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β galactosidase activity assay kit  (Sangon Biotech)
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Sangon Biotech β galactosidase activity assay kit
β Galactosidase Activity Assay Kit, supplied by Sangon Biotech, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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β galactosidase activity test  (Abbkine Inc)
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A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
β Galactosidase Activity Test, supplied by Abbkine Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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senescence detection  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc senescence detection
A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
Senescence Detection, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B2+galactosidase+activity/Senescence+beta-Galactosidase+Activity+Assay+Kit/pm41862889-73-20-25
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β galactosidase activity  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc β galactosidase activity
A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
β Galactosidase Activity, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B2+galactosidase+activity/Senescence+beta-Galactosidase+Staining+Kit/pm41683922-213-16-18
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sa β gal activity  (Cell Signaling Technology Inc)
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A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
Sa β Gal Activity, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/%CE%B2+galactosidase+activity/Senescence+beta-Galactosidase+Staining+Kit/bio_rxiv__64898__2026__02__05__703986-158-18-20
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sa β gal cellular senescence fluorometric assay kit  (Elabscience Biotechnology)
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A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
Sa β Gal Cellular Senescence Fluorometric Assay Kit, supplied by Elabscience Biotechnology, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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β galactosidase activity  (Valiant Co Ltd)
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A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
β Galactosidase Activity, supplied by Valiant Co Ltd, 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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positive β galactosidase activity  (Nikon)
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A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. <t>M</t> <t>β-Galactosidase</t> assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.
Positive β Galactosidase Activity, supplied by Nikon, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. M β-Galactosidase assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.

Journal: Oncogene

Article Title: CSF1R inhibitors mitigate CDK4/6 inhibitor-induced immunosuppression to increase antitumor immunity in HR+/HER2− breast cancer

doi: 10.1038/s41388-026-03786-w

Figure Lengend Snippet: A Pal alone did not directly modulate the polarization of PMA-induced THP-1-derived macrophages. B In mouse tumors, the IGF and FGF signaling pathways both presented a certain degree of increase among the top 30 conserved signaling pathways. C Ranking of cell communication received by macrophages revealed that Pal increased the strength of the ability of IGF to communicate with macrophages. D GSEA revealed that M2-like macrophages were enriched in the IGF1 pathway. E The probability of IGF and FGF communication between fibroblasts and M2-like macrophages was increased, whereas that between fibroblasts and M1-like macrophages was decreased. F Pal upregulated the expression of Igf1, Fgf7, Cdkn1a, Cdkn2a and Glb1, while downregulating Mki67 in mouse tumors (n = 4335). G ELISAanalysis revealed increased levels of IGF1 and FGF7 in fibroblasts from mouse tumor tissues . H Transcriptome analysis of the cell cycle revealed that Pal arrested fibroblasts in the G1 phase. I mIHC staining of mouse tumor tissues revealed that Pal suppressed Ki-67 expression in fibroblasts (a-SMA+Fap + ) and upregulated the senescence marker p16 (Veh: n = 3; Pal: n = 3). J mIHC analysis of HR⁺/HER2⁻ breast cancer tissues from patients treated with Pal also revealed reduced Ki-67 expression and increased P16 levels (Pre: n = 3; Post: n = 3). K ELISA results indicating that treatment of human primary mammary fibroblasts with Pal for four days upregulated the expression of IGF1 and FGF7. L Cell cycle analysis confirmed that Pal blocked the cell cycle of HMFs in the G1 phase. M β-Galactosidase assays indicated that Pal intervention caused senescence in human primary fibroblasts after four days ( n = 3). Veh: vehicle, Pal: palbociclib. The data are shown as the means ± SEMs. * P < 0.05, ** P < 0.01, *** P < 0.001, ns: not significant, t test, Welch’s one-way ANOVA and one-way ANOVA.

Article Snippet: Cellular senescence detection was accomplished using β-galactosidase activity test (KTA3030, Abbkine).

Techniques: Derivative Assay, Protein-Protein interactions, Expressing, Staining, Marker, Enzyme-linked Immunosorbent Assay, Cell Cycle Assay