Weiqi Zeng's research while affiliated with Central South University and other places

... FYN was found to regulate autoimmunity by binding to B-lymphocyte surface antigen CD19 [49] and interacting with immunoglobulin superfamily member CD147 [50]. Evidence has shown that FYN plays a role in cancer pathogenesis and drug resistance [51]. ...

... FYN was a nonreceptor tyrosine kinase (RTK) member of the Src family kinase (SFK) (55). It was reported that FYN promoted tumor progression in glioma (56), melanoma (57), colon cancer (58), gastric cancer (59), and pancreatic cancer through various mechanisms (60). Furthermore, FYN was found to suppress LUAD by downregulating PI3K/AKT and inhibiting the epithelial-tomesenchymal transition (61). ...

... When mutations occur at these sites, Ubc13's ability to bind to TRAF6 is compromised [11,14]. Research has previously demonstrated TRAF6's upregulation in various tumors and disease conditions, such as autoimmune diseases, liver cancer, and melanoma [15][16][17]. TRAF6's association with tumors significantly impacts their development and prognosis, resulting in unfavorable outcomes [8]. The suppression of TRAF6 expression leads to a notable decrease in the malignant characteristics both in vitro and in vivo, underscoring the pivotal role of TRAF6 in tumor metastasis. ...

... The guideline of animal experiment is required to minimize suffering and improve welfare of animals in research. Three groups of mice were assigned at random, including the solvent group (vehicle), AE007 30 mg/kg group, and AE007 60 mg/kg group (10 mice in each group), as previously described [24]. ...

... These findings are consistent with the results of the current study. Also, our results are consistent with the findings of many previous studies [5][6][7][8]34 . GLUT1 concentration and gene expression were elevated in skin biopsies from psoriatic lesions compared to non-lesioned skin and normal control skin 5 . ...

... Importantly, experimental glucocorticoid treatment partially ameliorated the autoimmune response and bleeding symptoms seen in genetically modified leptin pigs. These findings highlight the important role of leptin in the development of autoimmune diseases and highlight the potential of genetic modification of leptin as an important model to study SLE [4]. ...

... Hypoxia is the primary stimulator of VEGF through hypoxia-inducible factor (HIF-1), which is also known in bone healing. [6][7][8][9][10] Because of the important angiogenesis effect of VEGF on wound healing, recombinant human VEGF (rhVEGF) has been tried in treating diabetic ulcers. 11 The former FDA-approved drug Telbermin, a rhVEGF, has shown a tendency to increase complete ulcer healing and to reduce the time to complete healing. ...

... p-H2A.X, a hallmark for DNA damage, was not detected in the extrahepatic biliary duct tissues from the normal control mice, though increased in epithelial cells of the extrahepatic biliary ducts in Pten L/L /Pdx1-Cre mice (Fig. 2D), suggesting Pten deletion caused an accumulation of DNA damage. Ezh2, a histone epigenetic modulator for genes involved with regulating cell survival, proliferation, epithelial-to-mesenchymal transition, and immune/inflammation regulation [35,36], was also substantially upregulated (Fig. 2D, bottom row). The inflammatory cell infiltrations were further manifested via staining with markers of neutrophils (Gr-1) and cancer associated macrophages (CD206 and CD86) (Fig. 2E). ...

... Wei et al. (Wei et al., 2016) established that propranolol increased the cytotoxicity of vemurafenib and sensitized cells to the of this tyrosine kinase inhibitor (TKI) in thyroid cancer. Other studies showed a synergistic effect of the combination of propranolol and other TKI sunitinib on melanoma cells (Kuang et al., 2018). Studies have also shown the ability of carvedilol to enhance the activity of anticancer drugs, for example, it increased the efficacy of vincristine treatment against neuroblastoma (Pasquier et al., 2013). ...

... In addition to acidosis, our characterization of the distinct lipid metabolomics profile in the IMQ-induced psoriasis model revealed upregulation of several molecular species of LPC. This observation is also consistent with findings in humans, where LPC levels were significantly elevated in lesioned psoriatic skin compared with uninvolved and normal skin 53,54 . Importantly, our results, along with previous reports, indicate that LPC can evoke and enhance ASIC3 currents in the absence and presence of acidosis, respectively 41,42,55 . ...