immunoprecipitation (IP): 1-2 μg using lysates of HEK-293T cells over-expressing human SMAD1. western blot (chemiluminescent): 0.5-1.0 μg/mL using whole extracts of HEK-293T cells over-expressing human SMAD1.
Mothers against decapentaplegic homolog 1 (SMAD1) belongs to receptor-activated Smads (R-SMADs) subfamily. SMAD1 gene is mapped to human chromosome 4q31.21. The domain organization comprises of Mad homology 1 (MH1) domain andnuclear localisation signal (NLS) in the N-terminus. The C-terminal region has the Mad homology 1 (MH2), leucine-rich nuclear export signal (NES) and a proline-tyrosine (PY) motif.
Specificity
Anti-SMAD1 recognizes human SMAD1.
Immunogen
peptide corresponding to an internal region of human SMAD1, conjugated to KLH. The corresponding sequence is identical in mouse and differs by one amino acid in rat.
Application
Anti-SMAD1 antibody produced in rabbit may be used in immunoblotting and immunoprecipitation.
Biochem/physiol Actions
Mothers against decapentaplegic homolog 1 (SMAD1) is involved in mediating the signals of the bone morphogenetic proteins (BMP) and undergoes activation post phosphorylation by BMP receptor kinase. SMAD1 is a target for SMAD-specific E3 ubiquitin ligases, such as Smad ubiquitin regulatory factor 1 (SMURF1 and SMURF2) and undergoes ubiquitination and proteasome-mediated degradation. The phosphorylated form of SMAD1 forms a complex with SMAD4, which is important for its function in transcription regulation. SMAD1 is an oncogene which favors cancer cell growth and invasion especially in Glioma. It is a potential biomarker Diabetic nephropathy (DN pathology) along with urinary IgG4. An elevated extracellular signal-regulated kinases (ERKs) activity lead to higher activation of SMAD1 signaling which is implicated in the pathogenesis Cardio‐facio‐cutaneous (CFC) syndrome. Alternatively spliced transcript variants encoding the same protein have been observed. Variants of SMAD1 and other SMAD genes are implicated in pulmonary arterial hypertension (PAH). 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.
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 workingaliquots. 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.
Diabetic nephropathy (DN) is the major cause of end-stage kidney disease, but early biomarkers of DN risk are limited. Herein we examine urinary IgG4 and Smad1 as additional early DN biomarkers. We recruited 815 patients with type 2 diabetes; 554
Non-small cell lung cancer (NSCLC) is the major cause of cancer mortality worldwide. Though multidisciplinary therapies have been widely used for NSCLC, its overall prognosis remains very poor, presumably owing to lack of effective prognostic biomarkers. SMAD, a well-known transcription
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)
Heterozygous germline mutations of BMPR2 contribute to familial clustering of pulmonary arterial hypertension (PAH). To further explore the genetic basis of PAH in isolated cases, we undertook a candidate gene analysis to identify potentially deleterious variation. Members of the bone
Our team of scientists has experience in all areas of research including Life Science, Material Science, Chemical Synthesis, Chromatography, Analytical and many others.