Deletion of Exon I of SMAD7 in Mice Results in Altered B Cell Responses

No abstract is available for this paper.

• Publication year

  2006

• Venue

  Journal of Immunology

• Publication date

  2006-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.4049/jimmunol.176.11.6777PMID 16709837
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar, PubMed

• No claims are published for this paper.

• No concepts are published for this paper.

• TGF-beta 1 plays an important role in the mechanism of CD4+CD25+ regulatory T cell activity in both humans and mice.

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• Mechanisms of TGF-beta signaling from cell membrane to the nucleus.

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• Distinct endocytic pathways regulate TGF-beta receptor signalling and turnover.

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• Distinct endocytic pathways regulate TGF-β receptor signalling and turnover

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• Genetic Analysis of the Mammalian Transforming Growth Factor-β Superfamily

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• Smad7 mediates transforming growth factor-β–induced apoptosis in mesangial cells

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• Smurf1 Regulates the Inhibitory Activity of Smad7 by Targeting Smad7 to the Plasma Membrane* 210

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  2002cited by this paper
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• Apoptosis in podocytes induced by TGF-β and Smad7

  2001cited by this paper
• Dissection of inhibitory Smad proteins: both N- and C-terminal domains are necessary for full activities of Xenopus Smad6 and Smad7.

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• The N domain of Smad7 is essential for specific inhibition of transforming growth factor-β signaling

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• Apoptosis in podocytes induced by TGF-beta and Smad7.

  2001cited by this paper
• Smad7 inhibits the survival nuclear factor κB and potentiates apoptosis in epithelial cells

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• Smurf1 Interacts with Transforming Growth Factor-β Type I Receptor through Smad7 and Induces Receptor Degradation*

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• Smad7 mediates apoptosis induced by transforming growth factor beta in prostatic carcinoma cells.

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• Smad and AML Proteins Synergistically Confer Transforming Growth Factor β1 Responsiveness to Human Germ-line IgA Genes*

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• Smad7 mediates apoptosis induced by transforming growth factor β in prostatic carcinoma cells

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• Class switch recombination and hypermutation require activation-induced cytidine deaminase (AID), a potential RNA editing enzyme.

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• Functional analysis of the TGFbeta receptor/Smad pathway through gene ablation in mice.

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• A role for Smad6 in development and homeostasis of the cardiovascular system

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• Smad7 Is Induced by CD40 and Protects WEHI 231 B-lymphocytes from Transforming Growth Factor-β-induced Growth Inhibition and Apoptosis*

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• TGF-beta receptor controls B cell responsiveness and induction of IgA in vivo.

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

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• T-cell cytotoxicity assays for studying the functional interaction between the superantigen staphylococcal enterotoxin A and T-cell receptors.

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• TGF-β Receptor Controls B Cell Responsiveness and Induction of IgA In Vivo

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• Mice lacking Smad3 show accelerated wound healing and an impaired local inflammatory response

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• Angiogenesis defects and mesenchymal apoptosis in mice lacking SMAD5.

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• Differential Inhibition of Smad6 and Smad7 on Bone Morphogenetic Protein- and Activin-mediated Growth Arrest and Apoptosis in B Cells*

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• Smad5 knockout mice die at mid-gestation due to multiple embryonic and extraembryonic defects.

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• The tumor suppressor gene Smad4/Dpc4 is required for gastrulation and later for anterior development of the mouse embryo.

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• Smad7 Is an Activin-inducible Inhibitor of Activin-induced Growth Arrest and Apoptosis in Mouse B Cells*

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• REGULATION OF IMMUNE RESPONSES BY TGF-β*

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• Smad2 signaling in extraembryonic tissues determines anterior-posterior polarity of the early mouse embryo.

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• Dissecting the role of N-myc in development using a single targeting vector to generate a series of alleles.

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• The L45 loop in type I receptors for TGF‐β family members is a critical determinant in specifying Smad isoform activation

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• Smad3 mutant mice develop metastatic colorectal cancer.

  1998cited by this paper
• Smad6 inhibits signalling by the TGF-β superfamily

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• Vascular MADs: two novel MAD-related genes selectively inducible by flow in human vascular endothelium.

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• Smad6 inhibits signalling by the TGF-beta superfamily.

  1997cited by this paper
• The MAD-related protein Smad7 associates with the TGFbeta receptor and functions as an antagonist of TGFbeta signaling.

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

  1997cited by this paper
• Identification of Smad7, a TGFβ-inducible antagonist of TGF-β signalling

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• The MAD-Related Protein Smad7 Associates with the TGFβ Receptor and Functions as an Antagonist of TGFβ Signaling

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• TGFβ Superfamily Members as Regulators of B Cell Development and Function—Implications for Autoimmunity

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• MicroRNA-182 inhibits rat ovarian granulosa cell apoptosis by targeting Smad 7 in polycystic ovarian syndrome

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• Regulation of Innate and Adaptive Immunity by TGFβ.

  2017cites this paper
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  2017cites this paper
• SMAD7 deficiency stimulates Müller progenitor cell proliferation during the development of the mammalian retina

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• TGF-β in Development and Ageing

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  2016cites this paper
• A single intranasal immunization with a subunit vaccine formulation induces higher mucosal IgA production than live respiratory syncytial virus.

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• Smad7 protects against chronic aristolochic acid nephropathy in mice

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• Identification of novel long noncoding RNAs associated with TGF-β/Smad3-mediated renal inflammation and fibrosis by RNA sequencing.

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