Name | Smad (protein family or complex) |
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Synonyms | SMAD; SMAD, mothers against DPP homolog; SMAD, mothers against DPP homologs; Smad |
Name | SMA |
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CAS | sodium 2-chloroacetate |
PubMed | Abstract | RScore(About this table) | |
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20233786 | Corpuz PS, Lindaman LL, Mellon PL, Coss D: FoxL2 Is Required for Activin Induction of the Mouse and Human Follicle-Stimulating Hormone {beta}-Subunit Genes. Mol Endocrinol. 2010 Mar 16. We identify FoxL2 as a critical component in activin induction of FSHbeta, both for the mouse gene, induction of which is Sma- and Mad-related protein (Smad) dependent, and for the human gene that is Smad independent. |
6(0,0,1,1) | Details |
20160437 | Hu Y, Liang H, Du Y, Zhu Y, Wang X: Inhibits Transforming Growth Factor-beta Activity via Inhibition of Smad Signaling in HK-2 Cells. Am J Nephrol. 2010 Feb 17;31(4):332-341. |
4(0,0,0,4) | Details |
18552272 | Liu Q, Mao H, Nie J, Chen W, Yang Q, Dong X, Yu X: Transforming growth factor {beta}1 induces epithelial-mesenchymal transition by activating the JNK-Smad3 pathway in rat peritoneal mesothelial cells. Perit Dial Int. 2008 Jun;28 Suppl 3:S88-95. Phosphorylation of Smad proteins is required for TGFbeta1-induced EMT. |
3(0,0,0,3) | Details |
20193171 | Liu JQ, Hu DH, Zhang ZF, Guan H, She T, Zhang J, Bai XZ: [Effects of interferon-gamma on the transforming growth factor beta/Smad pathway in keloid-derived fibroblasts]. Zhonghua Shao Shang Za Zhi. 2009 Dec;25(6):454-9. |
3(0,0,0,3) | Details |
19516008 | Dawes LJ, Sleeman MA, Anderson IK, Reddan JR, Wormstone IM: TGFbeta/Smad4-dependent and -independent regulation of human lens epithelial cells. Invest Ophthalmol Vis Sci. 2009 Nov;50(11):5318-27. Epub 2009 Jun 10. The primary objective of the study was to determine the importance of Smad4 in TGFbeta2-induced transdifferentiation, matrix contraction, and Smad signaling by human lens epithelial cells. |
3(0,0,0,3) | Details |
18502066 | Yang Y, Yang S, Chen M, Zhang X, Zou Y, Zhang X: Compound Astragalus and Salvia miltiorrhiza Extract exerts anti-fibrosis by mediating TGF-beta/Smad signaling in myofibroblasts. J Ethnopharmacol. 2008 Jul 23;118(2):264-70. Epub 2008 Apr 18. |
2(0,0,0,2) | Details |
18065393 | Jeon ES, Moon HJ, Lee MJ, Song HY, Kim YM, Cho M, Suh DS, Yoon MS, Chang CL, Jung JS, Kim JH: Cancer-derived lysophosphatidic acid stimulates differentiation of human mesenchymal stem cells to myofibroblast-like cells. Stem Cells. 2008 Mar;26(3):789-97. Epub 2007 Dec 6. LPA elicited phosphorylation of Smad2/3, and siRNA-mediated depletion of endogenous Smad2/3 or adenoviral expression of Smad7, an inhibitory Smad, abrogated the LPA induced expression of alpha-SMA and phosphorylation of Smad2/3. |
2(0,0,0,2) | Details |
19193641 | Webber J, Meran S, Steadman R, Phillips A: Similarly inhibition of HAS2 by short interfering RNA prevented phenotypic activation without altering TGF-beta1-dependent Smad phosphorylation, thus suggesting that HA-dependent regulation of cell phenotype was independent of Smad activation. |
orchestrates transforming growth factor-beta1-dependent maintenance of myofibroblast phenotype. J Biol Chem. 2009 Apr 3;284(14):9083-92. Epub 2009 Feb 4.2(0,0,0,2) | Details |
18631173 | Vardouli L, Vasilaki E, Papadimitriou E, Kardassis D, Stournaras C: A novel mechanism of TGFbeta-induced actin reorganization mediated by Smad proteins and Rho GTPases. FEBS J. 2008 Aug;275(16):4074-87. Epub 2008 Jul 9. |
2(0,0,0,2) | Details |
18448597 | Huang XR, Chung AC, Wang XJ, Lai KN, Lan HY: Mice overexpressing latent TGF-beta1 are protected against renal fibrosis in obstructive kidney disease. Am J Physiol Renal Physiol. 2008 Jul;295(1):F118-27. Epub 2008 Apr 30. Transforming growth factor (TGF)-beta1, once activated, binds to its receptors and mediates renal fibrosis via the downstream Smad signaling pathway. |
1(0,0,0,1) | Details |
19543302 | Yan JD, Yang S, Zhang J, Zhu TH: BMP6 reverses TGF-beta1-induced changes in HK-2 cells: implications for the treatment of renal fibrosis. Acta Pharmacol Sin. 2009 Jul;30(7):994-1000. Epub 2009 Jun 22. MMP-2 activity was analyzed by zymography, whereas the activation of the MAPKs and Smad signaling were analyzed using Western blot assays and a reporter gene assay, respectively. |
1(0,0,0,1) | Details |
18988920 | Shukla MN, Rose JL, Ray R, Lathrop KL, Ray A, Ray P: Hepatocyte growth factor inhibits epithelial to myofibroblast transition in lung cells via Smad7. Am J Respir Cell Mol Biol. 2009 Jun;40(6):643-53. Epub 2008 Nov 6. HGF also induced the nuclear export of Smad7 and Smad ubiquitin regulatory factor 1 (Smurf1) to the cytoplasm. |
1(0,0,0,1) | Details |
20089843 | Tsapara A, Luthert P, Greenwood J, Hill CS, Matter K, Balda MS: The RhoA activator GEF-H1/Lfc is a transforming growth factor-beta target gene and effector that regulates alpha-smooth muscle actin expression and cell migration. Mol Biol Cell. 2010 Mar;21(6):860-70. Epub 2010 Jan 20. Cellular TGF-beta responses are stimulated by different signal transduction pathways: some are Smad dependent and others Smad independent. |
1(0,0,0,1) | Details |
18655827 | Kim YM, Jeon ES, Kim MR, Lee JS, Kim JH: Bradykinin-induced expression of alpha-smooth muscle actin in human mesenchymal stem cells. Cell Signal. 2008 Oct;20(10):1882-9. Epub 2008 Jul 4. Pretreatment with a TGF-beta type I receptor kinase inhibitor (SB-431542), small interfering RNA-mediated depletion of endogenous Smad2, or adenoviral expression of Smad7 (an inhibitory Smad isoform) all blocked BK-induced alpha-SMA expression and Smad2 phosphorylation. |
1(0,0,0,1) | Details |
17923018 | Xu GP, Li QQ, Cao XX, Chen Q, Zhao ZH, Diao ZQ, Xu ZD: [Effect of Smad7 on transforming growth factor-beta1-induced alveolar epithelial to mesenchymal transition]. Zhonghua Yi Xue Za Zhi. 2007 Jul 17;87(27):1918-23. CONCLUSION: Under TGF beta1 treatment, RLE-6TN undergoes a conversion process into myofibroblasts in vitro with the conversion mechanism related to Smad signaling pathway, and transfection of Smad7 gene can partly reverse this process. |
1(0,0,0,1) | Details |
19847872 | Guo H, Leung JC, Cheung JS, Chan LY, Wu EX, Lai KN: Non-viral Smad7 gene delivery and attenuation of postoperative peritoneal adhesion in an experimental model. Br J Surg. 2009 Nov;96(11):1323-35. Smad7, a protein that occupies a strategic position in fibrogenesis, inhibits the transforming growth factor (TGF) beta/Smad signalling pathway. |
1(0,0,0,1) | Details |
17997227 | Lacmann A, Hess D, Gohla G, Roussa E, Krieglstein K: Activity-dependent release of transforming growth factor-beta in a neuronal network in vitro. Neuroscience. 2007 Dec 12;150(3):647-57. Epub 2007 Sep 29. Notably, KCl stimulation caused Smad (composite term from SMA (C. elegans) and MAD=mothers against dpp (Drosophila)) translocation into the nucleus and upregulated TGF-beta inducible early gene (Tieg1) expression, demonstrating that activity-dependent released TGF-beta may exert autocrine actions and thereby activate the TGF-beta-dependent signaling pathway. |
1(0,0,0,1) | Details |
20061511 | Pechkovsky DV, Hackett TL, An SS, Shaheen F, Murray LA, Knight DA: Human Lung Parenchyma but not Proximal Bronchi Produces Fibroblasts with Enhanced TGF{beta} Signaling and {alpha}SMA Expression. Am J Respir Cell Mol Biol. 2010 Jan 8. In contrast to B-FBR, P-FBR displayed enhanced TGFbeta/Smad signaling at baseline, and inhibition of either ALK-5 or neutralization of endogenously produced and activated TGFbeta substantially decreased basal alphaSMA protein in P-FBR. |
1(0,0,0,1) | Details |
19158077 | Huang WY, Li ZG, Rus H, Wang X, Jose PA, Chen SY: RGC-32 mediates transforming growth factor-beta-induced epithelial-mesenchymal transition in human renal proximal tubular cells. J Biol Chem. 2009 Apr 3;284(14):9426-32. Epub 2009 Jan 21. TGF-beta function is mediated by several signaling pathways, but RGC-32 expression in HPTCs appears to be mainly regulated by Smad. |
1(0,0,0,1) | Details |
19578024 | Parapuram SK, Chang B, Li L, Hartung RA, Chalam KV, Nair-Menon JU, Hunt DM, Hunt RC: Differential effects of TGFbeta and vitreous on the transformation of retinal pigment epithelial cells. Invest Ophthalmol Vis Sci. 2009 Dec;50(12):5965-74. Epub 2009 Jul 2. RESULTS: Changes in phosphorylation or cellular localization of Smad -2, -3, or -4 indicated a TGFbeta-like activity in vitreous. |
1(0,0,0,1) | Details |
18840652 | Vaahtomeri K, Ventela E, Laajanen K, Katajisto P, Wipff PJ, Hinz B, Vallenius T, Tiainen M, Makela TP: Lkb1 is required for TGFbeta-mediated myofibroblast differentiation. J Cell Sci. 2008 Nov 1;121(Pt 21):3531-40. Epub 2008 Oct 7. Ablation of Lkb1 in primary mouse embryo fibroblasts (MEFs) leads to attenuated Smad activation and TGFbeta-dependent transcription. |
1(0,0,0,1) | Details |
17576240 | Fumagalli M, Musso T, Vermi W, Scutera S, Daniele R, Alotto D, Cambieri I, Ostorero A, Gentili F, Caposio P, Zucca M, Sozzani S, Stella M, Castagnoli C: Imbalance between activin A and follistatin drives postburn hypertrophic scar formation in human skin. Exp Dermatol. 2007 Jul;16(7):600-10. Activin A, a member of the TGF-beta family, shares the same intra-cellular Smad signalling pathway with TGF-beta, but binds to its own specific transmembrane receptors and to follistatin, a secreted protein that inhibits activin by sequestration. |
1(0,0,0,1) | Details |
18455002 | Carvajal G, Droguett A, Burgos ME, Aros C, Ardiles L, Flores C, Carpio D, Ruiz-Ortega M, Egido J, Mezzano S: Gremlin: a novel mediator of epithelial mesenchymal transition and fibrosis in chronic allograft nephropathy. Transplant Proc. 2008 Apr;40(3):734-9. Epithelial mesenchymal transition (EMT) has been identified as responsible for the presence of activated interstitial fibroblasts (myofibroblasts) and transforming growth factor beta (TGF-beta)/Smad is the key signaling mediator. |
1(0,0,0,1) | Details |
18355371 | Nonaka M, Pawankar R, Fukumoto A, Yagi T: Heterogeneous response of nasal and lung fibroblasts to transforming growth factor-beta 1. Clin Exp Allergy. 2008 May;38(5):812-21. Epub 2008 Mar 18. OBJECTIVE: We examined whether there is any heterogeneity between nasal and lung fibroblasts upon stimulation with TGF-beta (1) with regard to the synthesis of SMA, pro-collagen type I and vascular endothelial growth factor (VEGF) as well as translocation of Smad proteins. |
1(0,0,0,1) | Details |
18679024 | Ng YY, Chen YM, Tsai TJ, Lan XR, Yang WC, Lan HY: Pentoxifylline inhibits transforming growth factor-beta signaling and renal fibrosis in experimental crescentic glomerulonephritis in rats. Am J Nephrol. 2009;29(1):43-53. Epub 2008 Aug 5. Further studies revealed that severe renal fibrosis was associated with upregulation of renal TGF-beta1 and activation of TGF-beta/Smad signaling, which was blocked by treatment with PTX. |
1(0,0,0,1) | Details |
20123992 | Masszi A, Speight P, Charbonney E, Lodyga M, Nakano H, Szaszi K, Kapus A: Fate-determining mechanisms in epithelial-myofibroblast transition: major inhibitory role for Smad3. J Cell Biol. 2010 Feb 8;188(3):383-99. Epub 2010 Feb 1. Because the SMA promoter harbors both MRTF-responsive CC (A/T)-rich GG element (CArG) boxes and TGF-beta-responsive Smad-binding elements, we hypothesized that the myogenic program is mobilized by a synergy between MRTF and Smad3. |
1(0,0,0,1) | Details |
18380662 | Imura T, Tane K, Toyoda N, Fushiki S: Endothelial cell-derived bone morphogenetic proteins regulate glial differentiation of cortical progenitors. Eur J Neurosci. 2008 Apr;27(7):1596-606. Endothelial cells produce bone morphogenetic proteins (BMPs) to activate Sma- and Mad-related protein (Smad) signalling in progenitors and the effects of endothelial cells on glial differentiation are blocked by the BMP antagonist Noggin. |
82(1,1,1,2) | Details |
18032694 | Kane N, Jones M, Brosens JJ, Saunders PT, Kelly RW, Critchley HO: Transforming growth factor-beta1 attenuates expression of both the progesterone receptor and Dickkopf in differentiated human endometrial stromal cells. Mol Endocrinol. 2008 Mar;22(3):716-28. Epub 2007 Nov 21. Moreover, although TGFbeta1 was capable of signaling via the Sma- and mothers against decapentaplegic (MAD)-related protein (SMAD) pathway, the inhibitory effect on DKK was SMAD independent. |
82(1,1,1,2) | Details |
18813789 | Naumann U, Maass P, Gleske AK, Aulwurm S, Weller M, Eisele G: Glioma gene therapy with soluble transforming growth factor-beta receptors II and III. Int J Oncol. 2008 Oct;33(4):759-65. Binding of TGF-beta leads to the activation of an intracellular signaling cascade and subsequent phosphorylation of Sma and MAD-related proteins (SMAD). |
81(1,1,1,1) | Details |
17977791 | Bommireddy R, Doetschman T: TGFbeta1 and Treg cells: alliance for tolerance. Trends Mol Med. 2007 Nov;13(11):492-501. Epub 2007 Oct 30. TGFbeta1 prevents abnormal T-cell activation through the modulation of Ca2+-calcineurin signaling in a Caenorhabditis elegans Sma and Drosophila Mad proteins (SMAD) 3 and SMAD4-independent manner; however, in Treg cells, its effects are mediated, at least in part, through SMAD signaling. |
31(0,1,1,1) | Details |
19157940 | Makkar P, Metpally RP, Sangadala S, Reddy BV: Modeling and analysis of MH1 domain of Smads and their interaction with promoter DNA sequence motif. J Mol Graph Model. 2009 Apr;27(7):803-12. Epub 2008 Dec 24. The prototypic members of the Smad family, Mad and Sma, were first described in Drosophila and Caenorhabditis elegans, respectively. |
10(0,0,1,5) | Details |