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Lisa L. Maduzia

Researcher at Rutgers University

Publications -  7
Citations -  451

Lisa L. Maduzia is an academic researcher from Rutgers University. The author has contributed to research in topics: Signal transduction & Caenorhabditis elegans. The author has an hindex of 7, co-authored 7 publications receiving 440 citations.

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Specificity of TGFbeta signaling is conferred by distinct type I receptors and their associated SMAD proteins in Caenorhabditis elegans

TL;DR: The C. elegans model for TGFbeta-like signaling, in which distinct type I receptors determine specificity, may be a general mechanism of achieving specificity in other organisms and distinguish between the manner in which signaling specificity is achieved in TGF beta-like pathways and receptor tyrosine-kinase (RTK) pathways.
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The Drosophila gene Medea demonstrates the requirement for different classes of Smads in dpp signaling.

TL;DR: The identification of a new Drosophila class II Smad, Medea, a close homolog of the human tumor-suppressor gene DPC4 is reported, providing a paradigm for, and distinguish between, the requirement for class I and II Smads in Dpp/BMP signaling.
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Genetic screen for small body size mutants in C. elegans reveals many TGFβ pathway components

TL;DR: Two genes influence regulation of the developmentally arrested dauer larval stage, suggesting a role in a second characterized TGFβ pathway in C. elegans and homologs of these genes may be involved in tissue specificity and/or crosstalk of TGF β pathways in other animals.
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lon-1 regulates Caenorhabditis elegans body size downstream of the dbl-1 TGFβ signaling pathway

TL;DR: Lon-1 is identified as a novel downstream target gene of the dbl-1 TGF beta-like signaling pathway, a gene with homology to the cysteine-rich secretory protein (CRISP) family of proteins that regulates body size morphogenesis, but does not affect male tail development.
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C. elegans serine-threonine kinase KIN-29 modulates TGFβ signaling and regulates body size formation

TL;DR: kin-29 is a new modulator of the Sma/Mab pathway that functions in neurons and in the hypodermis to regulate body size, but does not affect all TGFβ outputs, such as tail morphogenesis.