Overexpression of Smad7 results in severe pathological alterations in multiple epithelial tissues. - Test2 - elhamkhani - TriplyDB

Overexpression of Smad7 results in severe pathological alterations in multiple epithelial tissues.

Overexpression of Smad7 results in severe pathological alterations in multiple epithelial tissues.

http://www.wikidata.org/entity/Q39647327

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Structural basis for the versatile interactions of Smad7 with regulator WW domains in TGF-β Pathways Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus Normal morphogenesis of epithelial tissues and progression of epithelial tumors.SMAD2 and SMAD7 involvement in the post-translational regulation of Muc4 via the transforming growth factor-beta and interferon-gamma pathways in rat mammary epithelial cells Noggin overexpression inhibits eyelid opening by altering epidermal apoptosis and differentiation.Oral Mucositis: Melatonin Gel an Effective New Treatment.Distinct mechanisms of TGF-beta1-mediated epithelial-to-mesenchymal transition and metastasis during skin carcinogenesis.Transforming growth factor beta-dependent sequential activation of Smad, Bim, and caspase-9 mediates physiological apoptosis in gastric epithelial cells.The role of Smad7 in oral mucositis.Temporal smad7 transgene induction in mouse epidermis accelerates skin wound healing Nonhistone protein acetylation as cancer therapy targets.Unraveling the biological functions of Smad7 with mouse models.Evidence for an Important Role of Smad-7 in Intervertebral Disc Degeneration.Smad7 Modulates Epidermal Growth Factor Receptor Turnover through Sequestration of c-Cbl.CtBP1 overexpression in keratinocytes perturbs skin homeostasis.A pair of transmembrane receptors essential for the retention and pigmentation of hair.Establishment and functioning of intrathymic microenvironments.The Role of TGFβ Signaling in Squamous Cell Cancer: Lessons from Mouse Models Integrated morphogen signal inputs in gammadelta versus alphabeta T-cell differentiation.Sma- and Mad-related protein 7 (Smad7) is required for embryonic eye development in the mouse.MicroRNA-195a-5p inhibits mouse medullary thymic epithelial cells proliferation by directly targeting Smad7 Maintenance of a normal thymic microenvironment and T-cell homeostasis require Smad4-mediated signaling in thymic epithelial cells.FGF-regulated BMP signaling is required for eyelid closure and to specify conjunctival epithelial cell fate.Preventive and therapeutic effects of Smad7 on radiation-induced oral mucositis Mutation in Mpzl3, a novel [corrected] gene encoding a predicted [corrected] adhesion protein, in the rough coat (rc) mice with severe skin and hair abnormalities.p63 Suppresses non-epidermal lineage markers in a bone morphogenetic protein-dependent manner via repression of Smad7.Commercial development of cell-based therapeutics: strategic considerations along the drug to tissue spectrum.Expression of signaling components in embryonic eyelid epithelium.Latent TGFbeta1 overexpression in keratinocytes results in a severe psoriasis-like skin disorder.Regulation of TGF-β Family Signaling by Inhibitory Smads.Smad7 induces G0/G1 cell cycle arrest in mesenchymal cells by inhibiting the expression of G1 cyclins.Repression of endogenous Smad7 by Ski.alpha3beta1 integrin-controlled Smad7 regulates reepithelialization during wound healing in mice.Ultraviolet irradiation induces Smad7 via induction of transcription factor AP-1 in human skin fibroblasts.Transforming Growth Factor Beta Signaling in Cutaneous Wound Healing: Lessons Learned from Animal Studies.Revisiting the Road Map of Medullary Thymic Epithelial Cell Differentiation.Smad signaling in the rat model of monocrotaline pulmonary hypertension.Smad7 enhances ATM activity by facilitating the interaction between ATM and Mre11-Rad50-Nbs1 complex in DNA double-strand break repair.YAP/TAZ regulates TGF-β/Smad3 signaling by induction of Smad7 via AP-1 in human skin dermal fibroblasts.Deregulation of Negative Controls on TGF-β1 Signaling in Tumor Progression.

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P2860

Overexpression of Smad7 results in severe pathological alterations in multiple epithelial tissues.

http://www.wikidata.org/entity/Q39647327

description

2002 nî lūn-bûn

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2002年の論文

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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The EMBO Journal

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Overexpression of Smad7 result ...... n multiple epithelial tissues.

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Allen G Li

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Biao Zheng

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Dongyan Wang

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Marie-José Goumans

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Peter Ten Dijke

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Shuhua Han

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Wei He

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Xiao-Jing Wang

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P2860

The TGF-beta2 isoform is both a required and sufficient inducer of murine hair follicle morphogenesis

Smad7 binds to Smurf2 to form an E3 ubiquitin ligase that targets the TGF beta receptor for degradation

Smurf1 interacts with transforming growth factor-beta type I receptor through Smad7 and induces receptor degradation

Smad6 inhibits BMP/Smad1 signaling by specifically competing with the Smad4 tumor suppressor

Lens-specific expression of transforming growth factor beta1 in transgenic mice causes anterior subcapsular cataracts

Inhibition of Bmp signaling affects growth and differentiation in the anagen hair follicle

The TGF-beta signaling inhibitor Smad7 enhances tumorigenicity in pancreatic cancer

The MAD-related protein Smad7 associates with the TGFbeta receptor and functions as an antagonist of TGFbeta signaling

Identification of Smad7, a TGFbeta-inducible antagonist of TGF-beta signalling

Enhanced expression of type I receptors for bone morphogenetic proteins during bone formation

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