| Perl Molson 2005-12-14, 10:59 am |
| http://www.sciencedaily.com/release...91018075747.htm
There was this above article posted in here before (I believe I've
posted it).
There is a conclussion that can be learned from this research papers,
that is, increased adiposity seems to be a trigger for herpes
replication.
So, beware, folks, the best way to keep herpes at bay is to keep your
weight low.
Clicking on each of the links I've posted in here will clarify the
issue pretty well I hope.
Perl von Molson
Nature. 2002 Nov 21;420(6913):333-6. Related Articles, Links
Activation of JNK provides a beneficial activity for viral replication.
HSV infection causes many changes to the infected cell, such as halting
cellular macromolecular synthesis, reorganizing the nucleus, and
causing cells to round up before they are ultimately lysed as a result
of the release of viral progeny (76). In this report, we describe an
additional event, the activation of SAPKs. Neither the mechanism for
activation nor its role in the infectious process of HSV is currently
known. The effect of JNK activation after infection could be complex
and cell-type specific, since activation of JNK under different
conditions in different cell types correlates with proliferation,
oncogenic transformation, or apoptosis (40, 92). Previously, only four
reports have described induction of JNK activity following virus
infection, and the significance of these inductions is also unknown
(20, 71, 81, 100).
http://jvi.asm.org/cgi/content/full/73/10/8415
http://www.biocarta.com/pathfiles/h_stressPathway.asp
http://www.biocarta.com/search/genesrchresults.asp
A central role for JNK in obesity and insulin resistance.
Hirosumi J, Tuncman G, Chang L, Gorgun CZ, Uysal KT, Maeda K, Karin M,
Hotamisligil GS.
Division of Biological Sciences and Department of Nutrition, Harvard
School of Public Health, 665 Huntington Avenue, Boston, Massachusetts
02115, USA.
Obesity is closely associated with insulin resistance and establishes
the leading risk factor for type 2 diabetes mellitus, yet the molecular
mechanisms of this association are poorly understood. The c-Jun
amino-terminal kinases (JNKs) can interfere with insulin action in
cultured cells and are activated by inflammatory cytokines and free
fatty acids, molecules that have been implicated in the development of
type 2 diabetes. Here we show that JNK activity is abnormally elevated
in obesity. Furthermore, an absence of JNK1 results in decreased
adiposity, significantly improved insulin sensitivity and enhanced
insulin receptor signalling capacity in two different models of mouse
obesity. Thus, JNK is a crucial mediator of obesity and insulin
resistance and a potential target for therapeutics.
PMID: 12447443 [PubMed - indexed for MEDLINE]
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