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Proteintech rabbit anti cxcl12 pab
Rabbit Anti Cxcl12 Pab, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech cxcl12 proteintech 17402 1 ap
Cxcl12 Proteintech 17402 1 Ap, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti cxcl12
Anti Cxcl12, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech cxcl12
SPOCD1 activates the <t>CXCL12/CXCR4</t> signaling pathway in CAFs through LAMA4, and promotes epithelial-to-mesenchymal transition (EMT) in tumor cells. ( A ) Changes in the expression of chemokine CXCL family members after co-culturing SPOCD1 knockout CRC cells with CAFs. ( B ) Protein expression changes of chemokine CXCL12 in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( C ) Expression of CXCL12 in CAFs after co-culturing with SPOCD1-overexpressing CRC cells and treating with recombinant LAMA4 protein. ( D ) Detection of LAMA4 protein levels in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( E ) Immunofluorescence analysis of CAFs after co-cultured with CRC cells transfected with SPOCD1-EGFP fusion plasmid. ( F ) Detection of CXCL12 mRNA stability in CAFs treated with recombinant LAMA4. ( G ) Correlation between SPOCD1 expression and the activation of signaling pathways in CRC. ( H ) Co-culture of CAFs with either knockdown or overexpression of CXCL12 and CRC cells, followed by assessment of tumor cell EMT. ( I ) Liver metastasis in mice after SPOCD1 overexpression and blocking the CXCL12/CXCR4 pathway
Cxcl12, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech primary antibodies against cxcl12
SPOCD1 activates the <t>CXCL12/CXCR4</t> signaling pathway in CAFs through LAMA4, and promotes epithelial-to-mesenchymal transition (EMT) in tumor cells. ( A ) Changes in the expression of chemokine CXCL family members after co-culturing SPOCD1 knockout CRC cells with CAFs. ( B ) Protein expression changes of chemokine CXCL12 in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( C ) Expression of CXCL12 in CAFs after co-culturing with SPOCD1-overexpressing CRC cells and treating with recombinant LAMA4 protein. ( D ) Detection of LAMA4 protein levels in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( E ) Immunofluorescence analysis of CAFs after co-cultured with CRC cells transfected with SPOCD1-EGFP fusion plasmid. ( F ) Detection of CXCL12 mRNA stability in CAFs treated with recombinant LAMA4. ( G ) Correlation between SPOCD1 expression and the activation of signaling pathways in CRC. ( H ) Co-culture of CAFs with either knockdown or overexpression of CXCL12 and CRC cells, followed by assessment of tumor cell EMT. ( I ) Liver metastasis in mice after SPOCD1 overexpression and blocking the CXCL12/CXCR4 pathway
Primary Antibodies Against Cxcl12, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech cxcl12 polyclonal antibody
SPOCD1 activates the <t>CXCL12/CXCR4</t> signaling pathway in CAFs through LAMA4, and promotes epithelial-to-mesenchymal transition (EMT) in tumor cells. ( A ) Changes in the expression of chemokine CXCL family members after co-culturing SPOCD1 knockout CRC cells with CAFs. ( B ) Protein expression changes of chemokine CXCL12 in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( C ) Expression of CXCL12 in CAFs after co-culturing with SPOCD1-overexpressing CRC cells and treating with recombinant LAMA4 protein. ( D ) Detection of LAMA4 protein levels in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( E ) Immunofluorescence analysis of CAFs after co-cultured with CRC cells transfected with SPOCD1-EGFP fusion plasmid. ( F ) Detection of CXCL12 mRNA stability in CAFs treated with recombinant LAMA4. ( G ) Correlation between SPOCD1 expression and the activation of signaling pathways in CRC. ( H ) Co-culture of CAFs with either knockdown or overexpression of CXCL12 and CRC cells, followed by assessment of tumor cell EMT. ( I ) Liver metastasis in mice after SPOCD1 overexpression and blocking the CXCL12/CXCR4 pathway
Cxcl12 Polyclonal Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anti cxcl12 antibody
Fig. 2. Identification of DEPs in lung tissue of three groups of mice. Validation of <t>Cxcl12</t> and Mrp14 change trends in proteomics. (A) heatmap, (B) volcano: LPS vs Control, (C) volcano: LPS + hucMSCs vs LPS, (D) histogram (n = 4 mice/group). (E) Western blotting method was used to detect the changes of Cxcl2 and Mrp14 in different groups of lung tissues. Quantification results of Cxcl2 and Mrp14 can be seen in (F) and (G). (H) RNA levels of Cxcl12 in lung tissue (n = 3 mice/group). (I) Serum Cxcl12 levels in mice (n = 9 mice/group). (J) RNA levels of Mrp14 in lung tissue (n = 3 mice/group). (K) Serum Mrp14 levels in mice (n = 6 mice/group). All data are expressed as the mean ± standard deviation of three independent experiments. ***p < 0.001 versus the control group; #p < 0.05, ###p < 0.01 versus the LPS group.
Anti Cxcl12 Antibody, supplied by Proteintech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/anti cxcl12 antibody/product/Proteintech
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Cayman Chemical chrysin 17402
Fig. 2. Identification of DEPs in lung tissue of three groups of mice. Validation of <t>Cxcl12</t> and Mrp14 change trends in proteomics. (A) heatmap, (B) volcano: LPS vs Control, (C) volcano: LPS + hucMSCs vs LPS, (D) histogram (n = 4 mice/group). (E) Western blotting method was used to detect the changes of Cxcl2 and Mrp14 in different groups of lung tissues. Quantification results of Cxcl2 and Mrp14 can be seen in (F) and (G). (H) RNA levels of Cxcl12 in lung tissue (n = 3 mice/group). (I) Serum Cxcl12 levels in mice (n = 9 mice/group). (J) RNA levels of Mrp14 in lung tissue (n = 3 mice/group). (K) Serum Mrp14 levels in mice (n = 6 mice/group). All data are expressed as the mean ± standard deviation of three independent experiments. ***p < 0.001 versus the control group; #p < 0.05, ###p < 0.01 versus the LPS group.
Chrysin 17402, supplied by Cayman Chemical, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


SPOCD1 activates the CXCL12/CXCR4 signaling pathway in CAFs through LAMA4, and promotes epithelial-to-mesenchymal transition (EMT) in tumor cells. ( A ) Changes in the expression of chemokine CXCL family members after co-culturing SPOCD1 knockout CRC cells with CAFs. ( B ) Protein expression changes of chemokine CXCL12 in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( C ) Expression of CXCL12 in CAFs after co-culturing with SPOCD1-overexpressing CRC cells and treating with recombinant LAMA4 protein. ( D ) Detection of LAMA4 protein levels in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( E ) Immunofluorescence analysis of CAFs after co-cultured with CRC cells transfected with SPOCD1-EGFP fusion plasmid. ( F ) Detection of CXCL12 mRNA stability in CAFs treated with recombinant LAMA4. ( G ) Correlation between SPOCD1 expression and the activation of signaling pathways in CRC. ( H ) Co-culture of CAFs with either knockdown or overexpression of CXCL12 and CRC cells, followed by assessment of tumor cell EMT. ( I ) Liver metastasis in mice after SPOCD1 overexpression and blocking the CXCL12/CXCR4 pathway

Journal: Journal of Translational Medicine

Article Title: Cancer cell SPOCD1 promotes colorectal cancer liver metastasis by activating the CXCL12/CXCR4 signaling pathway in cancer-associated fibroblasts

doi: 10.1186/s12967-025-06863-y

Figure Lengend Snippet: SPOCD1 activates the CXCL12/CXCR4 signaling pathway in CAFs through LAMA4, and promotes epithelial-to-mesenchymal transition (EMT) in tumor cells. ( A ) Changes in the expression of chemokine CXCL family members after co-culturing SPOCD1 knockout CRC cells with CAFs. ( B ) Protein expression changes of chemokine CXCL12 in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( C ) Expression of CXCL12 in CAFs after co-culturing with SPOCD1-overexpressing CRC cells and treating with recombinant LAMA4 protein. ( D ) Detection of LAMA4 protein levels in CAFs after co-culturing with SPOCD1 knockout and overexpressing CRC cells. ( E ) Immunofluorescence analysis of CAFs after co-cultured with CRC cells transfected with SPOCD1-EGFP fusion plasmid. ( F ) Detection of CXCL12 mRNA stability in CAFs treated with recombinant LAMA4. ( G ) Correlation between SPOCD1 expression and the activation of signaling pathways in CRC. ( H ) Co-culture of CAFs with either knockdown or overexpression of CXCL12 and CRC cells, followed by assessment of tumor cell EMT. ( I ) Liver metastasis in mice after SPOCD1 overexpression and blocking the CXCL12/CXCR4 pathway

Article Snippet: Antibodies against α-SMA (14395-1-AP, 1:1000), CXCL12 (17402-1-AP, 1:1000), DNMT1 (24206-1-AP, 1:1000), and β-actin (20536-1-AP, 1:5000) were sourced from Proteintech.

Techniques: Expressing, Knock-Out, Recombinant, Immunofluorescence, Cell Culture, Transfection, Plasmid Preparation, Activation Assay, Protein-Protein interactions, Co-Culture Assay, Knockdown, Over Expression, Blocking Assay

A schematic diagram of mechanism of SPOCD1 promotes colorectal cancer liver metastasis by activating the CXCL12/CXCR4 signaling pathway in cancer-associated fibroblasts

Journal: Journal of Translational Medicine

Article Title: Cancer cell SPOCD1 promotes colorectal cancer liver metastasis by activating the CXCL12/CXCR4 signaling pathway in cancer-associated fibroblasts

doi: 10.1186/s12967-025-06863-y

Figure Lengend Snippet: A schematic diagram of mechanism of SPOCD1 promotes colorectal cancer liver metastasis by activating the CXCL12/CXCR4 signaling pathway in cancer-associated fibroblasts

Article Snippet: Antibodies against α-SMA (14395-1-AP, 1:1000), CXCL12 (17402-1-AP, 1:1000), DNMT1 (24206-1-AP, 1:1000), and β-actin (20536-1-AP, 1:5000) were sourced from Proteintech.

Techniques:

Fig. 2. Identification of DEPs in lung tissue of three groups of mice. Validation of Cxcl12 and Mrp14 change trends in proteomics. (A) heatmap, (B) volcano: LPS vs Control, (C) volcano: LPS + hucMSCs vs LPS, (D) histogram (n = 4 mice/group). (E) Western blotting method was used to detect the changes of Cxcl2 and Mrp14 in different groups of lung tissues. Quantification results of Cxcl2 and Mrp14 can be seen in (F) and (G). (H) RNA levels of Cxcl12 in lung tissue (n = 3 mice/group). (I) Serum Cxcl12 levels in mice (n = 9 mice/group). (J) RNA levels of Mrp14 in lung tissue (n = 3 mice/group). (K) Serum Mrp14 levels in mice (n = 6 mice/group). All data are expressed as the mean ± standard deviation of three independent experiments. ***p < 0.001 versus the control group; #p < 0.05, ###p < 0.01 versus the LPS group.

Journal: Microvascular research

Article Title: Proteomics suggests the role of Cxcl12 secreted by hucMSCs in the treatment of lipopolysaccharide-acute lung injury.

doi: 10.1016/j.mvr.2025.104815

Figure Lengend Snippet: Fig. 2. Identification of DEPs in lung tissue of three groups of mice. Validation of Cxcl12 and Mrp14 change trends in proteomics. (A) heatmap, (B) volcano: LPS vs Control, (C) volcano: LPS + hucMSCs vs LPS, (D) histogram (n = 4 mice/group). (E) Western blotting method was used to detect the changes of Cxcl2 and Mrp14 in different groups of lung tissues. Quantification results of Cxcl2 and Mrp14 can be seen in (F) and (G). (H) RNA levels of Cxcl12 in lung tissue (n = 3 mice/group). (I) Serum Cxcl12 levels in mice (n = 9 mice/group). (J) RNA levels of Mrp14 in lung tissue (n = 3 mice/group). (K) Serum Mrp14 levels in mice (n = 6 mice/group). All data are expressed as the mean ± standard deviation of three independent experiments. ***p < 0.001 versus the control group; #p < 0.05, ###p < 0.01 versus the LPS group.

Article Snippet: LPS (L2880, Escherichia coli O55: B5, Sigma), anti-Cxcl12 antibody (17402-1-AP, Proteintech), anti-Mrp14 antibody (269992-1-AP, Proteintech), anti-β- actin (20536-1-AP, Proteintech), Mouse Cxcl12 ELISA Kit (ab100741, Abcam), Mouse Mrp14 ELISA Kit (EK1152, Boster).

Techniques: Biomarker Discovery, Control, Western Blot, Standard Deviation

Fig. 3. Effect of silencing Cxcl12 on the therapeutic effect of hucMSCs. (A) Western Blot detection of Cxcl12 expression in hucMSCs and shCxcl12 hucMSCs to verify the silencing efficiency. (B) Hematoxylin and eosin (HE) staining of lung tissues (200× magnification, scale bar: 50 μm). (C) Lung injury score. (D) The lung coefficient was utilized to assess the degree of lung edema. (E, F) Pulmonary vascular permeability were assessed by tail vein injection of FITC-dextran and Evans blue. (G, H) The transendothelial FITC-albumin permeability was detected and the transendothelial resistance reflected the permeability of endothelial cells by constructing the co-culture system of endothelial cells and hucMSCs. (All groups, n = 6 mice/group). ***p < 0.001 versus the control group; ##p < 0.01 versus the LPS group; ɎɎp < 0.01versus the sh Cxcl12 hucMSCs group.

Journal: Microvascular research

Article Title: Proteomics suggests the role of Cxcl12 secreted by hucMSCs in the treatment of lipopolysaccharide-acute lung injury.

doi: 10.1016/j.mvr.2025.104815

Figure Lengend Snippet: Fig. 3. Effect of silencing Cxcl12 on the therapeutic effect of hucMSCs. (A) Western Blot detection of Cxcl12 expression in hucMSCs and shCxcl12 hucMSCs to verify the silencing efficiency. (B) Hematoxylin and eosin (HE) staining of lung tissues (200× magnification, scale bar: 50 μm). (C) Lung injury score. (D) The lung coefficient was utilized to assess the degree of lung edema. (E, F) Pulmonary vascular permeability were assessed by tail vein injection of FITC-dextran and Evans blue. (G, H) The transendothelial FITC-albumin permeability was detected and the transendothelial resistance reflected the permeability of endothelial cells by constructing the co-culture system of endothelial cells and hucMSCs. (All groups, n = 6 mice/group). ***p < 0.001 versus the control group; ##p < 0.01 versus the LPS group; ɎɎp < 0.01versus the sh Cxcl12 hucMSCs group.

Article Snippet: LPS (L2880, Escherichia coli O55: B5, Sigma), anti-Cxcl12 antibody (17402-1-AP, Proteintech), anti-Mrp14 antibody (269992-1-AP, Proteintech), anti-β- actin (20536-1-AP, Proteintech), Mouse Cxcl12 ELISA Kit (ab100741, Abcam), Mouse Mrp14 ELISA Kit (EK1152, Boster).

Techniques: Western Blot, Expressing, Staining, Permeability, Injection, Co-Culture Assay, Control