scholarly journals High-Temperature Requirement A 1 Causes Photoreceptor Cell Death in Zebrafish Disease Models

2018 ◽  
Vol 188 (12) ◽  
pp. 2729-2744 ◽  
Author(s):  
Yoshihito Oura ◽  
Machiko Nakamura ◽  
Tohru Takigawa ◽  
Yoko Fukushima ◽  
Taku Wakabayashi ◽  
...  
2010 ◽  
Vol 177 (3) ◽  
pp. 1176-1186 ◽  
Author(s):  
Ze-Hua Zhu ◽  
Yan P. Yu ◽  
Zhong-Liang Zheng ◽  
Yang Song ◽  
Guo-Sheng Xiang ◽  
...  

Genetics ◽  
2003 ◽  
Vol 165 (2) ◽  
pp. 517-529
Author(s):  
Kentaro Ohkuni ◽  
Asuko Okuda ◽  
Akihiko Kikuchi

AbstractNbp2p is a Nap1-binding protein in Saccharomyces cerevisiae identified by its interaction with Nap1 by a two-hybrid system. NBP2 encodes a novel protein consisting of 236 amino acids with a Src homology 3 (SH3) domain. We showed that NBP2 functions to promote mitotic cell growth at high temperatures and cell wall integrity. Loss of Nbp2 results in cell death at high temperatures and in sensitivity to calcofluor white. Cell death at high temperature is thought not to be due to a weakened cell wall. Additionally, we have isolated several type-2C serine threonine protein phosphatases (PTCs) as multicopy suppressors and MAP kinase-kinase (MAPKK), related to the yeast PKC MAPK pathway, as deletion suppressors of the nbp2Δ mutant. Screening for deletion suppressors is a new genetic approach to identify and characterize additional proteins in the Nbp2-dependent pathway. Genetic analyses suggested that Ptc1, which interacts with Nbp2 by the two-hybrid system, acts downstream of Nbp2 and that cells lacking the function of Nbp2 prefer to lose Mkk1, but the PKC MAPK pathway itself is indispensable when Nbp2 is deleted at high temperature.


PLoS Genetics ◽  
2013 ◽  
Vol 9 (6) ◽  
pp. e1003555 ◽  
Author(s):  
Kyoung-in Cho ◽  
MdEmdadul Haque ◽  
Jessica Wang ◽  
Minzhong Yu ◽  
Ying Hao ◽  
...  

2014 ◽  
Vol 5 (5) ◽  
pp. e1269-e1269 ◽  
Author(s):  
H Matsumoto ◽  
Y Murakami ◽  
K Kataoka ◽  
H Lin ◽  
K M Connor ◽  
...  

2011 ◽  
Vol 52 (6) ◽  
pp. 3825 ◽  
Author(s):  
Mi In Roh ◽  
Yusuke Murakami ◽  
Aristomenis Thanos ◽  
Demetrios G. Vavvas ◽  
Joan W. Miller

Author(s):  
Arvind Kumar Gupta ◽  
Debashree Behera ◽  
Balasubramanian Gopal

The crystal structure of Mycobacterium tuberculosis high-temperature requirement A (HtrA) protein was determined at 1.83 Å resolution. This membrane-associated protease is essential for the survival of M. tuberculosis. The crystal structure reveals that interactions between the PDZ domain and the catalytic domain in HtrA lead to an inactive conformation. This finding is consistent with its proposed role as a regulatory protease that is conditionally activated upon appropriate environmental triggers. The structure provides a basis for directed studies to evaluate the role of this essential protein and the regulatory pathways that are influenced by this protease.


Toxicology ◽  
2011 ◽  
Vol 290 (2-3) ◽  
pp. 143
Author(s):  
Izabel Villela ◽  
Barbara Heidenreich ◽  
Manraj Cheema ◽  
Tiziana di Martino ◽  
Leona D. Samson ◽  
...  

2022 ◽  
Vol 13 (1) ◽  
Author(s):  
Soumyaparna Das ◽  
Valerie Popp ◽  
Michael Power ◽  
Kathrin Groeneveld ◽  
Jie Yan ◽  
...  

AbstractHereditary degeneration of photoreceptors has been linked to over-activation of Ca2+-permeable channels, excessive Ca2+-influx, and downstream activation of Ca2+-dependent calpain-type proteases. Unfortunately, after more than 20 years of pertinent research, unequivocal evidence proving significant and reproducible photoreceptor protection with Ca2+-channel blockers is still lacking. Here, we show that both D- and L-cis enantiomers of the anti-hypertensive drug diltiazem were very effective at blocking photoreceptor Ca2+-influx, most probably by blocking the pore of Ca2+-permeable channels. Yet, unexpectedly, this block neither reduced the activity of calpain-type proteases, nor did it result in photoreceptor protection. Remarkably, application of the L-cis enantiomer of diltiazem even led to a strong increase in photoreceptor cell death. These findings shed doubt on the previously proposed links between Ca2+ and retinal degeneration and are highly relevant for future therapy development as they may serve to refocus research efforts towards alternative, Ca2+-independent degenerative mechanisms.


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