Positional cloning of the mouse obese gene and its human homologue

Nature ◽  
1994 ◽  
Vol 372 (6505) ◽  
pp. 425-432 ◽  
Author(s):  
Yiying Zhang ◽  
Ricardo Proenca ◽  
Margherita Maffei ◽  
Marisa Barone ◽  
Lori Leopold ◽  
...  
Nature ◽  
1995 ◽  
Vol 374 (6521) ◽  
pp. 479-479 ◽  
Author(s):  
Yiying Zhang ◽  
Ricardo Proenca ◽  
Margherita Maffei ◽  
Marisa Barone ◽  
Lori Leopold ◽  
...  

2000 ◽  
Vol 10 (2) ◽  
pp. 99-108
Author(s):  
Tooru M. Mizuno ◽  
Andrew Ross ◽  
Charles V. Mobbs

ob/ob mice with mutations in the obese gene are extremely obese and hyperphagic and have characteristic neuroendocrine impairments, including impaired reproduction and low sex hormones, low thyroid hormone, low growth hormone, and elevated glucocorticoids, a pattern also observed in fasting mice. The product of the obese gene, called leptin, was originally characterized on the basis of positional cloning. Injections of leptin not only reversed many of the phenotypes of ob/ob mice, many of the neuroendocrine effects of fasting are also reversed by leptin injection.


2018 ◽  
Author(s):  
TT Cui ◽  
N Hallahan ◽  
W Jonas ◽  
P Gottmann ◽  
M Jähnert ◽  
...  
Keyword(s):  

Diabetes ◽  
1996 ◽  
Vol 45 (5) ◽  
pp. 675-678 ◽  
Author(s):  
T. Niki ◽  
H. Mori ◽  
Y. Tamori ◽  
M. Kishimoto-Hashirmoto ◽  
H. Ueno ◽  
...  

Genetics ◽  
1999 ◽  
Vol 152 (1) ◽  
pp. 319-344
Author(s):  
Thomas R Breen

Abstract trithorax (trx) encodes chromosome-binding proteins required throughout embryogenesis and imaginal development for tissue- and cell-specific levels of transcription of many genes including homeotic genes of the ANT-C and BX-C. trx encodes two protein isoforms that contain conserved motifs including a C-terminal SET domain, central PHD fingers, an N-terminal DNA-binding homology, and two short motifs also found in the TRX human homologue, ALL1. As a first step to characterizing specific developmental functions of TRX, I examined phenotypes of 420 combinations of 21 trx alleles. Among these are 8 hypomorphic alleles that are sufficient for embryogenesis but provide different levels of trx function at homeotic genes in imaginal cells. One allele alters the N terminus of TRX, which severely impairs larval and imaginal growth. Hypomorphic alleles that alter different regions of TRX equivalently reduce function at affected genes, suggesting TRX interacts with common factors at different target genes. All hypomorphic alleles examined complement one another, suggesting cooperative TRX function at target genes. Comparative effects of hypomorphic genotypes support previous findings that TRX has tissue-specific interactions with other factors at each target gene. Some hypomorphic genotypes also produce phenotypes that suggest TRX may be a component of signal transduction pathways that provide tissue- and cell-specific levels of target gene transcription.


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