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SMAD family member 2

The protein encoded by this gene belongs to the SMAD, a family of proteins similar to the gene products of the Drosophila gene 'mothers against decapentaplegic' (Mad) and the C. elegans gene Sma. SMAD proteins are signal transducers and transcriptional modulators that mediate multiple signaling pathways. This protein mediates the signal of the transforming growth factor (TGF)-beta, and thus regulates multiple cellular processes, such as cell proliferation, apoptosis, and differentiation. This protein is recruited to the TGF-beta receptors through its interaction with the SMAD anchor for receptor activation (SARA) protein. In response to TGF-beta signal, this protein is phosphorylated by the TGF-beta receptors. The phosphorylation induces the dissociation of this protein with SARA and the association with the family member SMAD4. The association with SMAD4 is important for the translocation of this protein into the nucleus, where it binds to target promoters and forms a transcription repressor complex with other cofactors. This protein can also be phosphorylated by activin type 1 receptor kinase, and mediates the signal from the activin. Alternatively spliced transcript variants encoding the same protein have been observed. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: TGF-beta, Smad3, Smad4, CAN, V1a
Papers using Smad2 antibodies
Nuclear factor I-C links platelet-derived growth factor and transforming growth factor beta1 signaling to skin wound healing progression.
Lee Sean Bong, In PLoS ONE, 2008
... Rabbit anti-p-Smad3 and total Smad2/3 antibodies were purchased from Cell Signaling Technology (Danvers, MA) ...
GADD34-PP1c recruited by Smad7 dephosphorylates TGF type I receptor.
Goumans Marie Jose, In PLoS ONE, 2003
... The antibodies used were as follows: anti-phospho-Smad2 (Ser465/467) (138D4) and anti-Smad2 (L16D3) antibodies were purchased from Cell Signaling.
The emerging role of lysophosphatidic acid in cancer
Quaranta Vito et al., In Journal of Oncology, 2002
... Polyclonal antibody (pAb) against phosphorylated Smad2 (Ser465/467), GAPDH, and monoclonal antibody (mAb) against Smad2/3 were purchased from Cell Signaling Technology (Danvers, MA), BD ...
Hmg-CoA reductase inhibitor modulates monocyte-endothelial cell interaction under physiological flow conditions in vitro: involvement of Rho GTPase-dependent mechanism
Kim Jae Ho et al., In Experimental & Molecular Medicine, 2000
... Anti-phospho-Smad2 (Ser465/467) and anti-Smad2 antibodies were obtained from Cell Signaling Technology (Beverly, MA) ...
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 ...
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Papers on Smad2
Epicardium is required for sarcomeric maturation and cardiomyocyte growth in the ventricular compact layer mediated by transforming growth factor β and fibroblast growth factor before the onset of coronary circulation.
Nakajima et al., Ōsaka, Japan. In Congenit Anom (kyoto), Aug 2014
Sarcomeric maturation (distance between Z-lines) and cardiomyocyte growth (size) were affected in the thin compact myocardium of epicardium-deficient ventricles, in which the amounts of phospho-smad2 and phospho-ERK as well as expression of transforming growth factor (TGF)β2 and fibroblast growth factor (FGF)2 were reduced.
Identification of a characteristic copy number alteration profile by high-resolution single nucleotide polymorphism arrays associated with metastatic sporadic colorectal cancer.
Sayagués et al., Salamanca, Spain. In Cancer, Aug 2014
CONCLUSIONS: In line with expectations, the copy number profile investigated involved multiple genes that were associated previously with sCRC (ie, SMAD2) and/or the metastatic process (ie, podocalyxin-like [PODXL]), and it also was associated with a poorer outcome.
Calcitriol modulates receptor for advanced glycation end products (RAGE) in diabetic hearts.
Chen et al., Taipei, Taiwan. In Int J Cardiol, Jun 2014
Western blot was used to evaluate protein expressions of myocardial RAGE, TNF-α, p65 subunit of NF-κB (p65), α subunit of inhibitor of κB (IκBα), subunits of NADPH oxidase (NOX4 and p22(phox)), angiotensin II type 1 receptor (AT1R), TGF-β1, TGF-β receptor I, total and phosphorylated SMAD2/3 and ERK, matrix metalloproteinases 2 (MMP2), tissue inhibitors of metalloproteinases 2 (TIMP2) and procollagen I. RESULTS: As compared to control, diabetic rats had increased expressions of cardiac RAGE, TNF-α, p22(phox), AT1R, and TGF-β1, which were significantly attenuated in the diabetic rats treated with calcitriol.
M2 macrophages promote beta-cell proliferation by up-regulation of SMAD7.
Gittes et al., Pittsburgh, United States. In Proc Natl Acad Sci U S A, May 2014
M2 macrophages not only release TGFβ1 to directly induce up-regulation of SMAD7 in beta cells but also release EGF to activate EGF receptor signaling that inhibits TGFβ1-activated SMAD2 nuclear translocation, resulting in TGFβ signaling inhibition.
Daidzein stimulates collagen synthesis by activating the TGF-β/smad signal pathway.
Ye et al., Shanghai, China. In Australas J Dermatol, Apr 2014
A Western blot analysis was applied to detect the levels of phosphorylated-Smad2 and Smad3.
De novo mutations in histone-modifying genes in congenital heart disease.
Lifton et al., New Haven, United States. In Nature, Jul 2013
There are also two de novo mutations in SMAD2, which regulates H3K27 methylation in the embryonic left-right organizer.
The kinase PKCα selectively upregulates interleukin-17A during Th17 cell immune responses.
Baier et al., Innsbruck, Austria. In Immunity, Feb 2013
We have shown that PKCα physically interacts and functionally cooperates with TGFβRI to promote robust SMAD2-3 activation.
TGF-β signaling in tissue fibrosis: redox controls, target genes and therapeutic opportunities.
Higgins et al., Albany, United States. In Cell Signal, 2013
ROS generation in response to TGF-β1 stimulation is rapid and precedes PAI-1 induction; engagement of non-SMAD (e.g., EGFR, Src kinase, MAP kinases, p53) and SMAD2/3 pathways are both required for PAI-1 expression and are ROS-dependent.
Regulation of cumulus expansion and hyaluronan synthesis in porcine oocyte-cumulus complexes during in vitro maturation.
Nagyova, Czech Republic. In Endocr Regul, 2012
Furthermore, SMAD2/3 signaling pathway is involved in the control of both cumulus expansion and steroidogenesis in porcine OCCs, since SMAD2/3 activation by GDF9/ TGFβ produced by oocyte and/or cumulus cells, significantly affects gonadotropin-induced HA and progesterone synthesis by porcine cumulus cells.
From tall to short: the role of TGFβ signaling in growth and its disorders.
Cormier-Daire et al., Paris, France. In Am J Med Genet C Semin Med Genet, 2012
We found an increased level of active TGFβ in the fibroblast medium from patients with FBN1 or ADAMTSL2 mutations and an enhanced phosphorylated SMAD2 level, allowing us to conclude at an enhanced TGFβ signaling in GD and AD.
Smad2 decelerates re-epithelialization during gingival wound healing.
Takashiba et al., Okayama, Japan. In J Dent Res, 2012
results indicated Smad2 has inhibitory effects in regulating keratinocyte migration during gingival wound healing. TGF-beta/Smad2 signaling mediating alteration of K16 expression must be tightly regulated during periodontal regeneration.
Post-translational regulation of TGF-β receptor and Smad signaling.
Derynck et al., San Francisco, United States. In Febs Lett, 2012
TGF-beta family signaling through Smads is conceptually a simple and linear signaling pathway, driven by sequential phosphorylation, with type II receptors activating type I receptors, which in turn activate R-Smads [review]
Dynamics of TGF-β/Smad signaling.
Liu et al., Freiburg, Germany. In Febs Lett, 2012
analysis of the dynamics of TGF-beta and Smad2/Smad3 signaling [review]
Smad2/Smad3 in endothelium is indispensable for vascular stability via S1PR1 and N-cadherin expressions.
Kato et al., Tsukuba, Japan. In Blood, 2012
Smad2/3 signaling in ECs is indispensable for maintenance of vascular integrity via the fine-tuning of N-cadherin, VE-cadherin, and S1PR1 expressions in the vasculature.
TGF-β1 → SMAD/p53/USF2 → PAI-1 transcriptional axis in ureteral obstruction-induced renal fibrosis.
Higgins et al., Albany, United States. In Cell Tissue Res, 2012
SMAD2/3, pp60(c-src), EGFR, and p53 activation are each increased in the obstructed kidney.
R-Smad competition controls activin receptor output in Drosophila.
O'Connor et al., Minneapolis, United States. In Plos One, 2011
Data show that dSmad2 directly influences Baboon's phosphorylation of Mad.
Signalling pathways from NADPH oxidase-4 to idiopathic pulmonary fibrosis.
Boczkowski et al., Paris, France. In Int J Biochem Cell Biol, 2011
TGF-β or PDGF induce myofibroblast proliferation, differentiation, migration, contractility and extracellular matrix production, through NOX4 and reactive oxygen species dependent SMAD2/3 phosphorylation.
The kinases MEKK2 and MEKK3 regulate transforming growth factor-β-mediated helper T cell differentiation.
Su et al., New Haven, United States. In Immunity, 2011
Map3k2(-/-)Map3k3(Lck-Cre/-) T cells exhibited impaired phosphorylation of SMAD2 and SMAD3 proteins at their linker regions, which negatively regulated the TGF-β responses in T cells.
Conserved and divergent roles of FGF signaling in mouse epiblast stem cells and human embryonic stem cells.
Schöler et al., Münster, Germany. In Cell Stem Cell, 2010
Our data suggest that FGF2 fails to cooperate with SMAD2/3 signaling in actively promoting EpiSC self-renewal through Nanog, in contrast to its role in hESCs.
SIP1 mediates cell-fate decisions between neuroectoderm and mesendoderm in human pluripotent stem cells.
Vallier et al., Cambridge, United Kingdom. In Cell Stem Cell, 2010
Here, we demonstrate that Smad-interacting protein 1 (SIP1) limits the mesendoderm-inducing effects of Activin-Nodal signaling without inhibiting the pluripotency-maintaining effects exerted by SMAD2/3.
More papers using Smad2 antibodies
Alpha 3 beta 1 adhesion to laminin-5 and invasin: critical and differential role of integrin residues clustered at the boundary between alpha 3 N-terminal repeats 2 and 3
Chapman Harold A. et al., In The Journal of Cell Biology, 1998
... Secondary HRP-conjugated antibodies and Smad2/3 pAb were purchased from Santa Cruz Biotechnology, Inc ...
Krox-20 inhibits Jun-NH2-terminal kinase/c-Jun to control Schwann cell proliferation and death
Jessen Kristjan R. et al., In The Journal of Cell Biology, 1998
... Antibody against c-Jun and SMAD2 were purchased from BD Biosciences.
Activin receptors: cellular signalling by receptor serine kinases
Hamada Hiroshi et al., In The Journal of Cell Biology, 1995
... ten Dijke, Leiden University Medical Center, Leiden, Netherlands), rabbit monoclonal antibodies to p-Smad2 (Cell Signaling Technology), and Alexa Fluor ...
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