References
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1) Ginsenoside Rh1, a novel casein kinase II subunit alpha (CK2α) inhibitor, retards metastasis via disrupting HHEX/CCL20 signaling cascade involved in tumor cell extravasation across endothelial barrier.
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2) Single-cell RNA sequencing reveals that HSD17B2 in cancer-associated fibroblasts promotes the development and progression of castration-resistant prostate cancer.
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3) Integrating network analysis and experimental validation to reveal the mitophagy-associated mechanism of Yiqi Huoxue (YQHX) prescription in the treatment of myocardial ischemia/reperfusion injury.
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4) LONP1 targets HMGCS2 to protect mitochondrial function and attenuate chronic kidney disease.
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5) The microglial innate immune receptors TREM-1 and TREM-2 in the anterior cingulate cortex (ACC) drive visceral hypersensitivity and depressive-like behaviors following DSS-induced colitis.
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6) α-Synuclein induces Th17 differentiation and impairs the function and stability of Tregs by promoting RORC transcription in Parkinson's disease.
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7) CircNf1-mediated CXCL12 expression in the spinal cord contributes to morphine analgesic tolerance.
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8) Preparation of Phillygenin-Hyaluronic acid composite milk-derived exosomes and its anti-hepatic fibrosis effect.
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9) Silica nanocarrier-mediated intracellular delivery of rapamycin promotes autophagy-mediated M2 macrophage polarization to regulate bone regeneration.
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10) Therapeutic potency of compound RMY-205 for pulmonary fibrosis induced by SARS-CoV-2 nucleocapsid protein.
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11) Downregulation of connexin 43-based gap junctions underlies propofol-induced excessive relaxation in hypertensive vascular smooth muscle cells.
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12) N-glycosylation acts as a switch for FGFR1 trafficking between the plasma membrane and nuclear envelope.
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13) WWP2 drives the progression of gastric cancer by facilitating the ubiquitination and degradation of LATS1 protein.
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14) Semaphorin 7A interacts with nuclear factor NF-kappa-B p105 via integrin β1 and mediates inflammation.
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15) CP-25 inhibits the hyperactivation of rheumatic synoviocytes by suppressing the switch in Gαs-Gαi coupling to the β2-adrenergic receptor.