Jay P. Morgenstern

TL;DR: It is predicted that the long intrACEllular domain form of OB-R is crucial for initiating intracellular signal transduction, and as a corollary, the inability to produce this form ofOB-R leads to the severe obese phenotype found in db/db mice.

TL;DR: The crystal structure of the tandem SH2 domains of human ZAP-70 in complex with a peptide derived from the ζ-subunit of the T-cell receptor reveals an unanticipated interaction between the two domains that constitutes one of the two critical phosphotyrosine binding sites.

TL;DR: In this article, a single amino acid substitution at position 269 (Gln → Pro) in the OB-R extracellular domain that results in the obese phenotype of the fatty rat was analyzed.

TL;DR: It is demonstrated that in CHO-IR cells, transfected Tub is phosphorylated on tyrosine in response to insulin and insulin-like growth factor-1 and that in PC12 cells, insulin but not EGF induced tyosine phosphorylation of endogenous Tub.

TL;DR: The results suggest that proteasome inhibition promotes cell death primarily by dysregulating Myc and polyamines, interfering with protein translation, and disrupting essential DNA damage repair pathways, leading to programmed cell death.