scholarly journals Using Subsets Sequence to Approach the Maximal Terminal Region for MPC

10.5772/18330 ◽  
2011 ◽  
Author(s):  
Yafeng Wang ◽  
Fuchun Sun ◽  
Youan Zhang ◽  
Huaping Liu ◽  
Haibo Mi
Keyword(s):  
Terminal Region

Antibodies against the COOH-terminal region of E. coli ClpP protease in patients with primary biliary cirrhosis

2000 ◽  
Vol 33 (4) ◽  
pp. 528-536 ◽  
Author(s):  
Isabel Mayo ◽  
Paz Arizti ◽  
Albert Pares ◽  
Joaquin Oliva ◽  
Rita Alvarez Doforno ◽  
...  
Keyword(s):  
Primary Biliary Cirrhosis ◽  
Terminal Region ◽  
Biliary Cirrhosis ◽  
E Coli

Human Cardiac Ryanodine Receptor: Preparation, Crystallization and Preliminary X-ray Analysis of the N-terminal Region

2013 ◽  
Vol 20 (11) ◽  
pp. 1211-1216 ◽  
Author(s):  
L’ubomír Borko ◽  
Július Kostan ◽  
Alexandra Zahradníkova ◽  
Vladimír Pevala ◽  
Juraj Gasperík ◽  
...  
Keyword(s):  
Ryanodine Receptor ◽  
Terminal Region ◽  
X Ray ◽  
Cardiac Ryanodine Receptor

scholarly journals Mutation of the N-Terminal Region of Chikungunya Virus Capsid Protein: Implications for Vaccine Design

mBio ◽  
2017 ◽  
Vol 8 (1) ◽  
Author(s):  
Adam Taylor ◽  
Xiang Liu ◽  
Ali Zaid ◽  
Lucas Y. H. Goh ◽  
Jody Hobson-Peters ◽  
...  
Keyword(s):  
Host Cell ◽  
Capsid Protein ◽  
Chikungunya Virus ◽  
Fluorescent Protein ◽  
Nuclear Translocation ◽  
Vaccine Design ◽  
Terminal Region ◽  
Site Directed Mutagenesis ◽  
Nucleolar Localization ◽  
Localization Sequence

ABSTRACTMosquito-transmitted chikungunya virus (CHIKV) is an arthritogenic alphavirus of theTogaviridaefamily responsible for frequent outbreaks of arthritic disease in humans. Capsid protein, a structural protein encoded by the CHIKV RNA genome, is able to translocate to the host cell nucleolus. In encephalitic alphaviruses, nuclear translocation induces host cell transcriptional shutoff; however, the role of capsid protein nucleolar localization in arthritogenic alphaviruses remains unclear. Using recombinant enhanced green fluorescent protein (EGFP)-tagged expression constructs and CHIKV infectious clones, we describe a nucleolar localization sequence (NoLS) in the N-terminal region of capsid protein, previously uncharacterized in CHIKV. Mutation of the NoLS by site-directed mutagenesis reduced efficiency of nuclear import of CHIKV capsid protein. In the virus, mutation of the capsid protein NoLS (CHIKV-NoLS) attenuated replication in mammalian and mosquito cells, producing a small-plaque phenotype. Attenuation of CHIKV-NoLS is likely due to disruption of the viral replication cycle downstream of viral RNA synthesis. In mice, CHIKV-NoLS infection caused no disease signs compared to wild-type CHIKV (CHIKV-WT)-infected mice; lack of disease signs correlated with significantly reduced viremia and decreased expression of proinflammatory factors. Mice immunized with CHIKV-NoLS, challenged with CHIKV-WT at 30 days postimmunization, develop no disease signs and no detectable viremia. Serum from CHIKV-NoLS-immunized mice is able to efficiently neutralize CHIKV infectionin vitro. Additionally, CHIKV-NoLS-immunized mice challenged with the related alphavirus Ross River virus showed reduced early and peak viremia postchallenge, indicating a cross-protective effect. The high degree of CHIKV-NoLS attenuation may improve CHIKV antiviral and rational vaccine design.IMPORTANCECHIKV is a mosquito-borne pathogen capable of causing explosive epidemics of incapacitating joint pain affecting millions of people. After a series of major outbreaks over the last 10 years, CHIKV and its mosquito vectors have been able to expand their range extensively, now making CHIKV a human pathogen of global importance. With no licensed vaccine or antiviral therapy for the treatment of CHIKV disease, there is a growing need to understand the molecular determinants of viral pathogenesis. These studies identify a previously uncharacterized nucleolar localization sequence (NoLS) in CHIKV capsid protein, begin a functional analysis of site-directed mutants of the capsid protein NoLS, and examine the effect of the NoLS mutation on CHIKV pathogenesisin vivoand its potential to influence CHIKV vaccine design. A better understanding of the pathobiology of CHIKV disease will aid the development of effective therapeutic strategies.

scholarly journals SYT associates with human SNF/SWI complexes and the C-terminal region of its fusion partner SSX1 targets histones.

2002 ◽  
Vol 277 (16) ◽  
pp. 14350
Author(s):  
Hiroyuki Kato ◽  
Agneta Tjernberg ◽  
Wenzhu Zhang ◽  
Andrew N. Krutchinsky ◽  
Woojin An ◽  
...  
Keyword(s):  
Terminal Region ◽  
Fusion Partner

scholarly journals Identification of the N-terminal region in rhodopsin kinase involved in its interaction with rhodopsin.

1993 ◽  
Vol 268 (8) ◽  
pp. 6004-6013 ◽  
Author(s):  
K. Palczewski ◽  
J. Buczyłko ◽  
L. Lebioda ◽  
J.W. Crabb ◽  
A.S. Polans
Keyword(s):  
Terminal Region ◽  
Rhodopsin Kinase
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