C
Chang Gong Liu
Researcher at University of Texas MD Anderson Cancer Center
Publications - 4
Citations - 697
Chang Gong Liu is an academic researcher from University of Texas MD Anderson Cancer Center. The author has contributed to research in topics: Infantile neuronal ceroid lipofuscinosis & Tripeptidyl peptidase I. The author has an hindex of 4, co-authored 4 publications receiving 675 citations. Previous affiliations of Chang Gong Liu include Center for Advanced Biotechnology and Medicine.
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Journal ArticleDOI
Association of Mutations in a Lysosomal Protein with Classical Late-Infantile Neuronal Ceroid Lipofuscinosis
David E. Sleat,Robert J. Donnelly,Henry Lackland,Henry Lackland,Chang Gong Liu,Istvan Sohar,Istvan Sohar,Raju K. Pullarkat,Peter Lobel,Peter Lobel +9 more
TL;DR: In this paper, the mannose 6-phosphate modification of newly synthesized lysosomal enzymes was used as an affinity marker, and a single protein was identified that is absent in LINCL.
Journal ArticleDOI
Mouse mutants lacking the cation-independent mannose 6-phosphate/insulin-like growth factor II receptor are impaired in lysosomal enzyme transport: Comparison of cation-independent and cation-dependent mannose 6-phosphate receptor-deficient mice
TL;DR: Each MPR has distinct functions for the targeting of lysosomal enzymes in vivo, and while lack of the CI-MPR appears to perturb lysOSome function to a greater degree than lack ofThe CD-M PR, each MPR is shown to have distinct roles for thetargeting of l Lysosomal enzyme activities in vivo.
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Structural organization and sequence of CLN2, the defective gene in classical late infantile neuronal ceroid lipofuscinosis
TL;DR: The complete sequence of the human CLN2 gene is presented and its physical relationship with two other genes that have been previously mapped to chromosome 11p15 is defined and will facilitate the molecular analysis of and genetic testing for classical LINCL.
Journal ArticleDOI
Using whole-exome sequencing to investigate the genetic bases of lysosomal storage diseases of unknown etiology.
Nan Wang,Yeting Zhang,Erika Gedvilaite,Jui Wan Loh,Timothy Lin,Xiuping Liu,Chang Gong Liu,Dibyendu Kumar,Robert J. Donnelly,Kimiyo Raymond,Edward H. Schuchman,David E. Sleat,Peter Lobel,Jinchuan Xing +13 more
TL;DR: It is demonstrated that whole‐exome sequencing can be used to identify causal mutations in suspected LSD cases and cases where a confounding clinical phenotype may potentially reflect more than one lysosomal protein defect.