Harvard College

The Brigham and Women's Hospital, Inc.

Dana-farber-cancer Institute Inc.

Beth Israel Deaconess Medical Center, Inc.

Jeffrey Wade Harper

Jianping Jin

Bert L Vallee

Alec C Kimmelman

Joseph D Mancias

Described herein are methods of modulating autophagic targeting of ferritin in a cell, wherein the method comprises modulating the level and/or activity of nuclear receptor coactivator 4 (NCOA4) in the cell. Also provided are related methods of treatment.

Compositions and methods for modulating NCOA4-mediated autophagic targeting of ferritin

A novel activating enzyme for ubiquitin, Uba6, is provided. Compositions and methods for inhibiting ubiquitin via the Uba6 pathway are provided. Methods of identifying novel inhibitors of ubiquitination are also provided. Novel RNAi molecules are also provided.

Activation and transfer cascade for ubiquitin

Site-specific mutagenesis of a gene for angiogenin producing DNA sequences encoding mutant proteins having increased angiogenic activity are disclosed. Expression vectors containing these sequences are introduced into host cells and direct the production of the mutant angiogenic proteins with markedly increased angiogenic and ribonucleolytic activity. Replacement of a single amino acid, the aspartic acid at position 116 of human angiogenin, with another amino acid including asparagine, alanine or histidine, yields mutant proteins with 8 to 15 fold increased ribonucleolytic activity toward tRNA and rRNA and 10 to 100 fold increased angiogenic potency in the chorioallantoic membrane assay. The mutant angiogenin proteins of this invention are useful therapeutic compositions to promote the development of a hemovascular network in a mammal or to promote wound healing, in particular, healing of torn or traumatized fibrocartilage material.

Mutant human angiogenin (angiogenesis factor with superior angiogenin

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Wellesley, MA, United States of America

Jeffrey Wade Harper