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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, TGF-beta, HAD, CAN, p16
Papers using Smad4 antibodies
Smad4 is required for the normal organization of the cartilage growth plate
Supplier
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
Supplier
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.
Supplier
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
Supplier
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
Supplier
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
Prognostic implication of the loss of TGFBR2 expression in oral carcinoma.
New
Kannan et al., In Neoplasma, 13 May 2015
A gradual decrease in the expression of TGFβ signalling members like SMAD2, SMAD4, TGFBR1 and TGFBR2 have been noted from normal to PMD in oral cancers.
Transcriptional regulation of tenascin-W by TGF-beta signaling in the bone metastatic niche of breast cancer cells.
New
Chiquet-Ehrismann et al., Basel, Switzerland. In Int J Cancer, 13 May 2015
Site-directed mutagenesis of a SMAD4 binding element in proximity of the TATA box strongly impaired promoter activity.
Aspirin blocks growth of breast tumor cells and tumor-initiating cells and induces reprogramming factors of mesenchymal to epithelial transition.
New
Banerjee et al., Kansas City, United States. In Lab Invest, 13 May 2015
The tumor growth-inhibitory and reprogramming roles of ASA could be mediated through inhibition of TGF-β/SMAD4 signaling pathway that is associated with growth, motility, invasion, and metastasis in advanced BCs.
The clinical and biological significance of MIR-224 expression in colorectal cancer metastasis.
New
Nicoloso et al., Houston, United States. In Gut, 24 Apr 2015
We identified SMAD4 as a miR-224 target and observed negative correlation (Spearman Rs=-0.44,
Modeling colorectal cancer using CRISPR-Cas9-mediated engineering of human intestinal organoids.
New
Impact
Sato et al., Tokyo, Japan. In Nat Med, 31 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.
New
Impact
Grimmond et al., Brisbane, Australia. In Nature, 26 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.
New
Impact
Houlston et al., London, United Kingdom. In J Clin Oncol, 10 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.
Novel Targets in Pancreatic Cancer Research.
Review
New
Brody et al., Philadelphia, United States. In Semin Oncol, Feb 2015
For example, PDA is driven by key activating, gain-of-function mutations in proto-oncogenes (eg, K-Ras) along with loss of function of tumor suppressor genes (eg, p16, SMAD4).
Radiotherapy for SMAD4-negative musculoskeletal lesions from pancreatic cancer: case report and review.
Review
New
Brunner et al., Freiburg, Germany. In Strahlenther Onkol, Jan 2015
Metastatic disease correlates with SMAD4 status.
Hereditary hemorrhagic telangiectasia: genetics and molecular diagnostics in a new era.
Review
New
Bayrak-Toydemir et al., Salt Lake City, United States. In Front Genet, Dec 2014
More recently, two additional genes in the same pathway, SMAD4 and GDF2, have been identified in a much smaller number of patients with a similar or overlapping phenotype to HHT.
Research on potential biomarkers in hereditary hemorrhagic telangiectasia.
New
Bernabéu et al., Madrid, Spain. In Front Genet, Dec 2014
Hereditary hemorrhagic telangiectasia (HHT) is a genetically heterogeneous disorder, involving mutations in two predominant genes known as Endoglin (ENG; HHT1) and activin receptor-like kinase 1 (ACVRL1/ALK1; HHT2), as well as in some less frequent genes, such as MADH4/SMAD4 (JP-HHT) or BMP9/GDF2 (HHT5).
Diagnosis and molecular aspects of solid-pseudopapillary neoplasms of the pancreas.
Review
New
Cavard et al., Paris, France. In Semin Diagn Pathol, Nov 2014
Distinctive molecular alterations such as the presence of CTNNB1 mutations are observed in nearly all cases, while mutations classically observed in ductal adenocarcinoma, such as KRAS, TP53, and SMAD4, are not observed in SPNs, reinforcing its distinct nature compared to all other pancreatic neoplasms.
Serous cystic neoplasms of the pancreas: clinicopathologic and molecular characteristics.
Review
New
Adsay et al., Atlanta, United States. In Semin Diagn Pathol, Nov 2014
Serous cystadenomas also lack the molecular alterations that characterize ductal neoplasms, such as mutation of KRAS (high prevalence in most mucinous ductal neoplasms), inactivation of SMAD4 (seen in ductal adenocarcinomas), and mutations in GNAS (seen in some IPMNs) and RNF43 (detected in MCNs and IPMNs).
Ordering of mutations in preinvasive disease stages of esophageal carcinogenesis.
New
Impact
OCCAMS Consortium et al., Cambridge, United Kingdom. In Nat Genet, Aug 2014
Only TP53 and SMAD4 mutations occurred in a stage-specific manner, confined to HGD and EAC, respectively.
Exome and whole-genome sequencing of esophageal adenocarcinoma identifies recurrent driver events and mutational complexity.
Impact
Bass et al., Boston, United States. In Nat Genet, 2013
Of these genes, five (TP53, CDKN2A, SMAD4, ARID1A and PIK3CA) have previously been implicated in EAC.
MicroRNA-146a modulates TGF-beta1-induced hepatic stellate cell proliferation by targeting SMAD4.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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.
GeneRIF
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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