Fig 2: Schematic representation of the effects of quercetin on tumor necrosis factor-α-induced matrix metallopeptidase-9 expression and cell migration in normal human gastric mucosa epithelial cells. Schematic diagram of the signaling pathways for quercetin-mediated attenuation of tumor necrosis factor-α (TNF-α)-induced inflammation via downregulation of matrix metallopeptidase-9 (MMP-9) expression in normal human gastric mucosa epithelial cells. Quercetin attenuates TNF-α-induced MMP-9 expression in normal human gastric mucosa epithelial cells through the proinflammatory TNFR-c-Src–extracellular-signal-regulated kinase 1/2–c-Fos and nuclear factor kappa B pathways. AP-1: Activator protein-1; c-Src: Proto-oncogene tyrosine-protein kinase Src; ERK: Extracellular-signal-regulated kinase; GES-1: Normal human gastric mucosa epithelial cell line; MAPK: Mitogen-activated protein kinase; MMP-9: Matrix metallopeptidase-9; MMP9i: MMP-9 inhibitor; NF-κB: Nuclear factor kappa B; TNF-α: Tumor necrosis factor-α; TSIIA: Tanshinone IIA.

Fig 3: Timeline, procedure, and summary of results. Male and female mice underwent surgical vomeronasal organ ablation (VNOx) or a sham procedure in peripuberty [postnatal day (PND) 28–30] or in adulthood (PND 58–62). Behavioral testing took place between PND 72–90 and included the buried food test, olfactory preference, resident-intruder paradigm, and sexual behavior test. Following behavior testing, mice were exposed to soiled-bedding from the opposite-sex, then brains were dissected 90-min later. One series of brain tissue was processed for FOS immunoreactivity (ir), a marker of neural activity, and a second series was Nissl stained to assess neuroanatomical features, including cell number and size, along the accessory olfactory pathway. We found that peripubertal VNOx decreased preference for female-soiled bedding, reduced territorial aggression in male mice, and decreased FOS-ir in response to opposite-sex odors. Conversely, adult VNOx resulted in subtle differences in sexual odor preferences compared with sham controls but did not alter aggression or FOS-ir in response to opposite-sex odors. Regardless of VNO condition, sex-typical copulatory behaviors were observed, and no differences in neuroanatomy were found. Figure created with Biorender.com.

Fig 4: Acute fasting increases the c-Fos expression in different sub-cortical areas. (A) Representative photomicrographs of c-Fos immunostaining in the sub-region of the cortex including paraventricular thalamus (PVT), dorsomedial hypothalamus (DMH), lateral hypothalamus (LH), and basal amygdala (BMA). There were a higher number of c-Fos+ cells in the fasting group (right panel) in comparison with the control group (left panel). Scale bars represent 50 μm. (B) Schematic illustration of the regions of interest. The red box (500 μm × 140 μm) indicates the captured and analyzed sub-region of the cortex. (C) The number of c-Fos+ cells in different sub-cortical areas. Note that the number of c-Fos+ cells was significantly elevated following 9-h fasting as compared to the control condition. Data are shown as mean ± SEM (Student’s t-test; ∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.001; n = 4–6 animals).

Fig 5: BRAF/MAPK/AP-1 axis promotes TBX3 transcription in PTC.a, b Western blot of TBX3 in PTC or normal thyroid cells (Nthy-ori-3-1) with BRAF or BRAFV600E over-expression (a) or K1 cells with BRAF knock-down (b). c K1 cells were treated with BRAF inhibitor PLX4032 or ERK1/2 inhibitor SCH772984 for 24 h, the level of TBX3 was analysis by western blot. d TBX3 and AP-1 factors levels in K1 cells over-expressing c-Jun, JunB, or c-Fos, and treated with PLX4032 or SCH772984. e TBX3 and AP-1 factors levels in K1 cells with BRAFV600E over-expression and AP-1 knock-down. f AP-1 binding motifs were analyzed through TBX3 promoter region using Jasper database. g Construction of TBX3 promoter GLuc with potential AP-1-binding sites. The predicted -358bp and -362bp site were overlapped as -360bp site. Arrows represented primers were used for qPCR. h, i Promoter GLuc activities were analyzed in HEK293T cells co-transfected with TBX3 truncated promoter (h) or TBX3-149-MUT promoter (i) and AP-1 expression constructs. j Quantitative ChIP (qChIP) analysis with anti-IgG, c-Jun, JunB and c-Fos for -149 site in K1 cells, primers targeting GAPDH gene were used as control. k Luciferase activities of GLuc-149 were analyzed in K1 cells treated with PLX4032 or SCH772984 for 12 h, 24 h or 36 h. l THCA datasets were downloaded from TCGA database to analyze the correlation between TBX3 and BRAF, n = 501. Densitometric analyses of western blot were shown (a–e). Two independent experiments were carried out with similar results for each kind of cells (a–c), and n = 3 biological independent samples (d, e, h–k). Data are shown as the mean ± s.d. (h–k). P values were calculated by unpaired two-tailed Student’s t test (h–k). Uncropped immunoblots and statistical source data are provided in Source Data.