This website uses cookies to ensure you get the best experience on our website.
- Table of Contents
Facts about Mothers against decapentaplegic homolog 1.
SMAD1/OAZ1/PSMB4 complex mediates the degradation of this CREBBP/EP300 repressor SNIP1. May act synergistically with SMAD4 and YY1 in bone morphogenetic protein (BMP)-mediated cardiac-specific gene expression.
Human | |
---|---|
Gene Name: | SMAD1 |
Uniprot: | Q15797 |
Entrez: | 4086 |
Belongs to: |
---|
dwarfin/SMAD family |
BSP1; BSP-1; hSMAD1; JV4-1SMAD, mothers against DPP homolog 1 (Drosophila); MAD homolog 1; MADH1JV41; MADR1MAD, mothers against decapentaplegic homolog 1 (Drosophila); Mad-related protein 1; mothers against decapentaplegic homolog 1; Mothers against DPP homolog 1; SMAD family member 1SMAD 1; SMAD, mothers against DPP homolog 1; Smad1; TGF-beta signaling protein 1; transforming growth factor-beta signaling protein 1
Mass (kDA):
52.26 kDA
Human | |
---|---|
Location: | 4q31.21 |
Sequence: | 4; NC_000004.12 (145481306..145559176) |
Ubiquitous. Highest expression seen in the heart and skeletal muscle.
Cytoplasm. Nucleus. Cytoplasmic in the absence of ligand. Migrates to the nucleus when complexed with SMAD4 (PubMed:15647271). Co-localizes with LEMD3 at the nucleus inner membrane (PubMed:15647271). Exported from the nucleus to the cytoplasm when dephosphorylated (By similarity).
You've come to the right spot if you're searching for an antibody that is a secondary antibody to the SMAD1 marker. Boster Bio has developed educational resources for educators, including PDFs. These materials can be used in your class. However you must mention Boster Bio and link back to this website. These materials are also available for download. We've listed some of the most effective uses for this antibody below.
SMAD1 is an important protein that is involved in the differentiation of epiblasts from germ cells. Phosphorylated SMAD1 is essential for this differentiation. It also plays an essential role in the commitment of germ cells to lineage. This specific protein function can be understood through the SMAD1 marker. Here are a few of its most useful uses. Learn more about it. You might also be interested:
When stimulated by BMP signals, Smad1 phosphorylates and translocates from the nucleus to the cytoplasm. Bimolecular complementation by fluorescence is a method that allows researchers to pinpoint the subcellular compartment in which Smad1 is located. It involves an Smad1 reporter protein that is split into two fragments and then fused to one of two interacting proteins. When they come into contact the two fragments of fluorescent will bind together. Functional YFP is responsible for the fluorescent signal that emerges from these fusions.
Endogenous PPM1H interacts with Smad1 in HaCaT and C2C12 cells. This mutant blocks Smad1 synthesis in the cytoplasm. It inhibits osteoprotegerin and the p21 gene. These are the two primary functions of the SMAD1 mark. You can get more details about its functions on the Internet. It is an excellent instrument to study the signaling in bone or cartilage.
In mice, Smad1 is necessary for chondrogenesis and osteoblast differentiation. The precise physiological function of Smad1 signaling has yet to be established. Kobayashi et al. recently reported that Smad1 and Smad5 are essential for chondrogenesis. To examine the process of Chondrogenesis the authors used Smad1 double-KO mice. They also developed mice that had specific for chondrocytes. SMAD1 cKO genes.
Recent research showed that the Boster Bio SB431542 SMAD2/3 inhibitor decreased cell invasion by TGFb1 within JEG-3 cells. The results showed that the inhibitor slowed cell invasion significantly, whereas a negative control showed no effects. The siRNA knockdown of Smad3 also reduced cell invasion. Silencing of Smad2 didn't result in any changes in cell invasion. Each condition was tested in triplicate.
The SMAD2/3 and SMAD4 proteins are receptor-regulated transcription factors that are activated upon binding to a ligand. They assemble into complexes that contain SMAD4 and regulate gene transcription. Cell proliferation and growth depend on activation of these receptor-regulated SMAD protein proteins. StAR expression is also regulated by the SMAD signaling pathway.
RNAi technology was used to shut down Smad2 and Smad3. SiRNAs that target Smad2 or Smad3 were designed and then transfected into JEG-3 cell lines. The RNAi-mediated siRNAs inhibited MMP-2 and 9 the most effectively. SB431542 also inhibits MMP-2. MMP-2 is also inhibited with siRNA targeting Smad3.
The SMAD2/3 inhibitor SB431541 blocks the expression of Smad2/3 within stem cells grown in a cell culture. This inhibitor inhibits both Smad2 and Smad3 in cells, which is essential in the process of regenerating tissues. It also blocks TGFb signaling as well as Smad1 but does not affect TGFb's other canonical targets.
The SMAD1 gene is a crucial regulator of the TP53 signaling pathways, is involved in regulating the metabolic rate of mRNA and expression of TFPI2. The dysregulation of this gene could be the cause of DN pathogenesis. However, there are still several questions that remain unanswered. The current literature suggests a number of possibilities for the SMAD1 gene, including kidney disease and cancer.
TSCs were isolated from mice and separated according to the level of SMAD1 expression. The mice were either given 50 mg/mL ADSC-Exos or a 10nM solution of dorsomorphin or SB431542. The mice were treated with the SMAD1 inhibitor for 30 min prior to consuming the drug. With this model, SMAD1 expression was detected in mice using an astrocytoma mouse model (Asterias atra-squama) or using either the murine or human myofibroblast cell-based assay.
Periodate Schiff staining increased in diabetic mice because of the increased expression of TFPI2 The kidney cortex also showed a decrease in glycogen levels after TFPI2 was reduced. This suggests that the SMAD1 protein could play a role in diabetic nephropathy. SMAD1 can be beneficial to diabetics, regardless of disease.
Boster Bio has educational resources that can be used by scientists to assist researchers conduct their research. Boster Bio has produced various educational resources that can be shared for free. Be sure to reference the source. Best Uses For The SMAD1 Marker
Due to similar amino acid sequences This secondary antibody for SMAD1 could cross-react with the AKAP6 antibody. This antibody recognizes SMAD1 as a receptor-regulated SMAD which mediates the degradation of the CREBBP/EP300 the repressor SNIP1. The antibody can also function in synergy with YY1 and SMAD4 proteins.
This primary antibody was developed against synthetic peptides that recognize the SMAD1 gene. These antibodies recognize SMAD1 from a variety of species. The antibody is 100 100% compatible with SMAD1/5/8/9) but may cross-react with SMAD2 or SMAD3.
GST-Smad2 proteins were quantified using Coomassie staining using BSA standards. The sample was separated using SDS-PAGE. It was then compared to six independent lysates taken from PE25 cells. The sample was then immunoblotted using a Smad2 antibody and enhanced chemiluminescence. The Trendline Excel tool was used to quantify the sample.
A secondary antibody that recognizes the SMAD1 targets of ubiquitin-ligases, which target the BMP pathway. The proteins that SMAD targets are involved in the formation of embryonic patterns. Ubc-like protein, such as Smurf1, are members of the SMAD family. It is recommended to use mIgG FcBP HRP to detect this antibody. Combine multiple molecules using mIgG HRP BP-HRP in order to determine the entire spectrum.
SANEp>The Sytokine which blocks the BMP-mediated Smad1 nucleotranslocation. It inhibits the phosphorylation of Smad1 caused by BMP and blocks nuclear translocation dependent on ligand. SMAD1 is a key regulator of embryonic neural growth. In the brain of the rat, it is located in the cerebellum. The expression of the gene is increased at P6. A significant portion of cerebellar cells are located in the outer germinal layer and undergo extensive differentiation.
Smurf1 interacts with Smad1 through an E3 ligase. This protein stimulates Smad1 ubiquitination. The inhibition of Smad1 can cause OS differentiation. This protein is also involved in the growth of tumors. It can inhibit tumor growth when it is present. However SMAD1 can be found in the skeletal bone tissue as well as osteosarcoma. The expression of Smurf1 in this tissue can increase the chance of metastasis.
PMID: 8673135 by Riggins G.J., et al. Mad-related genes in the human.
PMID: 8637600 by Liu F., et al. A human Mad protein acting as a BMP-regulated transcriptional activator.
*More publications can be found for each product on its corresponding product page