H
Harry Hou
Researcher at Albert Einstein College of Medicine
Publications - 19
Citations - 6049
Harry Hou is an academic researcher from Albert Einstein College of Medicine. The author has contributed to research in topics: Mutation & Caveolae. The author has an hindex of 19, co-authored 19 publications receiving 5738 citations. Previous affiliations of Harry Hou include Yeshiva University.
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Journal ArticleDOI
Caveolin-1 Null Mice Are Viable but Show Evidence of Hyperproliferative and Vascular Abnormalities
Babak Razani,Jeffery A. Engelman,Xiaobo Wang,William Schubert,Xiao Lan Zhang,Carolyn Marks,Frank P. Macaluso,Robert G. Russell,Maomi Li,Richard G. Pestell,Dolores Di Vizio,Harry Hou,Burkhard Kneitz,Guy Lagaud,George J. Christ,Winfried Edelmann,Michael P. Lisanti +16 more
TL;DR: The results indicate that eNOS activity is up-regulated in Cav-1 null animals, and this activity can be blunted by using a specific NOS inhibitor, nitro-l-arginine methyl ester.
Journal ArticleDOI
Role for N-CoR and histone deacetylase in Sin3-mediated transcriptional repression
Lelia Alland,Rebecca Muhle,Harry Hou,Jason Potes,Lynda Chin,Nicole Schreiber-Agus,Ronald A. DePinho +6 more
TL;DR: The identification of the nuclear receptor co-repressor (N-CoR) and histone deacetylase (HD1) provides a basis for Mxi1/Sin3-induced transcriptional repression and tumour suppression.
Journal ArticleDOI
Altered cell differentiation and proliferation in mice lacking p57 KIP2 indicates a role in Beckwith–Wiedemann syndrome
Pumin Zhang,Nanette J. Liégeois,Calvin Wong,Milton J. Finegold,Harry Hou,Janet C. Thompson,Adam Silverman,J. Wade Harper,Ronald A. DePinho,Stephen J. Elledge +9 more
TL;DR: Mice lacking the imprinted Cdk inhibitor p57KIP2 have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; and lens cell hyperproliferation and apoptosis.
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Somatic Inactivation of Pkd2 Results in Polycystic Kidney Disease
Guanqing Wu,Vivette D. D'Agati,Yiqiang Cai,Glen S. Markowitz,Jong Hoon Park,David Reynolds,Yoshiko Maeda,Thanh C. Le,Harry Hou,Raju Kucherlapati,Winfried Edelmann,Stefan Somlo +11 more
TL;DR: Somatic loss of Pkd2 expression is both necessary and sufficient for renal cyst formation in ADPKD, suggesting that PKD2 occurs by a cellular recessive mechanism.
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Caveolin-3 Null Mice Show a Loss of Caveolae, Changes in the Microdomain Distribution of the Dystrophin-Glycoprotein Complex, and T-tubule Abnormalities
Ferruccio Galbiati,Jeffrey A. Engelman,Daniela Volonté,Xiao Lan Zhang,Carlo Minetti,Maomi Li,Harry Hou,Burkhard Kneitz,Winfried Edelmann,Michael P. Lisanti +9 more
TL;DR: Analysis of skeletal muscle tissue from these caveolin-3 null mice reveals mild myopathic changes; an exclusion of the dystrophin-glycoprotein complex from lipid raft domains; and abnormalities in the organization of the T- Tubule system, with dilated and longitudinally oriented T-tubules.