University of Texas Southwestern Medical Center

About: University of Texas Southwestern Medical Center is a healthcare organization based out in Dallas, Texas, United States. It is known for research contribution in the topics: Population & Cancer. The organization has 39107 authors who have published 75242 publications receiving 4497256 citations. The organization is also known as: UT Southwestern & UT Southwestern Medical School.

Suppression of Ovarian Follicle Activation in Mice by the Transcription Factor Foxo3a

Abstract: Foxo transcription factors have been implicated in diverse biological processes, including metabolism, cellular stress responses, and aging Here, we show that Foxo3a-/- female mice exhibit a distinctive ovarian phenotype of global follicular activation leading to oocyte death, early depletion of functional ovarian follicles, and secondary infertility Foxo3a thus functions at the earliest stages of follicular growth as a suppressor of follicular activation In addition to providing a molecular entry point for studying the regulation of follicular growth, these results raise the possibility that accelerated follicular initiation plays a role in premature ovarian failure, a common cause of infertility and premature aging in women

p21ras is modified by a farnesyl isoprenoid.

Abstract: Association of oncogenic ras proteins with cellular membranes appears to be a crucial step in transformation, ras is synthesized as a cytosolic precursor, which is processed to a mature form that localizes to the plasma membrane. This processing involves, in part, a conserved sequence, Cys-Ali-Ali-Xaa (in which Ali is an amino acid with an aliphatic side chain and Xaa is any amino acid), at the COOH terminus of ras proteins. Yeast a-factor mating hormone precursor also possesses a COOH-terminal Cys-Ali-Ali-Xaa sequence. However, while the COOH-terminal cysteine has been implicated as a site of palmitoylation of ras proteins, in mature a-type mating factor this residue is modified by an isoprenoid, a farnesyl moiety. We asked whether the Cys-Ali-Ali-Xaa sequence signaled different modifications for the yeast peptides (farnesylation) than for ras proteins (palmitoylation) or whether ras proteins were similar to the mating factors and contained a previously undiscovered isoprenoid. We report here that the processing of ras proteins involves addition of a farnesyl moiety, apparently at the COOH-terminal cysteine analogous to the cysteine modified in the yeast peptides, and that farnesylation may be important for membrane association and transforming activity of ras proteins.

Congenital heart disease in adults: First of two parts

Abstract: Cyanotic Conditions Patients with cyanotic congenital heart disease have arterial oxygen desaturation resulting from the shunting of systemic venous blood to the arterial circulation. The magnitude of shunting determines the severity of desaturation. Most children with cyanotic heart disease do not survive to adulthood without surgical intervention. In adults, the most common causes of cyanotic congenital heart disease are tetralogy of Fallot61 and Eisenmenger's syndrome. Tetralogy of Fallot Tetralogy of Fallot, the most common cyanotic congenital heart defect after infancy, is characterized by a large ventricular septal defect, an aorta that overrides the left and right ventricles, obstruction of the . . .

Autophagy and viruses: adversaries or allies?

Abstract: The autophagy pathway is an essential component of host defense against viral infection, orchestrating pathogen degradation (xenophagy), innate immune signaling, and certain aspects of adaptive immunity. Single autophagy proteins or cassettes of the core autophagy machinery can also function as antiviral factors independently of the canonical autophagy pathway. Moreover, to survive and propagate within the host, viruses have evolved a variety of strategies to evade autophagic attack and manipulate the autophagy machinery for their own benefit. This review summarizes recent advances in understanding the antiviral and proviral roles of autophagy and previously unappreciated autophagy-independent functions of autophagy-related genes.