Misexpression of BRE gene in the developing chick neural tube affects neurulation and somitogenesis.

The brain and reproductive expression (BRE) gene is expressed in numerous adult tissues and especially in the nervous and reproductive systems. However, little is known about BRE expression in the developing embryo or about its role in embryonic development. In this study, we used in situ hybridization to reveal the spatiotemporal expression pattern for BRE in chick embryo during development.

Anti-apoptotic protein BRE/BRCC45 attenuates apoptosis through maintaining the expression of caspase inhibitor XIAP in mouse Lewis lung carcinoma D122 cells.

Brain and Reproductive Organ Expressed (BRE), or BRCC45, is a death receptor-associated antiapoptotic protein, which is also involved in DNA-damage repair, and K63-specific deubiquitination. BRE overexpression attenuates both death receptor- and stress-induced apoptosis, promotes experimental tumor growth, and is associated with human hepatocellular and esophageal carcinoma. How BRE mediates its antiapoptotic function is unknown.

Promyelocytic leukemia (PML) protein plays important roles in regulating cell adhesion, morphology, proliferation and migration.

PML protein plays important roles in regulating cellular homeostasis. It forms PML nuclear bodies (PML-NBs) that act like nuclear relay stations and participate in many cellular functions. In this study, we have examined the proteome of mouse embryonic fibroblasts (MEFs) derived from normal (PML(+/+)) and PML knockout (PML(-/-)) mice.

Cardiac telocytes were decreased during myocardial infarction and their therapeutic effects for ischaemic heart in rat.

Recently, cardiac telocytes were found in the myocardium. However, the functional role of cardiac telocytes and possible changes in the cardiac telocyte population during myocardial infarction in the myocardium are not known. In this study, the role of the recently identified cardiac telocytes in myocardial infarction (MI) was investigated.

BDNF-mediated migration of cardiac microvascular endothelial cells is impaired during ageing.

This study indicates that brain-derived neurotrophic factor (BDNF) can promote young cardiac microvascular endothelial cells (CMECs) to migrate via the activation of the BDNF-TrkB-FL-PI3K/Akt pathway, which may benefit angiogenesis after myocardial infarction (MI). However, the ageing of CMECs led to changes in the expression of receptor Trk isoforms in that among the three isoforms (TrkB-FL, TrkB-T1 and TrkB-T2), only one of its truncated isoforms, TrkB-T1, continued to be expressed, which leads to the dysfunction of its ligand, a decrease in the migration of CMECs and increased injury in ageing hearts. This shift in receptor isoforms in aged CMECs, together with changes in the ageing microenvironment, might predispose ageing hearts to decreased angiogenic potential and increased cardiac pathology.

Gene expression profiling of CD3gamma, delta, epsilon, and zeta chains in CD4(+) and CD8(+) T cells from human umbilical cord blood.

In order to elucidate the feature of T-cell immune status in umbilical cord blood (CB) from humans, the expression levels of CD3gamma, delta, epsilon, and zeta chain genes in CD4(+) and CD8(+) T cells of CB were analysed by real-time PCR. CD4(+) and CD8(+) T cells sorted from 12 cases of CB and 10 peripheral blood (PB) samples from healthy adults were used in the study. The beta2-microglobulin gene was used as an endogenous reference, and the evaluations of mRNA expression level of each CD3 gene were used by the 2(-DeltaC(t)) x 100% method.

Differential expression of a novel gene BRE (TNFRSF1A modulator/BRCC45) in response to stress and biological signals.

Stress-responsive genes play critical roles in many biological functions that includes apoptosis, survival, differentiation and regeneration. We have identified a novel stress-responsive gene called BRE which interacts with TNF-receptor-1 and blocks the apoptotic effect of TNF-alpha. BRE enhances tumor growth in vivo and is up-regulated in hepatocellular and esophageal carcinomas.

TRGV and TRDV repertoire distribution and clonality of T cells from umbilical cord blood.

Umbilical cord blood (CB) has been used as a valuable source of hematopoietic stem cells for allogeneic transplantation, specific CTL response and immunotherapy for decades. We previously analyzed the distribution and clonality of T-cell receptor alpha and beta variable region (TRAV) and (TRBV) of the subfamily T cell receptors in T cells from umbilical cord blood. Recent data indicated that gammadelta(+) T cells may play an important role in mediating the graft versus leukemia effect after stem cells transplantation and in anti-cancer response.

Comparative proteomic analysis reveals a function of the novel death receptor-associated protein BRE in the regulation of prohibitin and p53 expression and proliferation.

The brain and reproductive organ expressed (BRE) gene encodes a highly conserved stress-modulating protein. To gain further insight into the function of this gene, we used comparative proteomics to investigate the protein profiles of C2C12 and D122 cells resulting from small interfering RNA (siRNA)-mediated silencing as well as overexpression of BRE. Silencing of BRE in C2C12 cells, using siRNA, resulted in up-regulated Akt-3 and carbonic anhydrase III expression, while the 26S proteasome regulatory subunit S14 and prohibitin were down-regulated.

BRE enhances in vivo growth of tumor cells.

Human BRE, a death receptor-associating intracellular protein, attenuates apoptotic response of human and mouse tumor cell lines to death receptor stimuli in vitro. In this report, we addressed whether the in vitro antiapoptotic effect of BRE could impact on tumor growth in vivo. We have shown that the mouse Lewis lung carcinoma D122 stable transfectants of human BRE expression vector developed into local tumor significantly faster than the stable transfectants of empty vector and parental D122, in both the syngeneic C57BL/6 host and nude mice.

A death receptor-associated anti-apoptotic protein, BRE, inhibits mitochondrial apoptotic pathway.

BRE, brain and reproductive organ-expressed protein, was found previously to bind the intracellular juxtamembrane domain of a ubiquitous death receptor, tumor necrosis factor receptor 1 (TNF-R1), and to down-regulate TNF-alpha-induced activation of NF-kappaB. Here we show that BRE also binds to another death receptor, Fas, and upon overexpression conferred resistance to apoptosis induced by TNF-alpha, anti-Fas agonist antibody, cycloheximide, and a variety of stress-related stimuli. However, down-regulation of the endogenous BRE by small interfering RNA increased apoptosis to TNF-alpha, but nottoetoposide, indicating that the physiological antiapoptotic role of this protein is specific to death receptor-mediated apoptosis.

Expression of a conserved mouse stress-modulating gene, Bre: comparison with the human ortholog.

Mouse Bre, an evolutionarily conserved stress-modulating gene, like its human counterpart, is expressed in multiple alternative transcripts. The main transcript, which is ubiquitously expressed, encodes a protein that binds tumor necrosis factor receptor 1 (TNF-R1) and downregulates TNF-induced activation of NF-kappaB. Alternative splicing of mouse Bre occurs only at the 5' region of the gene, generating either nonfunctional transcripts or transcripts that can encode putative protein isoforms differ at the N-terminal sequence.