Results 91 to 100 of about 377,868 (302)
CDK4/6 inhibition promotes CD8+ T cell expansion through tumor‐macrophage crosstalk by activating HIF‐1α and enhancing MIF‐CD44/CD74 signaling. This reprograms TAMs to boost MHC‐I antigen presentation, and CDK4/6 inhibitor‐trained M1 TAM supernatant therapy synergizes with low‐dose PD‐1 blockade to restore antitumor immunity.
Lin He +17 more
wiley +1 more source
Особливості морфометричної реакції bcl-2+ клітин кори скроневої частки півкуль у ранньому та віддаленому періодах ішемічно-реперфузійного пошкодження головного мозку щурів із цукровим діабетом [PDF]
Вивчено особливості впливу каротидної ішемії з реперфузією різної тривалості на динаміку реакції морфометричних параметрів Bcl-2+-нервових та гліальних клітин кори скроневої частки головного мозку в щурів з експериментальним цукровим діабетом.
Кметь, Тарас Ігорович
core
SLUG is activated by nuclear factor kappa B and confers human alveolar epithelial A549 cells resistance to tumor necrosis factor-alpha-induced apoptosis [PDF]
BACKGROUND: The role of tumor necrosis factor alpha (TNF-α) in cancer is complex with both apoptotic and anti-apoptotic roles proposed. However the mechanism is not clear. In the study, we designed to investigate the effect of TNF-α on the activation and
Bin Yue +4 more
core +1 more source
TRMT6‐mediated m1A modification in CDK9 mRNA enhances its mRNA stability and translation efficiency, thereby increasing the protein levels of CDK9. Upregulated CDK9 promotes the progression of HCC by elevating the levels of oncogenic factors including p‐STAT3, MCL1, and BCL‐2. On the other hand, CDK9 phosphorylates TARDBP at Ser254 to activate HBV core
Rui Zhang +12 more
wiley +1 more source
Objective:B-cell lymphoma 2 (Bcl-2) is an important member of the Bcl-2 family of proteins that regulate the induction of apoptosis. This study aims to investigate whether Bcl-2 small interfering RNA (siRNA) combined with miR-15a oligonucleotides (ODN ...
Li Ding +6 more
doaj +1 more source
The BCL-2-specific inhibitor, ABT-199 (venetoclax) has exhibited remarkable clinical activity in nearly all cases of chronic lymphocytic leukemia. In contrast, responses are usually much less in diffuse large B-cell lymphoma (DLBCL), despite high level ...
Victoria M. Smith +11 more
doaj +1 more source
Unraveling the Molecular Mechanisms Underlying Spontaneous Multipolar Mitosis Through CIN‐seq
Multipolar mitosis, a hallmark of chromosomal instability (CIN), drives tumor heterogeneity but is challenging to study in live cells. Using CIN‐seq, a single‐cell multiomics method, we profiled rare CIN events and identified mechanisms associated with viable multipolar mitosis, including PTEN attenuation, Rho GTPase‐driven cytokinesis failure, and ...
Pin‐Rui Su +10 more
wiley +1 more source
Reaction of Bcl-2+ cells of the parietal lobe cortex of rats with experimental diabetes mellitus to ischemia-reperfusion [PDF]
The peculiarities of anti-apoptotic mechanisms in the nerve and glial cells of the parietal lobe cortex are studied by the density changes of Bcl-2+-cells location and concentration of Bcl-2 protein in them in rats with diabetes mellitus in the dynamics ...
Boychuk, T.M., Kmet, T.I., Tkachuk, S.S.
core
Anti-apoptotic BCL-2 family proteins in acute neural injury. [PDF]
Cells under stress activate cell survival and cell death signaling pathways. Cell death signaling frequently converges on mitochondria, a process that is controlled by the activities of pro- and anti-apoptotic B-cell lymphoma 2 (BCL-2) proteins.
Anilkumar, Ujval, Prehn, Jochen HM
core +1 more source
Zinc Exposure Causes Disulfidptosis to Induce Miscarriage by Up‐Regulating GATA1/METTL1/SLC7A11 Axis
Zn exposure up‐regulates GATA1, promoting GATA1‐mediated METTL1 and SLC7A11 transcription. It also enhances METTL1‐mediated m7G modification on SLC7A11 mRNA, increasing SLC7A11 mRNA stability. Ultimately, Zn exposure up‐regulates SLC7A11 at both transcriptional and post‐transcriptional levels, causing disulfidptosis. Knockdown of murine Slc7a11, Gata1,
Wenxin Huang +16 more
wiley +1 more source

