scispace - formally typeset
D

Deborah J. Good

Researcher at Virginia Tech

Publications -  61
Citations -  2871

Deborah J. Good is an academic researcher from Virginia Tech. The author has contributed to research in topics: Gene & Conjugated linoleic acid. The author has an hindex of 18, co-authored 55 publications receiving 2720 citations. Previous affiliations of Deborah J. Good include University of Massachusetts Amherst & National Institutes of Health.

Papers
More filters
Journal ArticleDOI

A tumor suppressor-dependent inhibitor of angiogenesis is immunologically and functionally indistinguishable from a fragment of thrombospondin

TL;DR: A secreted inhibitor of angiogenesis that is controlled by a tumor suppressor gene in hamster cells has been found to be similar to a fragment of the platelet and matrix protein thrombospondin, which demonstrates a function for the ubiquitous adhesive glycoprotein thromBosponin that is likely to be important in the normal physiological down-regulation of neovascularization.
Journal ArticleDOI

Peptides derived from two separate domains of the matrix protein thrombospondin-1 have anti-angiogenic activity

TL;DR: The results suggest that the large TSP1 molecule employs at least two different structural domains and perhaps two different mechanisms to accomplish a single physiological function, the inhibition of neovascularization.
Journal ArticleDOI

The SIL gene is required for mouse embryonic axial development and left-right specification.

TL;DR: It is shown that mouse embryos lacking the early-response gene SIL have axial midline defects, a block in midline Sonic hedgehog (Shh) signalling and randomized cardiac looping, and that the consequences of abnormal midline development for left–right patterning depend on the time of onset, duration and severity of disruption of the normal asymmetric patterns of expression of nodal, lefty-2 and Pitx2.
Journal ArticleDOI

Hypogonadism and obesity in mice with a targeted deletion of the Nhlh2 gene.

TL;DR: A role for Nhlh2 in the onset of puberty and the regulation of body weight metabolism is supported, as well as a disruption of the hypothalamic-pituitary axis in mice.
Journal ArticleDOI

Deletion of the Nhlh2 Transcription Factor Decreases the Levels of the Anorexigenic Peptides α Melanocyte-Stimulating Hormone and Thyrotropin-Releasing Hormone and Implicates Prohormone Convertases I and II in Obesity

TL;DR: It is shown that Nhlh2 is expressed throughout the adult hypothalamus, and a direct role for transcriptional control of neuropeptide processing enzymes in the etiology of adult-onset obesity is supported.