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CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and <t>STAT1</t> . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
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CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and <t>STAT1</t> . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
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CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and <t>STAT1</t> . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).
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Co-expression of EspF and ANXA6 decreases the expression level of LC3B-II and may contribute to autophagy regulation via the PI3K/AKT/mTOR pathway. (A) The expression levels of ANXA6, LC3B, and key proteins involved in PI3K/AKT/mTOR signaling in HeLa cells with and without plasmid transfection. (B–H) Expression level of LC3B-II, p-AKT and AKT, <t>p-p85α</t> and p85α, and p-mTOR and mTOR in HeLa cells. Legends indicate non-transfected cells (N), cells transfected with pEGFP (E), cells transfected with pEGFP-EspF (EE), and cells transfected with pEYFP-EspF-T2A-ANXA6 (EYEA). * Significant difference. * p < 0.05.
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Co-expression of EspF and ANXA6 decreases the expression level of LC3B-II and may contribute to autophagy regulation via the PI3K/AKT/mTOR pathway. (A) The expression levels of ANXA6, LC3B, and key proteins involved in PI3K/AKT/mTOR signaling in HeLa cells with and without plasmid transfection. (B–H) Expression level of LC3B-II, p-AKT and AKT, <t>p-p85α</t> and p85α, and p-mTOR and mTOR in HeLa cells. Legends indicate non-transfected cells (N), cells transfected with pEGFP (E), cells transfected with pEGFP-EspF (EE), and cells transfected with pEYFP-EspF-T2A-ANXA6 (EYEA). * Significant difference. * p < 0.05.
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CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

Journal: Animal Bioscience

Article Title: Transcriptomic analysis identifies CXCL12 as a novel candidate gene for litter size in rabbits

doi: 10.5713/ab.24.0640

Figure Lengend Snippet: CXCL12 and its receptor CXCR4 were expressed and localized in the ovary, with their binding activating the JAK/STAT signaling pathway. (A) Immunofluorescence staining of ovarian follicles revealed that CXCL12 was co-localized with its receptor CXCR4 in ovarian follicles. (B) CXCL12 overexpression significantly promoted the expression of CXCR4 , JAK2 and STAT1 . (C) Knocking down CXCL12 significantly inhibited the expression of CXCR4 , JAK2 and STAT1 . (D) CXCL12 overexpression in GCs promoted the protein expression of CXCR4, JAK2 and STAT1 as well as the phosphorylation of JAK2 and STAT1. When CXCL12 was knocked down, the results were reversed. (E) MSX-122 inhibitor-based treatment further confirmed that CXCL12 promoted the total protein and phosphorylation levels of JAK2 and STAT1 (The t test was used for the above analyses comparing two individual samples. * p<0.05; ** p<0.01; *** p<0.001).

Article Snippet: Protein detection was achieved using the following antibodies: anti-CCND1 mouse monoclonal antibody (1:250, Proteintech), anti-PCNA rabbit polyclonal antibody (1:250, Proteintech), anti-Bcl2 rabbit polyclonal antibody (1:250, Proteintech), anti-Bax rabbit polyclonal antibody (1:250, Proteintech), anti-CITED1 rabbit polyclonal antibody (1:50, Proteintech), anti-WNT10B mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-CXCR4 mouse monoclonal polyclonal antibody (1:250, Proteintech), anti-phospho-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam, Cambridge, UK), anti-JAK2 rabbit monoclonal polyclonal antibody (1:250, Abcam), anti-phospho-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-STAT1 rabbit polyclonal antibody (1:250, Proteintech), anti-GAPDH mouse monoclonal antibody (1:2,500, Proteintech), 1:1,000 goat anti-rabbit secondary antibody IgG (Proteintech) and 1:1,000 goat anti-mouse secondary antibody IgG (Proteintech).

Techniques: Binding Assay, Immunofluorescence, Staining, Over Expression, Expressing, Phospho-proteomics

Co-expression of EspF and ANXA6 decreases the expression level of LC3B-II and may contribute to autophagy regulation via the PI3K/AKT/mTOR pathway. (A) The expression levels of ANXA6, LC3B, and key proteins involved in PI3K/AKT/mTOR signaling in HeLa cells with and without plasmid transfection. (B–H) Expression level of LC3B-II, p-AKT and AKT, p-p85α and p85α, and p-mTOR and mTOR in HeLa cells. Legends indicate non-transfected cells (N), cells transfected with pEGFP (E), cells transfected with pEGFP-EspF (EE), and cells transfected with pEYFP-EspF-T2A-ANXA6 (EYEA). * Significant difference. * p < 0.05.

Journal: AIMS Microbiology

Article Title: Enterohemorrhagic Escherichia coli targets Annexin A6 and ATG16L1 to inhibit autophagy and induce inflammation

doi: 10.3934/microbiol.2025044

Figure Lengend Snippet: Co-expression of EspF and ANXA6 decreases the expression level of LC3B-II and may contribute to autophagy regulation via the PI3K/AKT/mTOR pathway. (A) The expression levels of ANXA6, LC3B, and key proteins involved in PI3K/AKT/mTOR signaling in HeLa cells with and without plasmid transfection. (B–H) Expression level of LC3B-II, p-AKT and AKT, p-p85α and p85α, and p-mTOR and mTOR in HeLa cells. Legends indicate non-transfected cells (N), cells transfected with pEGFP (E), cells transfected with pEGFP-EspF (EE), and cells transfected with pEYFP-EspF-T2A-ANXA6 (EYEA). * Significant difference. * p < 0.05.

Article Snippet: polyclonal rabbit anti-Phospho-PI3 Kinase p85α , Bioss , 3332 , 1:1000.

Techniques: Expressing, Plasmid Preparation, Transfection