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Barbara A. Hocevar
Researcher at Cleveland Clinic
Publications - 12
Citations - 1383
Barbara A. Hocevar is an academic researcher from Cleveland Clinic. The author has contributed to research in topics: Transforming growth factor beta & Transforming growth factor. The author has an hindex of 9, co-authored 12 publications receiving 1342 citations.
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TGF-beta induces fibronectin synthesis through a c-Jun N-terminal kinase-dependent, Smad4-independent pathway.
TL;DR: It is shown that c‐Jun N‐terminal kinase (JNK), a member of the MAP kinase family, is activated in response to TGF‐β in the human fibrosarcoma HT1080‐derived cell line BAHgpt, and it is demonstrated that TGF•β‐mediated fibronectin induction requires activation of JNK which in turn modulates the activity of c‐ Jun and ATF‐2 in a Smad4independent manner.
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The adaptor molecule Disabled-2 links the transforming growth factor β receptors to the Smad pathway
TL;DR: Exposure of wild‐type Dab2 in a TGFβ‐signaling mutant restores TGF β‐mediated Smad2 phosphorylation, Smad translocation to the nucleus and Smad‐dependent transcriptional responses, suggesting that Dab1 is part of a multiprotein signaling complex.
Journal Article
TGF-beta suppresses IFN-gamma induction of class II MHC gene expression by inhibiting class II transactivator messenger RNA expression.
Yi-Ju Lee,Yulong Han,Hong Tao Lu,Vincent Nguyen,Hongwei Qin,Philip H. Howe,Barbara A. Hocevar,Jeremy M. Boss,Richard M. Ransohoff,Etty N. Benveniste +9 more
TL;DR: Evidence is provided that TGF-beta suppresses IFN-gamma-induced class II MHC expression by inhibiting accumulation of CIITA mRNA.
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Regulation of the Wnt signaling pathway by disabled-2 (Dab2).
TL;DR: It is proposed that Dab2 functions as a negative regulator of canonical Wnt signaling by stabilizing the β‐catenin degradation complex, which may contribute to its proposed role as a tumor suppressor.
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Mechanisms of TGF-β-Induced Cell Cycle Arrest
TL;DR: Further research is required to elucidate how these effects of TGF-β on the cyclins, cdks, and cdk inhibitors are linked to the T GF-β receptor complex and the Smad proteins.