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Robert J. Lechleider

Researcher at National Institutes of Health

Publications -  30
Citations -  4133

Robert J. Lechleider is an academic researcher from National Institutes of Health. The author has contributed to research in topics: SMAD & Transforming growth factor beta. The author has an hindex of 24, co-authored 30 publications receiving 4002 citations. Previous affiliations of Robert J. Lechleider include Uniformed Services University of the Health Sciences.

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Journal ArticleDOI

Targeted disruption of SMAD3 results in impaired mucosal immunity and diminished T cell responsiveness to TGF-β

Xiao Yang, +7 more
- 01 Mar 1999 - 
TL;DR: The data suggest that SMAD3 has an important role in TGF‐β‐mediated regulation of T cell activation and mucosal immunity, and that the loss of these functions is responsible for chronic infection and the lethality of Smad3‐null mice.
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The Immunophilin FKBP12 Functions as a Common Inhibitor of the TGFβ Family Type I Receptors

Tongwen Wang, +8 more
- 09 Aug 1996 - 
TL;DR: Overexpression of a myristylated FKBP12 in Mv1Lu cell specifically inhibits two separate pathways activated by TGF beta, and two point mutations on FkBP12 abolish the inhibitory activity, suggesting that FK BP12 may dock a cytoplasmic protein to the type I receptors to inhibit TGFbeta family mediated signaling.
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Smad2 transduces common signals from receptor serine–threonine and tyrosine kinases

Mark P. de Caestecker, +6 more
- 01 Jun 1998 - 
TL;DR: It is demonstrated here that HGF and EGF, which signal through RTKs, can also mediate SMAD-dependent reporter gene activation and induce rapid phosphorylation of endogenous SMAD proteins by kinase(s) downstream of MEK1.
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A novel mitochondrial septin-like protein, ARTS, mediates apoptosis dependent on its P-loop motif.

Sarit Larisch, +18 more
- 01 Dec 2000 - 
TL;DR: A protein product of the human septin H5/PNUTL2/CDCrel2b gene called ARTS (for apoptosis-related protein in the TGF-β signalling pathway) was described in this article.
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Targeted Mutagenesis of Smad1 Reveals an Essential Role in Chorioallantoic Fusion

Robert J. Lechleider, +6 more
- 01 Dec 2001 - 
TL;DR: The data demonstrate that although highly similar structurally, Smad proteins are not functionally homologous, and suggest that the defect observed in the developing extraembryonic tissue is caused by a very specific loss of transcriptional activity regulated by Smad1.