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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, CAN, HAD, p16, TGF-beta
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
Nanopore sequencing detects structural variants in cancer.
New
Timp et al., Baltimore, United States. In Cancer Biol Ther, Feb 2016
We have tested nanopore sequencing to detect a series of well-characterized SVs, including large deletions, inversions, and translocations that inactivate the CDKN2A/p16 and SMAD4/DPC4 tumor suppressor genes in pancreatic cancer.
Bone Morphogenic Protein 4-Smad-Induced Upregulation of Platelet-Derived Growth Factor AA Impairs Endothelial Function.
New
Huang et al., Hong Kong, Hong Kong. In Arterioscler Thromb Vasc Biol, Feb 2016
SMAD4-shRNA lentivirus, SMAD1-shRNA, and SMAD5 shRNA adenovirus were used for knockdown in human endothelial cells.
SMAD4 is Involved in the Development of Endotoxin Tolerance in Microglia.
New
Cao et al., Nantong, China. In Cell Mol Neurobiol, Feb 2016
Smad4 plays important roles in the induction of LPS tolerance.
RAS signaling and anti-RAS therapy: lessons learned from genetically engineered mouse models, human cancer cells, and patient-related studies.
Review
New
Fang, Houston, United States. In Acta Biochim Biophys Sin (shanghai), Jan 2016
Studies on clinical specimens also demonstrated that KRAS mutations are present in premalignant tissues and that most of KRAS mutant human cancers have co-mutations in other cancer driver genes, including TP53, STK11, CDKN2A, and KMT2C in lung cancer; APC, TP53, and PIK3CA in colon cancer; and TP53, CDKN2A, SMAD4, and MED12 in pancreatic cancer.
From Barrett metaplasia to esophageal adenocarcinoma: the molecular background.
Review
New
Rugge et al., Padova, Italy. In Histol Histopathol, Jan 2016
Recent comprehensive mutational profiling studies identified that the inactivation of the TP53 and of the SMAD4 tumour suppressor genes occurred in a stage-specific manner, confined to (high grade) dysplastic and neoplastic lesions, respectively.
Using next-generation sequencing to determine potential molecularly guided therapy options for patients with resectable pancreatic adenocarcinoma.
New
Chung et al., Grand Rapids, United States. In Am J Surg, Jan 2016
The incidence of mutations was: Kirsten rat sarcoma viral oncogene homolong (KRAS) = 87%, tumor protein 53 (TP53) = 63%, cyclin-dependent kinase inhibitor 2A (CDKN2A) = 20%, Mothers Against Decapentaplegic Homolog 4 (SMAD4) = 20%, epidermal growth factor receptor (EGFR) = 7%.
It's a SMAD/SMAD World.
New
Impact
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].
Review
New
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.
New
Impact
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.
Modeling colorectal cancer using CRISPR-Cas9-mediated engineering of human intestinal organoids.
New
Impact
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.
New
Impact
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.
New
Impact
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.
Review
Coveler et al., Seattle, United States. In Drug Des Devel Ther, 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%).
Transducer of ERBB2.1 (TOB1) as a Tumor Suppressor: A Mechanistic Perspective.
Review
Shin et al., Seoul, South Korea. In Int J Mol Sci, 2014
The tumor-specific overexpression of TOB1 results in the activation of other tumor suppressor proteins, such as mothers against decapentaplegic homolog 4 (SMAD4) and phosphatase and tensin homolog-10 (PTEN), and blocks tumor progression.
Halichondrin B amide acts as tubulin binding agent to exhibit anti-tumor efficacy in hematologic cancers.
Liu et al., Shenyang, China. In Int J Clin Exp Med, 2014
The HCT116 DPC4 (-/-) colon cancer cell line was the most sensitive with an IC50 of 2.02 μM, compared to 3.78 μM in the parental HCT116.
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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