Download full-text PDF

Source

Publication Analysis

Top Keywords

repression fasl
4
fasl expression
4
expression dipfluzine
4
dipfluzine involves
4
involves mechanism
4
mechanism inhibition
4
inhibition nfatc
4
nfatc transactivation
4
repression
1
expression
1

Similar Publications

Background: B-cell-specific Moloney murine leukemia virus integration site 1 (BMI1) and Fas ligand (FasL) are two critical stemness genes believed to play a role in the development of colorectal cancer (CRC). This study aimed to investigate the expression levels of these genes in primary CRC tumors to assess their correlation with cancer progression and prognosis.

Methods: The relative expression levels of BMI1 and FasL were analyzed using real-time polymerase chain reaction in 100 primary CRC tumor samples along with paired adjacent non-cancerous tissues.

View Article and Find Full Text PDF

Background: Extensive attention has been given to the role of myeloid-derived suppressor cells (MDSCs) in driving tumor progression and treatment failure. Preclinical studies have identified multiple agents that eliminate MDSCs. However, none have been authorized in the cliniccal ues due to the safety reasons.

View Article and Find Full Text PDF

Targeted disruption of E2f2 in mice causes T-cell hyperactivation and a disproportionate cell cycle entry upon stimulation. However, mice do not develop a lymphoproliferative condition. We report that E2f2 plays a Fas-dependent anti-apoptotic function in vitro and in vivo.

View Article and Find Full Text PDF

Intestinal intraepithelial lymphocytes (IELs) are distributed along the length of the intestine and are considered the frontline of immune surveillance. The precise molecular mechanisms, especially epigenetic regulation, of their development and function are poorly understood. The trimethylation of histone 3 at lysine 27 (H3K27Me3) is a kind of histone modifications and associated with gene repression.

View Article and Find Full Text PDF

CD95 expression is preserved in triple-negative breast cancers (TNBCs), and CD95 loss in these cells triggers the induction of a pro-inflammatory program, promoting the recruitment of cytotoxic NK cells impairing tumor growth. Herein, we identify a novel interaction partner of CD95, Kip1 ubiquitination-promoting complex protein 2 (KPC2), using an unbiased proteomic approach. Independently of CD95L, CD95/KPC2 interaction contributes to the partial degradation of p105 (NF-κB1) and the subsequent generation of p50 homodimers, which transcriptionally represses NF-κB-driven gene expression.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!