SAB4200405
Anti-SMAD4 antibody produced in rabbit
~1.0 mg/mL, affinity isolated antibody
Synonym(s):
Anti-DPC4, Anti-Deleted in pancreatic carcinoma locus 4, Anti-Deletion target in pancreatic carcinoma 4, Anti-JIP, Anti-MAD homolog 4, Anti-MADH4, Anti-Mothers against DPP homolog 4, Anti-SMAD family member 4
Sign Into View Organizational & Contract Pricing
All Photos(1)
About This Item
UNSPSC Code:
12352203
NACRES:
NA.41
biological source
rabbit
conjugate
unconjugated
antibody form
affinity isolated antibody
antibody product type
primary antibodies
clone
polyclonal
form
buffered aqueous solution
mol wt
antigen ~60 kDa
species reactivity
human
concentration
~1.0 mg/mL
technique(s)
western blot: 1-2 μg/mL using whole extracts of HEK-293T cells over-expressing human SMAD4
UniProt accession no.
shipped in
dry ice
storage temp.
−20°C
target post-translational modification
unmodified
Gene Information
human ... SMAD4(4089)
mouse ... Smad4(17128)
rat ... Smad4(50554)
General description
Mothers against decapentaplegic homolog 4 (SMAD4) belongs to the common-mediator SMAD (co-SMAD) SAMD sub-family. It comprises Mad homology 1 (MH1) and nuclear localisation signal (NLS) in the N-terminus. The C-terminal region has the Mad homology 1 (MH2). SMAD4 also possesses leucine-rich nuclear export signal (NES) and an unique Smad4 activation domain (SAD). SMAD4 gene is mapped to human chromosome 18q21.2.
Specificity
Anti-SMAD4 recognizes human SMAD4.
Immunogen
A peptide corresponding to an internal region of human SMAD4, conjugated to KLH. The corresponding sequence is identical in mouse, rat, bovine, dog, pig and bovine.
Application
Anti-SMAD4 antibody produced in rabbit has been used in western blotting.[1]
Biochem/physiol Actions
Mothers against decapentaplegic homolog (SMADs), in general, mediate transmission of signals from the transforming growth factor-β (TGFβ) to the nucleus, and thus regulate multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. The tumor suppressor mothers against decapentaplegic homolog 4 (SMAD4), also named DPC4, is the common signaling effector in the TGFβ superfamily. Phosphorylated R-SMADs interact with SMAD4, and the complex translocates into the nucleus to regulate gene transcription. Mutations or deletions in the SMAD4 gene have been shown to result in pancreatic cancer, juvenile polyposis syndrome, and hereditary hemorrhagic telangiectasia syndrome. A missense mutation in the Mad homology 2 (MH2) SMAD4 gene is implicated in Myhre syndrome.
Physical form
Solution in 0.01 M phosphate buffered saline, pH 7.4, containing 15 mM sodium azide.
Storage and Stability
For continuous use, store at 2-8 °C for up to one month. For extended storage, freeze in working aliquots. Repeated freezing and thawing, or storage in “frost-free” freezers,is not recommended. If slight turbidity occurs upon prolonged storage, clarify the solution by centrifugation before use. Working dilutions should be discarded if not used within 12 hours.
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.
Not finding the right product?
Try our Product Selector Tool.
recommended
Product No.
Description
Pricing
Storage Class
10 - Combustible liquids
flash_point_f
Not applicable
flash_point_c
Not applicable
Choose from one of the most recent versions:
Certificates of Analysis (COA)
Lot/Batch Number
Don't see the Right Version?
If you require a particular version, you can look up a specific certificate by the Lot or Batch number.
Already Own This Product?
Find documentation for the products that you have recently purchased in the Document Library.
Dipen Maru et al.
Oncogene, 23(3), 859-864 (2003-12-03)
Appendiceal adenocarcinomas are uncommon, and the genetic alterations present in these tumors are not well characterized. We studied genetic alterations including loss of chromosome 18q (location of DCC, DPC4, and JV-18 genes), and mutations of the DPC4 (SMAD4) and beta-catenin
Carine Le Goff et al.
Nature genetics, 44(1), 85-88 (2011-12-14)
Myhre syndrome (MIM 139210) is a developmental disorder characterized by short stature, short hands and feet, facial dysmorphism, muscular hypertrophy, deafness and cognitive delay. Using exome sequencing of individuals with Myhre syndrome, we identified SMAD4 as a candidate gene that
Nithya K Iyer et al.
Thorax, 65(8), 745-746 (2010-08-06)
Juvenile polyposis syndrome (JPS) and hereditary haemorrhagic telangiectasia (HHT) are autosomal dominant disorders with characteristic clinical phenotypes. Recently, reports of the combined syndrome of JPS and HHT have been described in individuals with mutations in the SMAD4 gene, whose product-SMAD4-is
Y Zhang et al.
Proceedings of the National Academy of Sciences of the United States of America, 98(3), 974-979 (2001-02-07)
Smad proteins are key intracellular signaling effectors for the transforming growth factor-beta superfamily of peptide growth factors. Following receptor-induced activation, Smads move into the nucleus to activate transcription of a select set of target genes. The activity of Smad proteins
A Moustakas et al.
Journal of cell science, 114(Pt 24), 4359-4369 (2002-01-17)
Smad proteins transduce signals from transforming growth factor-beta (TGF-beta) superfamily ligands that regulate cell proliferation, differentiation and death through activation of receptor serine/threonine kinases. Phosphorylation of receptor-activated Smads (R-Smads) leads to formation of complexes with the common mediator Smad (Co-Smad)
Active Filters
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.
Contact Technical Service
