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The antibody against SMAD4 was raised in rabbit using the Human SMAD4 as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, WB.
The antibody against SMAD4 was raised in rabbit using the Human SMAD4 as the immunogen. This antibody exists as a non-conjugated isotype IgG, Antigen affinity purified. This antibody has been validated on ELISA, WB.
$600.00
| Cat.No | ADC-45872A | Clonality | Polyclonal |
|---|---|---|---|
| Host Species | Rabbit | Target Name | SMAD4 |
| Form | Liquid | Species Reactivity | Human, Mouse, Rat |
| Isotype | IgG | Storage Buffer | 50% Glycerol, Avoid freeze / thaw cycles., PBS with 0.1% Sodium Azide |
| Purification Method | Antigen affinity purified | Conjugate | Non-conjugated |
| Application | ELISA, WB | Storage | Upon receipt |
| Immunogen Description | Human SMAD4 | Target Species | Human |
|---|---|---|---|
| Immunogen Sequence | Complete sequences for the immunogen, target protein, and peptides are available upon request. | Uniprot ID | Q13485 |
Uniprot Id
Q13485
Target Species
Human
Target Name
SMAD4
Target Full Name
Mothers against decapentaplegic homolog 4
Target 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. 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.
Target Involvement
Pancreatic cancer (PNCA); Juvenile polyposis syndrome (JPS); Juvenile polyposis/hereditary hemorrhagic telangiectasia syndrome (JP/HHT); Colorectal cancer (CRC); Myhre syndrome (MYHRS)
Target Subcellular Location
Cytoplasm. Nucleus.
Target Protein Families
Dwarfin/SMAD family
Target Synonyms
(Small) Mothers Against Decapentaplegic; Deleted in Pancreatic Carcinoma 4; Deleted in Pancreatic Carcinoma; Deleted in pancreatic carcinoma locus 4; Deletion target in pancreatic carcinoma 4; DPC 4; DPC4; hSMAD4; JIP; MAD homolog 4; MAD mothers against decapentaplegic Drosophila homolog 4; MAD mothers against decapentaplegic homolog 4; MADH 4; MADH4; Med; Medea; Mothers against decapentaplegic homolog 4; Mothers against decapentaplegic; Drosophila; homolog of; 4; Mothers against DPP homolog 4; MYHRS; OTTHUMP00000163548; SMA- and MAD-related protein 4; SMAD 4; SMAD family member 4; SMAD mothers against DPP homolog 4; SMAD4; SMAD4_HUMAN
Target 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 transforming growth factor (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 protein acts as a tumor suppressor and inhibits epithelial cell proliferation. It may also have an inhibitory effect on tumors by reducing angiogenesis and increasing blood vessel hyperpermeability. The encoded protein is a crucial component of the bone morphogenetic protein signaling pathway. 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.
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