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human ca3 (Santa Cruz Biotechnology)

Name: human ca3
Brand: Santa Cruz Biotechnology
Rating: 91 (4 reviews)

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Santa Cruz Biotechnology human ca3

Figure 4. Sqle activates de novo lipogenesis via <t>CA3</t> in NASH. (A) Silver staining results of co-IP by using Sqle tg mice liver protein. (B) The interaction between SQLE and CA3 was further conﬁrmed by using Sqle tg mice liver protein and commercial recombinant human SQLE and CA3 protein. (C) Direct binding of SQLE and CA3 were conﬁrmed using enzyme-linked immunosorbent assay. (D–E) Western blot analysis showed that SQLE stabilizes CA3 protein expression by inhibiting auto- phagy-lysosome–dependent protein degradation pathway. (F) CA3 overexpression increase intracellular Triglyceride level and protein expression of SREBP1C, FASN, and p- IkBa and p-P65 NF-kB subunit in LO2 and HKCI10 cells. (G) Silence CA3 expression reverse SQLE induced TG level and protein expression of FASN and p-P65. (H) Western blot analysis showed Acetazolamide reduced liver TG and protein expression of CA3 and reduced SQLE-induced protein expression of ACC, FASN, p-P65, and p- IkBa in SQLE-tg mice. (I) Western blot analysis showed that cholesterol treatment cannot increase Car3 protein expression. *P < .05; **P < .01, ***P < .001

Human Ca3, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 91/100, based on 4 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/human ca3/product/Santa Cruz Biotechnology
Average 91 stars, based on 4 article reviews

human ca3 - by Bioz Stars, 2026-02

91/100 stars

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1) Product Images from "Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target."

Article Title: Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target.

Journal: Gastroenterology

doi: 10.1053/j.gastro.2021.02.051

Figure 4. Sqle activates de novo lipogenesis via CA3 in NASH. (A) Silver staining results of co-IP by using Sqle tg mice liver protein. (B) The interaction between SQLE and CA3 was further conﬁrmed by using Sqle tg mice liver protein and commercial recombinant human SQLE and CA3 protein. (C) Direct binding of SQLE and CA3 were conﬁrmed using enzyme-linked immunosorbent assay. (D–E) Western blot analysis showed that SQLE stabilizes CA3 protein expression by inhibiting auto- phagy-lysosome–dependent protein degradation pathway. (F) CA3 overexpression increase intracellular Triglyceride level and protein expression of SREBP1C, FASN, and p- IkBa and p-P65 NF-kB subunit in LO2 and HKCI10 cells. (G) Silence CA3 expression reverse SQLE induced TG level and protein expression of FASN and p-P65. (H) Western blot analysis showed Acetazolamide reduced liver TG and protein expression of CA3 and reduced SQLE-induced protein expression of ACC, FASN, p-P65, and p- IkBa in SQLE-tg mice. (I) Western blot analysis showed that cholesterol treatment cannot increase Car3 protein expression. *P < .05; **P < .01, ***P < .001

Figure Legend Snippet: Figure 4. Sqle activates de novo lipogenesis via CA3 in NASH. (A) Silver staining results of co-IP by using Sqle tg mice liver protein. (B) The interaction between SQLE and CA3 was further conﬁrmed by using Sqle tg mice liver protein and commercial recombinant human SQLE and CA3 protein. (C) Direct binding of SQLE and CA3 were conﬁrmed using enzyme-linked immunosorbent assay. (D–E) Western blot analysis showed that SQLE stabilizes CA3 protein expression by inhibiting auto- phagy-lysosome–dependent protein degradation pathway. (F) CA3 overexpression increase intracellular Triglyceride level and protein expression of SREBP1C, FASN, and p- IkBa and p-P65 NF-kB subunit in LO2 and HKCI10 cells. (G) Silence CA3 expression reverse SQLE induced TG level and protein expression of FASN and p-P65. (H) Western blot analysis showed Acetazolamide reduced liver TG and protein expression of CA3 and reduced SQLE-induced protein expression of ACC, FASN, p-P65, and p- IkBa in SQLE-tg mice. (I) Western blot analysis showed that cholesterol treatment cannot increase Car3 protein expression. *P < .05; **P < .01, ***P < .001

Techniques Used: Silver Staining, Co-Immunoprecipitation Assay, Recombinant, Binding Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Over Expression

Figure 6. Pharmacologic inhibition of SQLE and CA3 synergistically ameliorated NASH development. (A) Schematic diagram of combined drug treatment in HFHC diet–induced mouse NASH model. Combined terbinaﬁne and acetazolamide treatment signiﬁcantly reduced liver weight and liver-to-body weight ratio. (B) Terbinaﬁne plus Acetazolamide abolished HFHC diet– induced accumulation of liver triglyceride, FFA, and TBARS, (C) and accumulation of serum triglyceride, ALT, and AST and improved glucose tolerance test and ITT. (D) Liver histology showed that combined terbinaﬁne plus acetazolamide syner- gistically attenuated steatohepatitis, lipid accumulation, and liver ﬁbrosis (**P < .01; ***P < .001 vs PBS group). (E) Serum IL1a, IL1b, IL6, IL17, MCP-1, MIP-1b, and TNF-a concentration of 4 groups. (F) Western blot analysis showed that combined drug treatment decreased p-P65 and p-IkBa in HFHC-fed WT mice. (G) qPCR analysis indicated that terbinaﬁne plus acetazolamide synergistically suppressed mRNA expression of genes involved in lipogenesis, triglyceride biosynthesis, and ﬁbrosis. Scale bars, 100 mm. *P < .05; **P < .01; ***P < .001.

Figure Legend Snippet: Figure 6. Pharmacologic inhibition of SQLE and CA3 synergistically ameliorated NASH development. (A) Schematic diagram of combined drug treatment in HFHC diet–induced mouse NASH model. Combined terbinaﬁne and acetazolamide treatment signiﬁcantly reduced liver weight and liver-to-body weight ratio. (B) Terbinaﬁne plus Acetazolamide abolished HFHC diet– induced accumulation of liver triglyceride, FFA, and TBARS, (C) and accumulation of serum triglyceride, ALT, and AST and improved glucose tolerance test and ITT. (D) Liver histology showed that combined terbinaﬁne plus acetazolamide syner- gistically attenuated steatohepatitis, lipid accumulation, and liver ﬁbrosis (**P < .01; ***P < .001 vs PBS group). (E) Serum IL1a, IL1b, IL6, IL17, MCP-1, MIP-1b, and TNF-a concentration of 4 groups. (F) Western blot analysis showed that combined drug treatment decreased p-P65 and p-IkBa in HFHC-fed WT mice. (G) qPCR analysis indicated that terbinaﬁne plus acetazolamide synergistically suppressed mRNA expression of genes involved in lipogenesis, triglyceride biosynthesis, and ﬁbrosis. Scale bars, 100 mm. *P < .05; **P < .01; ***P < .001.

Techniques Used: Inhibition, Concentration Assay, Western Blot, Expressing

Figure 7. SQLE is up-regulated in human NASH and serum SQLE/CA3 are novel biomarkers for the clinical diagnosis of NASH. (A) SQLE mRNA and (B) protein expression was up-regulated in patients with NAFLD. (C) Serum SQLE concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (D) Correlation analysis between serum SQLE and clinical information of patients with NAFLD. (E) Serum CA3 concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (F) Correlation analysis between serum CA3 and clinical information of patients with NAFLD. (G) Correlation analysis between serum SQLE and serum CA3 concentration in patients with NAFLD. (H) AUROC of combined serum SQLE and CA3 in discriminating NAFLD and NASH in all patients.

Figure Legend Snippet: Figure 7. SQLE is up-regulated in human NASH and serum SQLE/CA3 are novel biomarkers for the clinical diagnosis of NASH. (A) SQLE mRNA and (B) protein expression was up-regulated in patients with NAFLD. (C) Serum SQLE concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (D) Correlation analysis between serum SQLE and clinical information of patients with NAFLD. (E) Serum CA3 concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (F) Correlation analysis between serum CA3 and clinical information of patients with NAFLD. (G) Correlation analysis between serum SQLE and serum CA3 concentration in patients with NAFLD. (H) AUROC of combined serum SQLE and CA3 in discriminating NAFLD and NASH in all patients.

Techniques Used: Biomarker Discovery, Expressing, Concentration Assay

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Journal: Gastroenterology

Article Title: Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target.

doi: 10.1053/j.gastro.2021.02.051

Figure Lengend Snippet: Figure 4. Sqle activates de novo lipogenesis via CA3 in NASH. (A) Silver staining results of co-IP by using Sqle tg mice liver protein. (B) The interaction between SQLE and CA3 was further conﬁrmed by using Sqle tg mice liver protein and commercial recombinant human SQLE and CA3 protein. (C) Direct binding of SQLE and CA3 were conﬁrmed using enzyme-linked immunosorbent assay. (D–E) Western blot analysis showed that SQLE stabilizes CA3 protein expression by inhibiting auto- phagy-lysosome–dependent protein degradation pathway. (F) CA3 overexpression increase intracellular Triglyceride level and protein expression of SREBP1C, FASN, and p- IkBa and p-P65 NF-kB subunit in LO2 and HKCI10 cells. (G) Silence CA3 expression reverse SQLE induced TG level and protein expression of FASN and p-P65. (H) Western blot analysis showed Acetazolamide reduced liver TG and protein expression of CA3 and reduced SQLE-induced protein expression of ACC, FASN, p-P65, and p- IkBa in SQLE-tg mice. (I) Western blot analysis showed that cholesterol treatment cannot increase Car3 protein expression. *P < .05; **P < .01, ***P < .001

Article Snippet: SiRNA of human CA3 (sc-60309) and control (siCTL) were ordered from Santa Cruz (Dallas, USA).

Techniques: Silver Staining, Co-Immunoprecipitation Assay, Recombinant, Binding Assay, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Over Expression

Journal: Gastroenterology

Article Title: Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target.

doi: 10.1053/j.gastro.2021.02.051

Figure Lengend Snippet: Figure 6. Pharmacologic inhibition of SQLE and CA3 synergistically ameliorated NASH development. (A) Schematic diagram of combined drug treatment in HFHC diet–induced mouse NASH model. Combined terbinaﬁne and acetazolamide treatment signiﬁcantly reduced liver weight and liver-to-body weight ratio. (B) Terbinaﬁne plus Acetazolamide abolished HFHC diet– induced accumulation of liver triglyceride, FFA, and TBARS, (C) and accumulation of serum triglyceride, ALT, and AST and improved glucose tolerance test and ITT. (D) Liver histology showed that combined terbinaﬁne plus acetazolamide syner- gistically attenuated steatohepatitis, lipid accumulation, and liver ﬁbrosis (**P < .01; ***P < .001 vs PBS group). (E) Serum IL1a, IL1b, IL6, IL17, MCP-1, MIP-1b, and TNF-a concentration of 4 groups. (F) Western blot analysis showed that combined drug treatment decreased p-P65 and p-IkBa in HFHC-fed WT mice. (G) qPCR analysis indicated that terbinaﬁne plus acetazolamide synergistically suppressed mRNA expression of genes involved in lipogenesis, triglyceride biosynthesis, and ﬁbrosis. Scale bars, 100 mm. *P < .05; **P < .01; ***P < .001.

Article Snippet: SiRNA of human CA3 (sc-60309) and control (siCTL) were ordered from Santa Cruz (Dallas, USA).

Techniques: Inhibition, Concentration Assay, Western Blot, Expressing

Journal: Gastroenterology

Article Title: Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target.

doi: 10.1053/j.gastro.2021.02.051

Figure Lengend Snippet: Figure 7. SQLE is up-regulated in human NASH and serum SQLE/CA3 are novel biomarkers for the clinical diagnosis of NASH. (A) SQLE mRNA and (B) protein expression was up-regulated in patients with NAFLD. (C) Serum SQLE concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (D) Correlation analysis between serum SQLE and clinical information of patients with NAFLD. (E) Serum CA3 concentration in 72 healthy people, 65 patients with steatosis, and 80 patients with NASH. (F) Correlation analysis between serum CA3 and clinical information of patients with NAFLD. (G) Correlation analysis between serum SQLE and serum CA3 concentration in patients with NAFLD. (H) AUROC of combined serum SQLE and CA3 in discriminating NAFLD and NASH in all patients.

Article Snippet: SiRNA of human CA3 (sc-60309) and control (siCTL) were ordered from Santa Cruz (Dallas, USA).

Techniques: Biomarker Discovery, Expressing, Concentration Assay

Figure 3: A) Western blot analysis using Ca III and GAPDH antibodies, of whole cell protein extracts derived from both untransfected and transfected 3T3-L1 cells with Ca III siRNA. The positions of 27 kDa Ca III and 35 kDa GAPDH proteins are labeled. B) Histogram of percentage viability (MTT assay) of untransfected and transfected 3T3-L1 cells with Ca III siRNA in the presence or absence of 70 µM PK-11195. The columns

Journal: INTERNATIONAL RESEARCH JOURNAL OF PHARMACY

Article Title: PK-11195: A POTENTIAL DRUG IN LEUKEMIA TREATMENT

doi: 10.7897/2230-8407.050337

Figure Lengend Snippet: Figure 3: A) Western blot analysis using Ca III and GAPDH antibodies, of whole cell protein extracts derived from both untransfected and transfected 3T3-L1 cells with Ca III siRNA. The positions of 27 kDa Ca III and 35 kDa GAPDH proteins are labeled. B) Histogram of percentage viability (MTT assay) of untransfected and transfected 3T3-L1 cells with Ca III siRNA in the presence or absence of 70 µM PK-11195. The columns

Article Snippet: Anti-Ca III (P-17, sc-50715) and antiEvi1 (E-19, sc-54198), anti-GAPDH (V-18, sc-20357) and rabbit anti-goat IgG-HRP (sc-2768) antibodies and Ca III siRNA (sc-60310) were purchased from Santa Cruz Biotechnology, Inc. Caspase 3/7®Glo assay system (G8090) was purchased from Promega.

Techniques: Western Blot, Derivative Assay, Transfection, Labeling, MTT Assay

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1) Product Images from "Squalene Epoxidase Induces Nonalcoholic Steatohepatitis Via Binding to Carbonic Anhydrase III and is a Therapeutic Target."

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