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SMAD family member 4

Smad4, DPC4
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] (from NCBI)
Top mentioned proteins: p53, HAD, CAN, p16, TGF-beta
Papers using Smad4 antibodies
Smad4 is required for the normal organization of the cartilage growth plate
Glimcher Laurie H et al., In The EMBO Journal, 2004
... (Santa Cruz); anti-Smad2, anti-phospho-Smad1/5/8, anti-phospho-Smad2 (S465/467), and anti-phospho-p38 (Cell Signaling); anti-Smad1 (Invitrogen); anti-Flag (M2, Sigma); anti-Smad4 (Abcam); anti-XIAP (Stressgen); and anti-GAPDH ...
Transforming growth factor-beta-induced inhibition of myogenesis is mediated through Smad pathway and is modulated by microtubule dynamic stability
Kapus András et al., In The Journal of Cell Biology, 2003
tubulin (Sigma-Aldrich), cofilin, Smad2, phospho-Smad3, Smad4 (Cell Signaling Technology), c-Myc (clone 9E10), ...
Insulin-like growth factor-I inhibits transcriptional responses of transforming growth factor-beta by phosphatidylinositol 3-kinase/Akt-dependent suppression of the activation of Smad3 but not Smad2.
Nurminsky Dmitry I., In PLoS ONE, 2002
... ab65252), HDAC4 (Cell Signaling, #2072), HAND2 (Abcam, ab56590), Tropomyosin C (Santacruz, sc73225), DnaJB1 (Santacruz, sc-1800) and SMAD4 (Abcam, ab1341) ...
CHMP5 is essential for late endosome function and down-regulation of receptor signaling during mouse embryogenesis
Ghosh Sankar et al., In The Journal of Cell Biology, 1999
... The antibodies used were anti–phospho-Erk1/2 (Cell Signaling Technology), anti–phospho-Smad2 (Cell Signaling Technology), anti-Smad4 (Santa Cruz Biotechnology, Inc; H552), anti-Smad2 (Cell ...
Regulation of growth and prostatic marker expression by activin A in an androgen-sensitive prostate cancer cell line LNCAP
Nishio K et al., In British Journal of Cancer, 1996
... The following antibodies were used: anti-p21, anti-cdk2, anti-cyclin D, anti-phospho-Rb, anti-Smad2, anti-phospho-Smad2, anti-Smad3, anti-Smad4, and secondary antibodies (Cell Signaling, Beverly, MA, USA); anti- ...
Papers on Smad4
Zinc affects miR-548n, SMAD4, SMAD5 expression in HepG2 hepatocyte and HEp-2 lung cell lines.
Tripp et al., Athens, United States. In Biometals, 26 Oct 2015
The purpose of this study was to determine the effects of Zn concentration in cell culture on the expression of miR-548n, SMAD4 and SMAD5 in hepatocyte (HepG2) and lung epithelium (HEp-2) cell lines.
Characterization of pancreatic ductal adenocarcinoma using whole transcriptome sequencing and copy number analysis by single-nucleotide polymorphism array.
Biasco et al., Bologna, Italy. In Mol Med Report, 22 Oct 2015
From this analysis, alterations in the known oncogenes associated with PDAC were observed, including Kirsten rat sarcoma viral oncogene homolog (KRAS) mutations (93.7%) and inactivation of cyclin‑dependent kinase inhibitor 2A (CDKN2A) (50%), mothers against decapentaplegic homolog 4 (SMAD4) (50%), and tumor protein 53 (TP53) (56%).
Executive summary of the 11th HHT international scientific conference.
Wooderchak-Donahue et al., Essen, Germany. In Angiogenesis, 21 Oct 2015
HHT has a worldwide incidence of about 1:5000 and approximately 80 % of cases are due to mutations in ENG, ALK1 (aka activin receptor-like kinase 1 or ACVRL1) and SMAD4.
Activin B induces human endometrial cancer cell adhesion, migration and invasion by up-regulating integrin β3 via SMAD2/3 signaling.
Leung et al., Vancouver, Canada. In Oncotarget, 28 Sep 2015
Moreover, we show that activin B treatment increases integrin β3 mRNA and protein levels via SMAD2/3-SMAD4 signaling.
Stem vs non-stem cell origin of colorectal cancer.
Sansom et al., Glasgow, United Kingdom. In Br J Cancer, Jul 2015
The progression of this cancer from an early adenoma to carcinoma is accompanied by a well-characterised set of mutations including KRAS, SMAD4 and TP53.
It's a SMAD/SMAD World.
Maitra et al., Houston, United States. In Cell, Jul 2015
DPC4/SMAD4 mutations are associated with aggressive pancreatic cancer.
[Advance in the biology of pancreatic of cancer].
Cordelier et al., Toulouse, France. In Bull Cancer, Jun 2015
P16, TP53, DPC4/Smad4 tumor suppressor pathways are genetically inactivated in the majority of pancreatic carcinomas, whereas oncogenic k-ras is activated.
Sequential cancer mutations in cultured human intestinal stem cells.
Clevers et al., Utrecht, Netherlands. In Nature, Jun 2015
Here we utilize CRISPR/Cas9 technology for targeted gene modification of four of the most commonly mutated colorectal cancer genes (APC, P53 (also known as TP53), KRAS and SMAD4) in cultured human intestinal stem cells.
Pathogenesis of cholangiocarcinoma: From genetics to signalling pathways.
Teh et al., Singapore, Singapore. In Best Pract Res Clin Gastroenterol, Apr 2015
A series of highly recurrent mutations in genes such as TP53, KRAS, SMAD4, BRAF, MLL3, ARID1A, PBRM1 and BAP1, which are known to be involved in cell cycle control, cell signalling pathways and chromatin dynamics, have led to investigations of their roles, through molecular to mouse modelling studies, in cholangiocarcinogenesis.
Modeling colorectal cancer using CRISPR-Cas9-mediated engineering of human intestinal organoids.
Sato et al., Tokyo, Japan. In Nat Med, Mar 2015
By modulating the culture conditions to mimic that of the intestinal niche, we selected isogenic organoids harboring mutations in the tumor suppressor genes APC, SMAD4 and TP53, and in the oncogenes KRAS and/or PIK3CA.
Whole genomes redefine the mutational landscape of pancreatic cancer.
Grimmond et al., Brisbane, Australia. In Nature, Mar 2015
Chromosomal rearrangements leading to gene disruption were prevalent, affecting genes known to be important in pancreatic cancer (TP53, SMAD4, CDKN2A, ARID1A and ROBO2) and new candidate drivers of pancreatic carcinogenesis (KDM6A and PREX2).
Genetic diagnosis of high-penetrance susceptibility for colorectal cancer (CRC) is achievable for a high proportion of familial CRC by exome sequencing.
Houlston et al., London, United Kingdom. In J Clin Oncol, Mar 2015
PATIENTS AND METHODS: To quantify the impact of germline mutation to familial CRC, we sequenced the mismatch repair genes (MMR) APC, MUTYH, and SMAD4/BMPR1A in 626 early-onset familial CRC cases ascertained through a population-based United Kingdom national registry.
Pancreatic cancer: optimizing treatment options, new, and emerging targeted therapies.
Coveler et al., Seattle, United States. In Drug Des Devel Ther, Dec 2014
Pancreatic adenocarcinoma is characterized by several germline or acquired genetic mutations, the most common being KRAS (90%), CDK2NA (90%), TP53 (75%-90%), DPC4/SMAD4 (50%).
Comprehensive serial molecular profiling of an "N of 1" exceptional non-responder with metastatic prostate cancer progressing to small cell carcinoma on treatment.
Cooney et al., Ann Arbor, United States. In J Hematol Oncol, Dec 2014
RESULTS: A deleterious somatic SMAD4 L535fs variant was present in both prostate and liver specimens; however, a TP53 R282W mutation was exclusively enriched in the liver specimen.
[Genetic aspects of pancreatic cancer].
Tov et al., In Eksp Klin Gastroenterol, 2013
Currently, the most significant genes for PC include KRAS2, p16/CDKN2, TP53, SMAD4/DPC4.
MicroRNA-146a modulates TGF-beta1-induced hepatic stellate cell proliferation by targeting SMAD4.
Li et al., Hefei, China. In Cell Signal, 2012
Bioinformatics analyses predict that Smad4 is the potential target of miR-146a.
Vascular smooth muscle cell Smad4 gene is important for mouse vascular development.
Chen et al., Birmingham, United States. In Arterioscler Thromb Vasc Biol, 2012
Provide important insight into the role of Smad4 and its upstream Smads in regulating vascular smooth muscle function and vascular development of mice.
Transforming growth factor-β/SMAD Target gene SKIL is negatively regulated by the transcriptional cofactor complex SNON-SMAD4.
Macías-Silva et al., Mexico. In J Biol Chem, 2012
when the SNON-SMAD4 complex is absent as in some cancer cells lacking SMAD4 the regulation of some TGF-beta target genes is modified
Dynamics of TGF-β signaling reveal adaptive and pulsatile behaviors reflected in the nuclear localization of transcription factor Smad4.
Brivanlou et al., New York City, United States. In Proc Natl Acad Sci U S A, 2012
TGF-beta signaling has a role in nuclear localization of transcription factor Smad4
Mutations of SMAD4 account for both LAPS and Myhre syndromes.
Thibodeau et al., In Am J Med Genet A, 2012
Missense mutations of SMAD4 account for both LAPS and Myhre syndromes.
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