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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
Exchange Protein Directly Activated by cAMP (EPAC1) Modulates Regulatory T Cell-Mediated Immune Suppression.
New
Cheng et al., In Biochem J, 23 Nov 2014
Mechanistically, EPAC1 inhibition enhanced activation of the transcription factor STAT3 and up-regulated SMAD7 expression while down-regulating expression of SMAD4.
The Downregulation of MicroRNA-146a Modulates TGF-β Signaling Pathways Activity in Glioblastoma.
New
Ma et al., Beijing, China. In Mol Neurobiol, 19 Nov 2014
MiRNA-146a overexpression significantly reduced SMAD4 protein expression instead of p-SMAD2.
Nuclear factor I-C expression pattern in developing teeth and its important role in odontogenic differentiation of human molar stem cells from the apical papilla.
New
Ge et al., Beijing, China. In Eur J Oral Sci, 10 Nov 2014
NFIC knockdown in hSCAPs significantly inhibited expression of DSPP and promoted that of dentin matrix protein 1 (DMP1), meanwhile upregulated the expression of TGF-β1 and downregulated SMAD3 and SMAD4.
Gene expression differences in primary colorectal tumors and matched liver metastases: chemotherapy related or tumoral heterogeneity?
New
Feliu et al., Madrid, Spain. In Clin Transl Oncol, 10 Nov 2014
For the remaining genes, where no significant differences were observed, only SMAD4 (r s = 0.447, p = 0.010), ERCC1 (r s = 0.423, p = 0.016) and VEGF A (r s = 0.453, p = 0.009) showed significant correlation in expression between the two tissues.
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.
The genetic basis of pulmonary arterial hypertension.
Review
New
Chung et al., New York City, United States. In Hum Genet, May 2014
Mutations in ALK-1, ENG, SMAD4 and SMAD8, other TGFβ family members, are additional rare causes of PAH.
Molecular genetics of pancreatic neoplasms and their morphologic correlates: an update on recent advances and potential diagnostic applications.
Review
New
Adsay et al., Atlanta, United States. In Am J Clin Pathol, Feb 2014
RESULTS: Mutations in KRAS, P16/CDKN2A, TP53, and SMAD4/DPC4 are commonly seen in ductal neoplasia but not in nonductal tumors; ductal adenocarcinomas with SMAD4/DPC4 loss are associated with widespread metastasis and poor prognosis.
Molecular pathology of pancreatic cancer.
Review
New
Horii et al., Sendai, Japan. In Pathol Int, Jan 2014
The comprehensive studies of the pancreatic cancer genome have revealed that most genetic alterations are identified to be associated with specific core signaling pathways including high-frequency mutated genes such as KRAS, CDKN2A, TP53, and SMAD4 along with several low-frequency mutated genes.
Meta-analysis of the prognostic value of smad4 immunohistochemistry in various cancers.
New
Liu et al., Nanjing, China. In Plos One, Dec 2013
BACKGROUND: Accumulating evidence indicates that Smad4 (DPC4) plays a fundamental role in the development and prognosis of several types of cancer.
Contributions of molecular analysis to the diagnosis and treatment of gastrointestinal neoplasms.
Review
New
Bellizzi, Iowa City, United States. In Semin Diagn Pathol, Nov 2013
The first section describes clinical applications of 11 immunohistochemical stains (p53, HER2, KIT, SDHB, SMAD4, beta-catenin, L-FABP, MLH1, PMS2, MSH2, and MSH6), the results of which directly reflect underlying genetic or epigenetic events.
[Kras oncogene and pancreatic cancer: thirty years after].
Review
New
Buscail et al., Toulouse, France. In Med Sci (paris), Nov 2013
These models are induced on the basis of Kras mutation (Pdx1-Cre ; Kras(G12D) mice) associated or not to the inactivation of tumour suppressor genes (TP53, DPC4, INK4A).
Exome and whole-genome sequencing of esophageal adenocarcinoma identifies recurrent driver events and mutational complexity.
New
Impact
Bass et al., Boston, United States. In Nat Genet, May 2013
Of these genes, five (TP53, CDKN2A, SMAD4, ARID1A and PIK3CA) have previously been implicated in EAC.
COUP-TFII inhibits TGF-β-induced growth barrier to promote prostate tumorigenesis.
New
Impact
Tsai et al., Houston, United States. In Nature, Feb 2013
Here we show that COUP transcription factor II (COUP-TFII, also known as NR2F2), a member of the nuclear receptor superfamily, serves as a key regulator to inhibit SMAD4-dependent transcription, and consequently overrides the TGF-β-dependent checkpoint for PTEN-null indolent tumours.
Pancreatic cancer genomes reveal aberrations in axon guidance pathway genes.
Impact
Grimmond et al., Sydney, Australia. In Nature, 2012
We define 16 significantly mutated genes, reaffirming known mutations (KRAS, TP53, CDKN2A, SMAD4, MLL3, TGFBR2, ARID1A and SF3B1), and uncover novel mutated genes including additional genes involved in chromatin modification (EPC1 and ARID2), DNA damage repair (ATM) and other mechanisms (ZIM2, MAP2K4, NALCN, SLC16A4 and MAGEA6).
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
Comprehensive molecular characterization of human colon and rectal cancer.
Impact
Cancer Genome Atlas Network, In Nature, 2012
Twenty-four genes were significantly mutated, and in addition to the expected APC, TP53, SMAD4, PIK3CA and KRAS mutations, we found frequent mutations in ARID1A, SOX9 and FAM123B.
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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