Rockefeller University

About: Rockefeller University is a education organization based out in New York, New York, United States. It is known for research contribution in the topics: Population & Gene. The organization has 15867 authors who have published 32938 publications receiving 2940261 citations. The organization is also known as: Rockefeller University & Rockefeller Institute.

Obesity in the new millennium.

Abstract: Obesity has increased at an alarming rate in recent years and is now a worldwide public health problem. In addition to suffering poor health and an increased risk of illnesses such as hypertension and heart disease, obese people are often stigmatized socially. But major advances have now been made in identifying the components of the homeostatic system that regulates body weight, including several of the genes responsible for animal and human obesity. A key element of the physiological system is the hormone leptin, which acts on nerve cells in the brain (and elsewhere) to regulate food intake and body weight. The identification of additional molecules that comprise this homeostatic system will provide further insights into the molecular basis of obesity, and possibilities for new treatments.

POT1 as a terminal transducer of TRF1 telomere length control

Abstract: Human telomere maintenance is essential for the protection of chromosome ends, and changes in telomere length have been implicated in ageing and cancer. Human telomere length is regulated by the TTAGGG-repeat-binding protein TRF1 and its interacting partners tankyrase 1, TIN2 and PINX1 (refs 5-9). As the TRF1 complex binds to the duplex DNA of the telomere, it is unclear how it can affect telomerase, which acts on the single-stranded 3' telomeric overhang. Here we show that the TRF1 complex interacts with a single-stranded telomeric DNA-binding protein--protection of telomeres 1 (POT1)--and that human POT1 controls telomerase-mediated telomere elongation. The presence of POT1 on telomeres was diminished when the amount of single-stranded DNA was reduced. Furthermore, POT1 binding was regulated by the TRF1 complex in response to telomere length. A mutant form of POT1 lacking the DNA-binding domain abrogated TRF1-mediated control of telomere length, and induced rapid and extensive telomere elongation. We propose that the interaction between the TRF1 complex and POT1 affects the loading of POT1 on the single-stranded telomeric DNA, thus transmitting information about telomere length to the telomere terminus, where telomerase is regulated.

Cell adhesion molecules: implications for a molecular histology

Abstract: PERSPECTIVES AND SUMMARY ... . . ... . . .. . . . .. . . . ..... . . . .. . . . .... . . ... . . ... . 155 CAM TYPES, STRUCTURE, AND BINDING ........ ..... ........ .... . . . ... ..... . . ... . . ..... 1 56 Stru ctu re. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 157 B in ding. . . . .. . ... .... . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 1 6 1 Transfect ion as a M olecular Histological Tool.. ..... . . ... . . . ... . . ... . . ....... ....... ...... 1 63 CHROMOSOMAL LOCALIZATION, GENE STRUCTURE, AND ALTERNATIVE RNA SPLICING . .. . . . . . . . . . .. . . . . . . . . .... . . 165 EXPRESSION AND SYNTHESIS . . . . .. .. ... . .... . . . . .. . . . . . .. . . ......... . . . . . .. ... 166 B ioc hem ical M odific at ions . . .. ....... . . ... . . . .. . . . .. . . . .. . . . . .. . . ..... ... ..... . . . . . . . . . . . . . . . . . . 167 Signals R egu lating CAM Synth esis In vitro a nd In vivo.. . ... ..... .... . . .... . . . . . . . . . . . . . 168 MORPHOREGULATORY ACTIVITY OF CAMs . . . . .. . . . ... . . .... . . ....... . . . . . . . .. . . . . . . . . . 169 Place-D ep en dent Exp ression and I nt eract ions . . .... .. ... .. .. ..... . . .. . . . . . . . . . . .. . . . . . . . . . . 169 C;oreg ulatill,n with SAM Exp ression .... ..... ......... . .... . . ... . . . .... ... ........ ... 1 7 1 R epu !sln s . . . .. . . . . . . .. . . ... . ... . . . . . . . . . . . . .. . . .. .. . . . ..... .. . . . . . . . . . . . . .. .. . . . .. . .. 1 73 Pertu rb ation of CAM B inding an d Exp ression.. . . ... . . . .. . . . .. . . . . . . .. .. ...... . . . 174 EVOLUTIONARY RELATIONSHIPS 1 75 CAMs IN DISEASE 178 Neuromuscula r an d Neu rol ogical D is orders.. . . . ... . . ... . . . ... .. . ...... . ......... . . . . ... .... 179 Transform ed Cells, Tum ors, an d M etastasis ..... . ........ ...... . . .. . . . ... . . ... . . . . . . . . ..... 1 79 PROSPECTS FOR A MOLECULAR HISTOLOGy 1 8 1