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SIRT1 inhibited <t>GOT1</t> enzyme activity by catalyzing its lysine deacetylation. A The concentration of Asp in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). B The concentration of malate in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). C The activity of GOT1 in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). D The subcellular localization of SIRT1 and GOT1 in primary osteoblasts. E The protein level and Kac level of GOT1 upon Sirt1 deletion or overexpression in 3T3E1 cells. F The Kac level of GOT1 in Sirt1 knockout 3T3E1 cells upon Sirt1 overexpression. G The Kac level of GOT1 in 3T3E1 cells treated with SRT2104 or EX-527. H The Kac level of GOT1 protein immunoprecipitated from 3T3E1 cells transfected with SIRT1 plasmids or mutant SIRT1-H355A plasmids. I Control and Sirt1 knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The Kac level of GOT1 protein immunoprecipitated from the above cells. J Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The GOT1 activity was measured in the above cells. K Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of F6P in glycolysis were measured in the above cells. L Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of PEP in glycolysis were measured in the above cells. M Sirt1-knockout/Got1- knockout 3T3E1 cells were infected with Wild-type GOT1 or GOT1-K318R mutant virus. The ALP staining of osteoblast mineralization was conducted in the above cells. Data are presented as the mean ± SD, Student’s t test (a, b, c); one-way ANOVA with Tukey’s test (j, k, l), *P < 0.05, **P < 0.01, ***P < 0.001
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SIRT1 inhibited GOT1 enzyme activity by catalyzing its lysine deacetylation. A The concentration of Asp in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). B The concentration of malate in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). C The activity of GOT1 in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). D The subcellular localization of SIRT1 and GOT1 in primary osteoblasts. E The protein level and Kac level of GOT1 upon Sirt1 deletion or overexpression in 3T3E1 cells. F The Kac level of GOT1 in Sirt1 knockout 3T3E1 cells upon Sirt1 overexpression. G The Kac level of GOT1 in 3T3E1 cells treated with SRT2104 or EX-527. H The Kac level of GOT1 protein immunoprecipitated from 3T3E1 cells transfected with SIRT1 plasmids or mutant SIRT1-H355A plasmids. I Control and Sirt1 knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The Kac level of GOT1 protein immunoprecipitated from the above cells. J Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The GOT1 activity was measured in the above cells. K Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of F6P in glycolysis were measured in the above cells. L Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of PEP in glycolysis were measured in the above cells. M Sirt1-knockout/Got1- knockout 3T3E1 cells were infected with Wild-type GOT1 or GOT1-K318R mutant virus. The ALP staining of osteoblast mineralization was conducted in the above cells. Data are presented as the mean ± SD, Student’s t test (a, b, c); one-way ANOVA with Tukey’s test (j, k, l), *P < 0.05, **P < 0.01, ***P < 0.001

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: SIRT1 maintains bone homeostasis by regulating osteoblast glycolysis through GOT1

doi: 10.1007/s00018-023-05043-9

Figure Lengend Snippet: SIRT1 inhibited GOT1 enzyme activity by catalyzing its lysine deacetylation. A The concentration of Asp in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). B The concentration of malate in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). C The activity of GOT1 in the femurs of the control and cKO mice aged 8 weeks measured by an ELISA Kit (n = 8/group). D The subcellular localization of SIRT1 and GOT1 in primary osteoblasts. E The protein level and Kac level of GOT1 upon Sirt1 deletion or overexpression in 3T3E1 cells. F The Kac level of GOT1 in Sirt1 knockout 3T3E1 cells upon Sirt1 overexpression. G The Kac level of GOT1 in 3T3E1 cells treated with SRT2104 or EX-527. H The Kac level of GOT1 protein immunoprecipitated from 3T3E1 cells transfected with SIRT1 plasmids or mutant SIRT1-H355A plasmids. I Control and Sirt1 knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The Kac level of GOT1 protein immunoprecipitated from the above cells. J Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The GOT1 activity was measured in the above cells. K Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of F6P in glycolysis were measured in the above cells. L Sirt1-knockout/Got1- knockout 3T3E1 cells were transfected with Wild-type GOT1 or GOT1-K318R mutant plasmids. The levels of PEP in glycolysis were measured in the above cells. M Sirt1-knockout/Got1- knockout 3T3E1 cells were infected with Wild-type GOT1 or GOT1-K318R mutant virus. The ALP staining of osteoblast mineralization was conducted in the above cells. Data are presented as the mean ± SD, Student’s t test (a, b, c); one-way ANOVA with Tukey’s test (j, k, l), *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: To inhibit the activity of GOT1, mice aged 8 weeks were treated with vehicle (saline) and/or 10 mg/kg aminooxyacetic acid (AOA) (MedChemExpress, HY-107994) every other day until dissection at 16 weeks, and osteoblasts were treated with vehicle or 100 μM AOA for 48 h.

Techniques: Activity Assay, Concentration Assay, Control, Enzyme-linked Immunosorbent Assay, Over Expression, Knock-Out, Immunoprecipitation, Transfection, Mutagenesis, Infection, Virus, Staining

SIRT1 affected the acetylation level of GOT1 and glycolysis to regulate bone mass. A Schematic of experimental design. The 8-week cKO mice treated with vehicle or AOA until dissection at 16 weeks. B GOT1 activity of 16-week cKO mice treated with vehicle or AOA (n = 8/group). C The concentration of Asp in 16-week cKO mice treated with vehicle or AOA (n = 8/group). D The concentration of malate in 16-week cKO mice treated with vehicle or AOA (n = 8/group). E Representative micro-CT images of the femurs in 16-week cKO mice treated with vehicle or AOA. F Quantification of the BV/TV, Tb.N, Tb.Th, and Tb.Sp from the distal femurs in 16-week cKO mice treated with vehicle or AOA (n = 7/group). G Quantification of the metabolites in glycolysis after AOA treatment in 16-week cKO mice (n = 8/group). H Relative mRNA expression of Runx2, Col1a1, Alpl, and Bglap in Sirt1KO osteoblasts treated with vehicle or AOA (n = 6/group). I Representative images of ALP staining of Sirt1KO osteoblasts treated with vehicle or AOA. J Representative images of Alizarin Red S staining of Sirt1KO osteoblasts treated with vehicle or AOA. K Quantification of caspase-3 activity in Sirt1KO osteoblasts treated with vehicle or AOA (n = 6/group). BV/TV: bone volume fraction; Tb.Th: trabecular thickness; Tb.N: trabecular number; Tb.Sp: trabecular separation; Cort.Th: cortical bone thickness; Tt.Ar: total cortical bone area. Data are presented as the mean ± SD, Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: SIRT1 maintains bone homeostasis by regulating osteoblast glycolysis through GOT1

doi: 10.1007/s00018-023-05043-9

Figure Lengend Snippet: SIRT1 affected the acetylation level of GOT1 and glycolysis to regulate bone mass. A Schematic of experimental design. The 8-week cKO mice treated with vehicle or AOA until dissection at 16 weeks. B GOT1 activity of 16-week cKO mice treated with vehicle or AOA (n = 8/group). C The concentration of Asp in 16-week cKO mice treated with vehicle or AOA (n = 8/group). D The concentration of malate in 16-week cKO mice treated with vehicle or AOA (n = 8/group). E Representative micro-CT images of the femurs in 16-week cKO mice treated with vehicle or AOA. F Quantification of the BV/TV, Tb.N, Tb.Th, and Tb.Sp from the distal femurs in 16-week cKO mice treated with vehicle or AOA (n = 7/group). G Quantification of the metabolites in glycolysis after AOA treatment in 16-week cKO mice (n = 8/group). H Relative mRNA expression of Runx2, Col1a1, Alpl, and Bglap in Sirt1KO osteoblasts treated with vehicle or AOA (n = 6/group). I Representative images of ALP staining of Sirt1KO osteoblasts treated with vehicle or AOA. J Representative images of Alizarin Red S staining of Sirt1KO osteoblasts treated with vehicle or AOA. K Quantification of caspase-3 activity in Sirt1KO osteoblasts treated with vehicle or AOA (n = 6/group). BV/TV: bone volume fraction; Tb.Th: trabecular thickness; Tb.N: trabecular number; Tb.Sp: trabecular separation; Cort.Th: cortical bone thickness; Tt.Ar: total cortical bone area. Data are presented as the mean ± SD, Student’s t test; *P < 0.05, **P < 0.01, ***P < 0.001

Article Snippet: To inhibit the activity of GOT1, mice aged 8 weeks were treated with vehicle (saline) and/or 10 mg/kg aminooxyacetic acid (AOA) (MedChemExpress, HY-107994) every other day until dissection at 16 weeks, and osteoblasts were treated with vehicle or 100 μM AOA for 48 h.

Techniques: Dissection, Activity Assay, Concentration Assay, Micro-CT, Expressing, Staining

Schematic diagram of SIRT1 deacetylating GOT1 to regulate glycolysis in osteoblasts. SIRT1 deletion induced acetylation of GOT1, thereby inhibited the process of glycolysis to decrease bone formation by osteoblasts. The decreased bone formation then inhibited bone resorption. Thus, bone mass decreased

Journal: Cellular and Molecular Life Sciences: CMLS

Article Title: SIRT1 maintains bone homeostasis by regulating osteoblast glycolysis through GOT1

doi: 10.1007/s00018-023-05043-9

Figure Lengend Snippet: Schematic diagram of SIRT1 deacetylating GOT1 to regulate glycolysis in osteoblasts. SIRT1 deletion induced acetylation of GOT1, thereby inhibited the process of glycolysis to decrease bone formation by osteoblasts. The decreased bone formation then inhibited bone resorption. Thus, bone mass decreased

Article Snippet: To inhibit the activity of GOT1, mice aged 8 weeks were treated with vehicle (saline) and/or 10 mg/kg aminooxyacetic acid (AOA) (MedChemExpress, HY-107994) every other day until dissection at 16 weeks, and osteoblasts were treated with vehicle or 100 μM AOA for 48 h.

Techniques: