD binding elements (SBEs) (5′-GTCT/AGAC-3′) within BMP response element (BMPRE) of cardiac activating regions (By similarity). Common SMAD (co-SMAD) is the coactivator and mediator of signal transduction by TGF-beta (transforming growth factor). Component of the heterotrimeric SMAD2/SMAD3-SMAD4 complex that forms in the nucleus and is required for the TGF-mediated signaling. Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. Component of the multimeric SMAD3/SMAD4/JUN/FOS complex which forms at the AP1 promoter site; required for synergistic transcriptional activity in response to TGF-beta. May act as a tumor suppressor. 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|| |
Pancreatic cancer (PNCA) [MIM:260350]: A malignant neoplasm of the pancreas. Tumors can arise from both the exocrine and endocrine portions of the pancreas, but 95% of them develop from the exocrine portion, including the ductal epithelium, acinar cells, connective tissue, and lymphatic tissue. . Note: The gene represented in this entry may be involved in disease pathogenesis.; Juvenile polyposis syndrome (JPS) [MIM:174900]: Autosomal dominant gastrointestinal hamartomatous polyposis syndrome in which patients are at risk for developing gastrointestinal cancers. The lesions are typified by a smooth histological appearance, predominant stroma, cystic spaces and lack of a smooth muscle core. Multiple juvenile polyps usually occur in a number of Mendelian disorders. Sometimes, these polyps occur without associated features as in JPS; here, polyps tend to occur in the large bowel and are associated with an increased risk of colon and other gastrointestinal cancers. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome (JP/HHT) [MIM:175050]: JP/HHT syndrome phenotype consists of the coexistence of juvenile polyposis (JIP) and hereditary hemorrhagic telangiectasia (HHT) [MIM:187300] in a single individual. JIP and HHT are autosomal dominant disorders with distinct and non-overlapping clinical features. The former, an inherited gastrointestinal malignancy predisposition, is caused by mutations in SMAD4 or BMPR1A, and the latter is a vascular malformation disorder caused by mutations in ENG or ACVRL1. All four genes encode proteins involved in the transforming-growth-factor-signaling pathway. Although there are reports of patients and families with phenotypes of both disorders combined, the genetic etiology of this association is unknown. . Note: The disease is caused by mutations affecting the gene represented in this entry.; Colorectal cancer (CRC) [MIM:114500]: 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. . Note: The disease may be caused by mutations affecting the gene represented in this entry.; Note: SMAD4 variants may be associated with susceptibility to pulmonary hypertension, a disorder characterized by plexiform lesions of proliferating endothelial cells in pulmonary arterioles. The lesions lead to elevated pulmonary arterial pression, right ventricular failure, and death. The disease can occur from infancy throughout life and it has a mean age at onset of 36 years. Penetrance is reduced. Although familial pulmonary hypertension is rare, cases secondary to known etiologies are more common and include those associated with the appetite-suppressant drugs. .; Myhre syndrome (MYHRS) [MIM:139210]: A syndrome characterized by pre- and postnatal growth deficiency, mental retardation, generalized muscle hypertrophy and striking muscular build, decreased joint mobility, cryptorchidism, and unusual facies. Dysmorphic facial features include microcephaly, midface hypoplasia, prognathism, and blepharophimosis. Typical skeletal anomalies are short stature, square body shape, broad ribs, iliac hypoplasia, brachydactyly, flattened vertebrae, and thickened calvaria. Other features, such as congenital heart disease, may also occur. . Note: The disease is caused by mutations affecting the gene represented in this entry.
|Protein sequence and domain|| |
The MH1 domain is required for DNA binding. / The MH2 domain is required for both homomeric and heteromeric interactions and for transcriptional regulation. Sufficient for nuclear import. / Belongs to the dwarfin/SMAD family. / Contains 1 MH1 (MAD homology 1) domain. / Contains 1 MH2 (MAD homology 2) domain.
|Protein post-translational modifications|| |
Phosphorylated by PDPK1. / Monoubiquitinated on Lys-519 by E3 ubiquitin-protein ligase TRIM33. Monoubiquitination hampers its ability to form a stable complex with activated SMAD2/3 resulting in inhibition of TGF-beta/BMP signaling cascade. Deubiqitination by USP9X restores its competence to mediate TGF-beta signaling.
|Protein cellular localization|| |
Cytoplasm / Nucleus
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St John’s Laboratory Ltd.
|Product type|| |
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