Potent subversion of these responses thus becomes mandatory for the successful establishment of a primary infection Selleckchem SU5402 following viral entry as well as for efficient viral assembly and egress.
This review gives a concise overview of the induction of the type I IFN signaling pathways in response to viral infection and provides a comprehensive understanding of the antagonizing effects exerted by KSHV on type I IFN pathways wielded at various stages of the viral life cycle. Information garnered from this review should result in a better understanding of KSHV biology essential for the development of immunotherapeutic strategies targeted toward KSHV-associated malignancies.”
“X-chromosome inactivation has long served as an experimental model system for understanding the epigenetic regulation of gene expression. Central to this phenomenon is the long, non-coding RNA Xist that is specifically expressed from the inactive X chromosome
and spreads along the entire length of the chromosome in cis. Recently, two of the proteins originally identified as components of the nuclear scaffold/matrix (S/MAR-associated proteins) have been shown S63845 order to control the principal features of X-chromosome inactivation; specifically, context-dependent competency and the chromosome-wide association of Xist RNA. These findings implicate the involvement of nuclear S/MAR-associated proteins in the organization of epigenetic machinery. Here, we describe a model for the functional role of S/MAR-associated proteins in the regulation of key epigenetic processes.”
“Current psychiatric diagnostic schema segregate symptom clusters into discrete entities, however, large proportions of patients suffer from comorbid conditions that fit neither diagnostic nor therapeutic schema. Similarly, psychotropic treatments ranging from lithium and antipsychotics to serotonin reuptake inhibitors (SSRIs) and acetylcholinesterase inhibitors have been shown to be efficacious
in a wide spectrum of psychiatric disorders ranging from autism, schizophrenia (SZ), depression, and bipolar disorder (BD) to Alzheimer’s disease (AD). This apparent lack of specificity suggests that psychiatric symptoms as well as treatments may share MM-102 aspects of pathophysiology and mechanisms of action that defy current symptom-based diagnostic and neuron-based therapeutic schema.
A myelin-centered model of human brain function can help integrate these incongruities and provide novel insights into disease etiologies and treatment mechanisms. Available data are integrated herein to suggest that widely used psychotropic treatments ranging from antipsychotics and antidepressants to lithium and electroconvulsive therapy share complex signaling pathways such as Akt and glycogen synthase kinase-3 (GSK3) that affect myelination, its plasticity, and repair.