antibodies against echs1  (Proteintech)

Journal: Journal of Translational Autoimmunity

Article Title: Downregulated ECHS1 and HADH-mediated fatty acid β-oxidation contributes to mitochondrial dysfunction in salivary glands of Sjögren's syndrome

doi: 10.1016/j.jtauto.2026.100350

Figure Lengend Snippet: Bioinformatic analysis of transcriptome DEGs and mitochondria-related genes, and validation of MR-DEG hub genes using the GEO database. (A) Venn diagram showing the intersection of transcriptome DEGs and mitochondria-related genes. (B) KEGG enrichment analysis of MR-DEGs. (C) GO functional annotation of MR-DEGs. (D) PPI network analysis for screening hub genes. (E, F) RNA expression of hub genes ECHS1, HADH, ACADM, ACACA, FASN, and ACLY in the public GEO dataset ( GSE40611 ). P-values: Healthy control vs. SS group: ECHS1 ( P < 0.01), HADH ( P < 0.01), ACADM ( P = 0.4579), ACACA ( P = 0.2790), FASN ( P = 0.7094), ACLY ( P = 0.2003); SS group vs. non-SS control group: ECHS1 ( P < 0.0001), HADH ( P < 0.0001), ACADM ( P < 0.05), ACACA ( P < 0.0001), FASN ( P = 0.0688), ACLY ( P < 0.01). Only ECHS1 and HADH showed significant differences in both comparison sets.

Article Snippet: After blocking, the sections were incubated with primary antibodies against ECHS1 (11305-1-AP, Proteintech, China, 1:100 dilution) and HADH (HA601203-50, HuaAn Biotechnology, China, 1:200 dilution) at 4 °C overnight.

Techniques: Biomarker Discovery, Functional Assay, RNA Expression, Control, Comparison

Journal: Journal of Translational Autoimmunity

Article Title: Downregulated ECHS1 and HADH-mediated fatty acid β-oxidation contributes to mitochondrial dysfunction in salivary glands of Sjögren's syndrome

doi: 10.1016/j.jtauto.2026.100350

Figure Lengend Snippet: Validation of ECHS1 and HADH expression in human and mouse salivary glands. (A) Representative immunofluorescence images of ECHS1 and HADH in salivary glands of non-SS controls (40x). (B) Representative immunofluorescence images of ECHS1 and HADH in salivary glands of SS patients (40x). (C) PCR statistical results for ECHS1 in ICR-control vs. NOD mouse salivary glands ( n = 5 , P < 0.01). (D) PCR statistical results for HADH in ICR-control vs. NOD mouse salivary glands ( n = 5 , P < 0.01). (E) Statistical results of mean fluorescence intensity for ECHS1 in non-SS controls vs. SS patients ( n = 6 , P < 0.001). (F) Statistical results of mean fluorescence intensity for HADH in non-SS controls vs. SS patients ( n = 6 , P < 0.0001).

Article Snippet: After blocking, the sections were incubated with primary antibodies against ECHS1 (11305-1-AP, Proteintech, China, 1:100 dilution) and HADH (HA601203-50, HuaAn Biotechnology, China, 1:200 dilution) at 4 °C overnight.

Techniques: Biomarker Discovery, Expressing, Immunofluorescence, Control, Fluorescence

Journal: OncoTargets and Therapy

Article Title: The Expression and Clinical Significance of ALDOA in Breast Cancer

doi: 10.2147/OTT.S518473

Figure Lengend Snippet: ALDOA expression in human BC tissues. ( A ) ALDOA expression in tumor and normal tissues in TIMER database. ( B – D ) ALDOA expression in BC tumor and normal tissues in bc‐GenExMiner v5.1 ( B ), UALCAN ( C ) and GEPIA ( D ) databases. ( E ) Representative IHC staining of ALDOA in human BC tissues and normal tissues. ( F ) Analysis of ALDOA IHC scores in human BC tissues and normal tissues. *** P < 0.001.

Article Snippet: Following defined procedures, the paraffin-embedded tissues were sectioned to a thickness of 5 μm, incubated at 4°C overnight with a monoclonal human ALDOA antibody (dilution 1:100; #11305-1-AP, Proteintech), stained using a staining kit (Zhongshan Biotechnology, Bei-jing, China), followed by visualization.

Techniques: Expressing, Immunohistochemistry