R
Riddhi Bhattacharyya
Researcher at Albert Einstein College of Medicine
Publications - 5
Citations - 893
Riddhi Bhattacharyya is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Sanfilippo syndrome & Lysosomal storage disease. The author has an hindex of 5, co-authored 5 publications receiving 830 citations. Previous affiliations of Riddhi Bhattacharyya include Yeshiva University.
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Journal ArticleDOI
Histone H1 Depletion in Mammals Alters Global Chromatin Structure but Causes Specific Changes in Gene Regulation
Yuhong Fan,Tatiana Nikitina,Jie Zhao,Tomara J. Fleury,Riddhi Bhattacharyya,Eric E. Bouhassira,Arnold Stein,Christopher L. Woodcock,Arthur I. Skoultchi +8 more
TL;DR: Results indicate that linker histones can participate in epigenetic regulation of gene expression by contributing to the maintenance or establishment of specific DNA methylation patterns.
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A mouse model for mucopolysaccharidosis type III A (Sanfilippo syndrome)
Mantu Bhaumik,Vivienne J. Muller,Tina Rozaklis,Johnson Linda,Kostantin Dobrenis,Riddhi Bhattacharyya,Sarah Wurzelmann,Peter Finamore,John J. Hopwood,Steven U. Walkley,Pamela Stanley +10 more
TL;DR: A spontaneous mouse mutant is described that replicates many of the features found in MPS III A in children, and provides an excellent model for evaluating pathogenic mechanisms of disease and for testing treatment strategies, including enzyme or cell replacement and gene therapy.
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A novel missense mutation in lysosomal sulfamidase is the basis of MPS III A in a spontaneous mouse mutant
TL;DR: It is shown that the sulfamidase gene of the MPS III A mouse carries a novel mutation (G91A) that gives an amino acid change likely to interfere with the coordination of a divalent metal ion in the active site of this sulfatase.
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Truncated, InactiveN-Acetylglucosaminyltransferase III (GlcNAc-TIII) Induces Neurological and Other Traits Absent in Mice That Lack GlcNAc-TIII
TL;DR: The Mgat3 T37/T37 homozygotes in a mixed or 129SvJ background were retarded in growth rate and exhibited an altered leg clasp reflex, an altered gait, and defective nursing behavior, which may be the basis of the unexpected neurological phenotype induced by truncated, inactive GlcNAc-TIII in the mouse.
Journal Article
New evidence for an extra-hepatic role of N-acetylglucosaminyltransferase III in the progression of diethylnitrosamine-induced liver tumors in mice
TL;DR: The combined data provide strong evidence that retarded progression of tumors in mice lacking GlcNAc-TIII is due to the absence of the bisecting Glc NAc residue on N-glycans of a circulating glycoprotein(s) from a tissue other than liver.