“…Recently, increasing data on miR-203 in regulating neuroinflammation and neuronal apoptosis has raised extensive concern about the biological function of this microRNA. …”
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“…The antidepressant effect of DZXY may be related to its regulation of neuroinflammation and apoptosis.…”
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“…The effect of cdk4 or cdk6 deficiency on cell apoptosis and the cell cycle was analyzed using flow cytometry. …”
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“…Abbreviations: antibody drug conjugate (ADC), acute lymphocytic leukemia (ALL), constant domain of IgE (Cε), receptor of Cε (CεRI or CεRII), cluster of differentiation (CD), constant domain of heavy chain (C(H)), constant domain of light chain (C(L)), (single-chain) diabody ((sc)Db), diabody-immunoglobulin (Db-Ig), dynamic light scattering (DLS), Fragment antigen-binding (Fab), Fab with hetEHD2 (eFab), Fab-EHD2 with T121G in chain 1 and S10I in chain 2 (EFab), bispecific Ig domain containing hetEHD2 (eIg), extracellular domain (ECD), epidermal growth factor receptor 1, 2, 3 (EGFR, HER2, HER3), heavy chain domain 2 of IgE (EHD2), EHD2 domain with C102S (EHD2-1), EHD2 domain with C14S and N39Q (EHD2-2), (human or mouse) fragment crystalline ((hu or mo)Fc), heavy chain (HC), heterodimerized second domain of IgE (hetEHD2), high molecular weight (HMW), immunoglobulin (Ig), light chain (LC), liquid chromatography-mass spectrometry (LC-MS), mesenchymal epithelial transition factor (MET), heavy chain domain 2 of IgM (MHD2), peripheral blood mononuclear cell (PBMC), prolactin receptor (PRLP), Stokes radius (R(S)), single-chain Fragment variable (scFv), tumor necrosis factor (TNF), TNF receptor 2 (TNFR2), single-chain TNF-related apoptosis-inducing ligand (scTRAIL), variable domain of heavy chain (V(H)), variable domain of light chain (V(L)).…”
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“…For example, the HCG22 hub inhibited cell proliferation and invasion and induced apoptosis in oral squamous cell carcinoma (OSCC) cells. …”
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“…The chromosome segregation 1-like (CSE1L) protein, which regulates cellular mitosis and apoptosis, was previously found to be overexpressed in colorectal cancer (CRC) cells harboring mutations. …”
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“…Annexin V/PI staining was implemented to assess cell apoptosis. Luciferase assay, biotin-coupled microRNA capture, and RIP assay were used to validate the interaction among potential targets. …”
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“…Lastly, we found that IL-21 acts on mouse primary ischemic neurons to activate the JAK/STAT pathway and induce caspase 3/7-mediated apoptosis in vitro. CONCLUSION: These findings identify a novel mechanism for how pro-inflammatory T cells are recruited to the ischemic brain to propagate stroke damage and provide a potential new therapeutic target for stroke.…”
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“…CONCLUSION: Determining the key molecular mechanisms by which Phb1 facilitates the formation of p-p53 (ser15)-Bak-Phb1 and its involvement in the regulation of mitochondrial dynamics and apoptosis may ultimately contribute to the current understanding of molecular and cellular basis of chemoresistance in this gynecologic cancer. …”
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“…Many of the associated genes appeared highly relevant for muscle structure and function/weakness, including genes involved in myogenesis, muscle regeneration, nerve/muscle membrane excitability, muscle denervation/re‐innervation, axon guidance/myelination/degeneration/regeneration, synapse function, ion channelling with especially calcium signalling, metabolism (glucose, protein, and fat), insulin signalling, neuroendocrine hormone regulation, mitochondrial function, autophagy, apoptosis, oxidative stress, Wnt signalling, transcription regulation, muscle fat infiltration during regeneration, and fibrosis. …”
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“…Mechanistically, Gene Set Enrichment Analysis (GSEA) results revealed high stemness score group was enriched in interferon gamma response, interferon alpha response, P53 pathway, coagulation, apoptosis, KRAS signaling upregulation, complement, epithelial–mesenchymal transition (EMT) and IL6-mediated JAK-STAT signaling gene sets. …”
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“…CGA pretreatment inhibited neuronal apoptosis induced by HI by reducing inflammation and oxidative stress. …”
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“…Analysis of RTX-treated spheroids demonstrated apoptosis and necrosis essentially in the outer cell-layers. …”
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“…RESULTS: SNX2112 significantly inhibited cellular proliferation, induced G2/M cell cycle arrest and apoptosis in PRCC lines overexpressing MET. In contrast to TKIs targeting MET, SNX2112 inhibited both MET and known downstream mediators of MET activity (AKT, pAKT1/2 and pERK1/2) in PRCC cell lines. …”
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“…A literature-based pathway analysis showed that 42 proteins are associated with fibrosis, oxidative stress and apoptosis. This included the increased expression of Heat shock protein HSP 90-alpha, CD44 antigen and Carbonic anhydrase 1 which are inhibited by potential drugs against CAA. …”
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“…Functional analysis studies demonstrated that knockdown of eIF6 inhibited ESCA cell growth and migration, and fueled cell apoptosis. Moreover, the Bulk RNA gene analysis revealed a significant inverse association between eIF6 and the tumor-infiltrating immune cells (macrophages, T cells, or Th1 cells) and immunomodulators in the ESCA microenvironment. …”
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“…CONCLUSIONS: Genes annotated to these CpGs were found to be involved in secretion and transportation, nuclear signaling, Hippo signaling pathways, apoptosis, intracellular trafficking and neuronal signaling. …”
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“…Apoptotic and necroptotic proteins were determined by specific antibodies in western blotting. Cell viability/apoptosis was determined by the XTT and flow cytometry analyses. …”
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“…Histomorphological and immunohistochemical analyses were performed to calculate follicle number and assess proliferation and apoptosis of granulosa cells (GCs). Immunofluorescence staining was used to evaluate angiogenesis. …”
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“…PDK1 overexpression partly reversed the biological function of miR-148a—including miR-148a’s ability to increase cell sensitivity to Adriamycin (ADR) treatment—inhibiting cell glycolysis, invasion and epithelial–mesenchymal transition (EMT), and inducing apoptosis and repressing tumor growth. Furthermore, we identified a novel mechanism: DNMT1 directly bound to EZH2 and recruited EZH2 and HDAC2 complexes to the promoter region of miR-148a, leading to miR-148a downregulation. …”
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