Name: Smad4 Monoclonal Antibody
SKU: WM0422
Price: 268 USD
Availability: InStock

Product details

Background:
This gene encodes a member of the Smad family of signal transduction proteins. Smad proteins are phosphorylated and activated by transmembrane serine-threonine receptor kinases in response to TGF-beta signaling. The product of this gene forms homomeric complexes and heteromeric complexes with other activated Smad proteins, which then accumulate in the nucleus and regulate the transcription of target genes. This protein binds to DNA and recognizes an 8-bp palindromic sequence (GTCTAGAC) called the Smad-binding element (SBE). The Smad proteins are subject to complex regulation by post-translational modifications. Mutations or deletions in this gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome. [provided by RefSeq, Oct 2009],

Specifications

Target	Smad4
Reactivity	Human
Applications	WB, IHC, IF, FC, ELISA
MW(Calculated)	60kD
MW(Observed)
Host Species	Mouse
Isotype
Conjugate/Modification	Unmodified
Modification
Recommended Dilution Ratio	WB 1:500-1:2000; IHC 1:200-1:1000; IF 1:200-1:1000; Flow Cyt 1:200-1:400; ELISA 1:10000; Not yet tested in other applications. / Note: For IHC, we suggest antigen retrieval with TE buffer pH 9.0 (Cat#YS0004)
Formulation	Liquid in PBS containing 50% glycerol, 0.5% BSA and 0.02% sodium azide.
Source
Purification	Affinity purification
Purity
Storage	-15°C to -25°C/1 year(Do not lower than -25°C)
Concentration
Clonality	Monoclonal
Clone Number	20H1
Immunogen	Purified recombinant fragment of human Smad4 expressed in E. Coli.
Sequence
Specificity	Smad4 Monoclonal Antibody detects endogenous levels of Smad4 protein.
Gene Name	SMAD4
Protein Name	Mothers against decapentaplegic homolog 4
Other Name	SMAD4; / DPC4; / MADH4; / 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
Species	Human
Gene ID-1	4089
Uniprot	Q13485
Species.1
Gene ID-2
Uniprot.1
Species.2
Gene ID-3
Uniprot.2
Organism-4
Gene ID-4
SwissProt-4
Background	This gene encodes a member of the Smad family of signal transduction proteins. Smad proteins are phosphorylated and activated by transmembrane serine-threonine receptor kinases in response to TGF-beta signaling. The product of this gene forms homomeric complexes and heteromeric complexes with other activated Smad proteins, which then accumulate in the nucleus and regulate the transcription of target genes. This protein binds to DNA and recognizes an 8-bp palindromic sequence (GTCTAGAC) called the Smad-binding element (SBE). The Smad proteins are subject to complex regulation by post-translational modifications. Mutations or deletions in this gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome. [provided by RefSeq, Oct 2009],
Cellular Localization	Cytoplasm . Nucleus . Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD (PubMed:15799969). PDPK1 prevents its nuclear translocation in response to TGF-beta (PubMed:17327236). .
Tissue Expression	Fetal brain,Muscle,Placenta,
Signaling_pathway	Cellular Processes >> Cell growth and death >> Cell cycle;Cellular Processes >> Cellular community - eukaryotes >> Adherens junction;Cellular Processes >> Cellular community - eukaryotes >> Signaling pathways regulating pluripotency of stem cells;Organismal Systems >> Immune system >> Th17 cell differentiation;Human Diseases >> Cancer: overview >> Pathways in cancer;Human Diseases >> Cancer: specific types >> Colorectal cancer;Human Diseases >> Cancer: specific types >> Pancreatic cancer;Human Diseases >> Cancer: specific types >> Hepatocellular carcinoma;Human Diseases >> Cancer: specific types >> Gastric cancer;Human Diseases >> Cancer: specific types >> Chronic myeloid leukemia;Environmental Information Processing >> Signal transduction >> Wnt signaling pathway;Environmental Information Processing >> Signal transduction >> TGF-beta signaling pathway;Environmental Information Processing >> Signal transduction >> Hippo signaling pathway;Environmental Information Processing >> Signal transduction >> Apelin signaling pathway;Environmental Information Processing >> Signal transduction >> FoxO signaling pathway
Research Areas	>>FoxO signaling pathway; / >>Cell cycle; / >>Wnt signaling pathway; / >>TGF-beta signaling pathway; / >>Apelin signaling pathway; / >>Hippo signaling pathway; / >>Adherens junction; / >>Signaling pathways regulating pluripotency of stem cells; / >>Th17 cell differentiation; / >>AGE-RAGE signaling pathway in diabetic complications; / >>Hepatitis B; / >>Human T-cell leukemia virus 1 infection; / >>Pathways in cancer; / >>Colorectal cancer; / >>Pancreatic cancer; / >>Chronic myeloid leukemia; / >>Hepatocellular carcinoma; / >>Gastric cancer
Function	Disease:Defects in SMAD4 are a cause of juvenile polyposis syndrome (JPS) [MIM:174900]; also known as juvenile intestinal polyposis (JIP). JPS is an 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.,Disease:Defects in SMAD4 are a cause of 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 aetiology of this association is unknown.,Disease:Defects in SMAD4 are a cause of pancreatic carcinoma [MIM:260350].,Disease:Defects in SMAD4 may be a cause of colorectal cancer (CRC) [MIM:114500].,Function:Common mediator of signal transduction by TGF-beta (transforming growth factor) superfamily; SMAD4 is the common SMAD (co-SMAD). Promotes binding of the SMAD2/SMAD4/FAST-1 complex to DNA and provides an activation function required for SMAD1 or SMAD2 to stimulate transcription. May act as a tumor suppressor.,PTM: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.,similarity:Belongs to the dwarfin/SMAD family.,similarity:Contains 1 MH1 (MAD homology 1) domain.,similarity:Contains 1 MH2 (MAD homology 2) domain.,subcellular location:Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with R-SMAD.,subunit:May form trimers with receptor-regulated SMAD (R-SMAD). Found in a ternary complex composed of SMAD4, STK11 and STK11IP. Interacts with ATF2, COPS5, DACH1, MSG1, SKI, STK11, STK11IP and TRIM33. Associates with ZNF423 or ZNF521 in response to BMP2 leading to activate transcription of BMP target genes. Interacts with USP9X.,
RRID