Institution
University of Texas Southwestern Medical Center
Healthcare•Dallas, Texas, United States•
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.
Topics: Population, Cancer, Signal transduction, Receptor, Transplantation
Papers published on a yearly basis
Papers
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TL;DR: It has been shown that in the presence of a NADPH2-generating system prostatic nuclei convert testosterone to dihydrotestosterone, whereas prostatic cytoplasm reduces dihydotestosterone to androstandiol.
985 citations
TL;DR: The reduced forms of the redox cofactors, NAD(H) and NADP(H), strongly enhance DNA binding of the Clock:BMal1 and NPAS2:BMAL1 heterodimers, whereas the oxidized forms inhibit, raising the possibility that food, neuronal activity, or both may entrain the circadian clock by direct modulation of cellular redox state.
Abstract: Clock:BMAL1 and NPAS2:BMAL1 are heterodimeric transcription factors that control gene expression as a function of the light-dark cycle. Although built to fluctuate at or near a 24-hour cycle, the clock can be entrained by light, activity, or food. Here we show that the DNA-binding activity of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers is regulated by the redox state of nicotinamide adenine dinucleotide (NAD) cofactors in a purified system. The reduced forms of the redox cofactors, NAD(H) and NADP(H), strongly enhance DNA binding of the Clock:BMAL1 and NPAS2:BMAL1 heterodimers, whereas the oxidized forms inhibit. These observations raise the possibility that food, neuronal activity, or both may entrain the circadian clock by direct modulation of cellular redox state.
983 citations
TL;DR: This work has shown that the activity of PARP family members, such as PARP1 and PARP2, is tied to cellular signalling pathways, and through poly(ADP-ribosyl)ation (PARylation) they ultimately promote changes in gene expression, RNA and protein abundance, and the location and activity of proteins that mediate signalling responses.
Abstract: Poly(ADP-ribose) polymerases (PARPs) are enzymes that transfer ADP-ribose groups to target proteins and thereby affect various nuclear and cytoplasmic processes. The activity of PARP family members, such as PARP1 and PARP2, is tied to cellular signalling pathways, and through poly(ADP-ribosyl)ation (PARylation) they ultimately promote changes in gene expression, RNA and protein abundance, and the location and activity of proteins that mediate signalling responses. PARPs act in a complex response network that is driven by the cellular, molecular and chemical biology of poly(ADP-ribose) (PAR). This PAR-dependent response network is crucial for a broad array of physiological and pathological responses and thus is a good target for chemical therapeutics for several diseases.
983 citations
Washington University in St. Louis1, Mayo Clinic2, University of California, Santa Cruz3, University of Texas MD Anderson Cancer Center4, University of California, San Francisco5, Duke University6, Good Samaritan Hospital7, University of Texas Southwestern Medical Center8, Howard Hughes Medical Institute9
TL;DR: To correlate the variable clinical features of oestrogen-receptor-positive breast cancer with somatic alterations, pretreatment tumour biopsies accrued from patients in two studies of neoadjuvant aromatase inhibitor therapy are studied by massively parallel sequencing and analysis.
Abstract: Whole-genome analysis of oestrogen-receptor-positive tumours in patients treated with aromatase inhibitors show that distinct phenotypes are associated with specific patterns of somatic mutations; however, most recurrent mutations are relatively infrequent so prospective clinical trials will require comprehensive sequencing and large study populations.
981 citations
TL;DR: Findings indicate an essential role for EDNRB in the development of two neural crest-derived cell lineages, myenteric ganglion neurons and epidermal melanocytes, and postulate that defects in the human ED NRB gene cause a hereditary form of Hirschsprung's disease that has recently been mapped to human chromosome 13.
978 citations
Authors
Showing all 39410 results
| Name | H-index | Papers | Citations |
|---|---|---|---|
| Eugene Braunwald | 230 | 1711 | 264576 |
| Joseph L. Goldstein | 207 | 556 | 149527 |
| Eric N. Olson | 206 | 814 | 144586 |
| Craig B. Thompson | 195 | 557 | 173172 |
| Thomas C. Südhof | 191 | 653 | 118007 |
| Scott M. Grundy | 187 | 841 | 231821 |
| Michael S. Brown | 185 | 422 | 123723 |
| Eric Boerwinkle | 183 | 1321 | 170971 |
| Jiaguo Yu | 178 | 730 | 113300 |
| John J.V. McMurray | 178 | 1389 | 184502 |
| Eric J. Nestler | 178 | 748 | 116947 |
| John D. Minna | 169 | 951 | 106363 |
| Yuh Nung Jan | 162 | 460 | 74818 |
| Andrew P. McMahon | 162 | 415 | 90650 |
| Elliott M. Antman | 161 | 716 | 179462 |