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CXCL12 and its <t>receptor</t> <t>CXCR4</t> 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).
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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

CXCL12 targets the receptor CXCR4 to activate the JAK/STAT signaling pathway and regulate the expression of related genes.

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 targets the receptor CXCR4 to activate the JAK/STAT signaling pathway and regulate the expression of related genes.

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: Expressing

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: These samples were then treated with 0.3% TritonX-100 (Beyotime) and 1% bovine serum albumin (Sigma, St. Louis, MO, USA) for 60 min prior to overnight incubation at 4°C with the following primary antibodies: anti-CXCL12 rabbit polyclonal antibody (1:250, Proteintech, Wuhan, China) and anti-CXCR4 rabbit polyclonal antibody (1:250, Proteintech).

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

CXCL12 targets the receptor CXCR4 to activate the JAK/STAT signaling pathway and regulate the expression of related genes.

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 targets the receptor CXCR4 to activate the JAK/STAT signaling pathway and regulate the expression of related genes.

Article Snippet: These samples were then treated with 0.3% TritonX-100 (Beyotime) and 1% bovine serum albumin (Sigma, St. Louis, MO, USA) for 60 min prior to overnight incubation at 4°C with the following primary antibodies: anti-CXCL12 rabbit polyclonal antibody (1:250, Proteintech, Wuhan, China) and anti-CXCR4 rabbit polyclonal antibody (1:250, Proteintech).

Techniques: Expressing

Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma

Journal: BMC Oral Health

Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

doi: 10.1186/s12903-025-07544-4

Figure Lengend Snippet: Prediction of CXCR4-associated biological processes in the OSCC. A The differentially expressing genes in the OSCC were identified by the R software and presented as volcano plots. B The CXCR4-associated biological processes were presented by the bubble plot. CXCR4, C-X-C chemokine receptor type 4; OSCC, oral squamous cell carcinoma

Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

Techniques: Expressing, Software

Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

Journal: BMC Oral Health

Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

doi: 10.1186/s12903-025-07544-4

Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the bone resorption degree by HSC-3 cells in vivo. A The effect of CXCR4 inhibitor on bone resorption by HSC-3 in vivo was examined using µCT. B - H Semi-quantification of bone resorption degree according to different indicators. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

Techniques: In Vivo, Standard Deviation

Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase

Journal: BMC Oral Health

Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

doi: 10.1186/s12903-025-07544-4

Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the activation of osteoclasts in the microenvironment of HSC-3 in vivo. A H&E staining was used to present the histological findings in the different groups. B TRAP staining was used to present the TRAP-positive cells in the different groups. C Quantification of TRAP-positive cells in different groups. Black arrow indicated the TRAP-positive cells. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. ** P < 0.01. CXCR4, C-X-C chemokine receptor type 4; TRAP, tartrate-resistant acid phosphatase

Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

Techniques: Activation Assay, In Vivo, Staining, Standard Deviation

Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

Journal: BMC Oral Health

Article Title: Inhibition of CXCR4 suppresses bone invasion in a murine model of oral squamous cell carcinoma

doi: 10.1186/s12903-025-07544-4

Figure Lengend Snippet: Examination of the effect of the CXCR4 inhibitor on the invasion and migration of HSC-3 cells in vivo. A , C , E and G Immunohistochemical staining was used to test the expression of CXCR4 ( A ), MMP9 ( C ), Snail ( E ) and vimentin ( G ) in the HSC-3 in vivo. B , D , F and H Semi-quantification of CXCR4 ( B ), MMP9 ( D ), Snail ( F ) and vimentin ( H ) expression in different groups. Data are shown as mean ± standard deviation and analyzed using the unpaired student’s t-test. * P < 0.05. CXCR4, C-X-C chemokine receptor type 4

Article Snippet: The sections were then incubated with primary antibodies against CXCR4 (Bioss, cat. no. bs-20317R), MMP9 (Bioss, cat. no. bs-4593R), Snail (Bioss, cat. no. bs-1371R) and Vimentin (Bioss, cat. no. bs-0756R) in 4 ̊C overnight.

Techniques: Migration, In Vivo, Immunohistochemical staining, Staining, Expressing, Standard Deviation