Strengths and limitations of web servers for the modeling of TCRpMHC complexes.

Cellular immunity relies on the ability of a T-cell receptor (TCR) to recognize a peptide (p) presented by a class I major histocompatibility complex (MHC) receptor on the surface of a cell. The TCR-peptide-MHC (TCRpMHC) interaction is a crucial step in activating T-cells, and the structural characteristics of these molecules play a significant role in determining the specificity and affinity of this interaction. Hence, obtaining 3D structures of TCRpMHC complexes offers valuable insights into various aspects of cellular immunity and can facilitate the development of T-cell-based immunotherapies.

The nuclear receptor Hr46/Hr3 is required in the blood brain barrier of mature males for courtship.

The blood brain barrier (BBB) forms a stringent barrier that protects the brain from components in the circulation that could interfere with neuronal function. At the same time, the BBB enables selective transport of critical nutrients and other chemicals to the brain. Beyond these functions, another recently recognized function is even less characterized, specifically the role of the BBB in modulating behavior by affecting neuronal function in a sex-dependent manner.

p11 mediates the BDNF-protective effects in dendritic outgrowth and spine formation in B27-deprived primary hippocampal cells.

Background: p11 (S100A10) is a key regulator of depression-like behaviors and antidepressant drug response in rodent models. Recent studies suggest that p11 mediates the behavioral antidepressant action of brain-derived neurotrophic factor (BDNF) in rodents. BDNF improves neural plasticity, which is linked to the cellular actions of antidepressant drugs.

Early life stress increases stress vulnerability through BDNF gene epigenetic changes in the rat hippocampus.

Early life stress (ELS) exerts long-lasting epigenetic influences on the brain and makes an individual susceptible to later depression. It is poorly understood whether ELS and subsequent adult chronic stress modulate epigenetic mechanisms. We examined the epigenetic mechanisms of the BDNF gene in the hippocampus, which may underlie stress vulnerability to postnatal maternal separation (MS) and adult restraint stress (RS).