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Kin Ming Kwan

Researcher at The Chinese University of Hong Kong

Publications -  52
Citations -  3090

Kin Ming Kwan is an academic researcher from The Chinese University of Hong Kong. The author has contributed to research in topics: Cerebellum & Medicine. The author has an hindex of 23, co-authored 46 publications receiving 2676 citations. Previous affiliations of Kin Ming Kwan include University of Texas MD Anderson Cancer Center & Baylor College of Medicine.

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Distinct and sequential tissue-specific activities of the LIM-class homeobox gene Lim1 for tubular morphogenesis during kidney development

TL;DR: It is demonstrated that the nephric duct is essential for the elongation and maintenance of the adjacent Müllerian duct, the anlage of the female reproductive tract, and that Lim1 functions in distinct tissue compartments of the developing metanephros for both proper development of the ureteric buds and the patterns of renal vesicles for nephron formation.
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Abnormal Compartmentalization of Cartilage Matrix Components in Mice Lacking Collagen X: Implications for Function

TL;DR: It is proposed that collagen X plays a role in the normal distribution of matrix vesicles and proteoglycans within the growth plate matrix, which would accommodate the previously conflicting views of the function of collagen X and of the molecular pathogenesis of SMCD.
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Surviving endoplasmic reticulum stress is coupled to altered chondrocyte differentiation and function

TL;DR: Altered differentiation in terminally differentiating hypertrophic chondrocytes expressing unfolded or misfolded proteins may be part of an adaptive response that facilitates survival and recovery from the ensuing ER stress, however, the altered differentiation disrupts the highly coordinated events of endochondral ossification culminating in chondrodysplasia.
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Lim1 is required in both primitive streak-derived tissues and visceral endoderm for head formation in the mouse

TL;DR: It is indicated that Lim1 is required in both primitive streak-derived tissues and visceral endoderm for head formation and that its inactivation in these tissues produces cell non-autonomous defects.