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Baoli Yang

Researcher at University of Iowa

Publications -  77
Citations -  7167

Baoli Yang is an academic researcher from University of Iowa. The author has contributed to research in topics: Glia maturation factor & Gene. The author has an hindex of 38, co-authored 76 publications receiving 6645 citations. Previous affiliations of Baoli Yang include Roy J. and Lucille A. Carver College of Medicine & University of North Carolina at Chapel Hill.

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The mammalian sodium channel BNC1 is required for normal touch sensation.

TL;DR: It is shown that disrupting the mouse BNC1 gene markedly reduces the sensitivity of a specific component of mechanosensation: low-threshold rapidly adapting mechanoreceptors, and this data identify the B NC1 channel as essential for the normal detection of light touch and indicate that BNC 1 may be a central component of a mechanosensory complex.
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Requirement for the leukocyte-specific adapter protein SLP-76 for normal T cell development

TL;DR: The leukocyte-specific adapter molecule SLP-76 plays a crucial role in translating signals mediated by pre-T cell receptors into distal biochemical events and is required for normal thymocyte development.
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Bbs2-null mice have neurosensory deficits, a defect in social dominance, and retinopathy associated with mislocalization of rhodopsin

TL;DR: It is demonstrated that BBS2 retinopathy involves normal retina development followed by apoptotic death of photoreceptors, the primary ciliated cells of the retina, indicating a defect in transport.
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Bardet-Biedl syndrome type 4 (BBS4)-null mice implicate Bbs4 in flagella formation but not global cilia assembly.

TL;DR: It is shown that mice lacking the Bbs4 protein have major components of the human phenotype, including obesity and retinal degeneration, and homology comparisons of BBS proteins in model organisms find that they are specifically conserved in ciliated organisms.
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Abnormal skin, limb and craniofacial morphogenesis in mice deficient for interferon regulatory factor 6 ( Irf6 )

TL;DR: It is reported that mice deficient for Irf6 have abnormal skin, limb and craniofacial development, and Histological and gene expression analyses indicate that the primary defect is in keratinocyte differentiation and proliferation.