Human APOC2 ELISA
- Known as:
- Human APOC2 Enzyme-linked immunosorbent assay test
- Catalog number:
- kt-7424
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Kamiya biomedical company
- Gene target:
- Human APOC2 ELISA
Related genes to: Human APOC2 ELISA
- Gene:
- APOC2 NIH gene
- Name:
- apolipoprotein C2
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 19q13.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-06-22
- Date modifiied:
- 2016-10-05
Related products to: Human APOC2 ELISA
Related articles to: Human APOC2 ELISA
- Triple-negative breast cancer (TNBC) is an aggressive breast cancer subtype characterized by an immunosuppressive tumor microenvironment and resistance to chemotherapy. Previous studies have indicated that apolipoprotein C-II (APOC2) is involved in the immune microenvironment of several malignancies and is upregulated in breast cancer; however, the molecular mechanisms through which APOC2 regulates the immune microenvironment in TNBC remain poorly understood. In the present study, we found that APOC2 was upregulated in TNBC tissues and was negatively correlated with M1 macrophage infiltration. APOC2 overexpression in 4 T1 cells promoted tumor progression by enhancing cell proliferation, migration, and invasion, while suppressing M1 macrophage polarization. In addition, KLHL1, a substrate adaptor for the Cullin3-RING E3 ubiquitin ligase complex, was found to interact with APOC2, and KLHL1 overexpression reversed the biological effects induced by APOC2. Mechanistically, KLHL1 promoted APOC2 protein degradation through the ubiquitin-proteasome pathway, thereby enhancing M1 macrophage polarization and suppressing the malignant behavior of tumor cells. Finally, in vivo xenograft experiments demonstrated that APOC2 reduced M1 macrophage polarization and increased tumor weight and volume, whereas KLHL1 overexpression counteracted the oncogenic effects of APOC2. Collectively, these findings reveal that activation of the KLHL1/APOC2 axis enhances M1 macrophage polarization and inhibits TNBC progression, providing novel insights into the immune regulatory mechanisms underlying TNBC development. - Source: PubMed
Publication date: 2026/08/14
He ZiranZhang ZhenhuaDing LiLong ShanYang LiuHu CeLong MengXueLiu Zhiqiang - Data on the interaction between dietary patterns, single nucleotide polymorphisms (SNPs), and cardiometabolic markers remain limited in genetically admixed populations, particularly among individuals with established cardiovascular disease (CVD). This study aimed to evaluate how SNPs modulate the effects of dietary interventions on apolipoprotein concentrations (A-I, A-II, B, C-II, C-III, and E) in Brazilians undergoing secondary cardiovascular prevention. - Source: PubMed
Publication date: 2026/08/05
Bersch-Ferreira Angela CSantos Renato Hideo NRogero Marcelo MMachado Rachel Helena VBressan JosefinaMoreira Annie Seixas BAmaral Cristiane KMarcadenti Aline - Renal amyloidosis is an important cause of kidney injury that is often associated with significant morbidity and mortality. In this study, we aim to characterise the clinicopathological patterns and identify potential prognostic factors in renal amyloidosis at an Australian tertiary referral centre over a decade. A total of 63 biopsy-diagnosed cases of renal amyloidosis from 2011 to 2021 were retrospectively reviewed. Cases were initially subtyped by immunofluorescence and immunohistochemistry. Mass spectrometry was performed when rare subtypes were suspected. Histological characteristics were correlated with clinical parameters at the time of biopsy. The primary outcome was severe renal impairment (SRI), defined as an estimated glomerular filtration rate (eGFR) <10 mL/min/1.73 m or commencement of renal replacement therapy. Amyloid light chain (AL) amyloidosis was the most common subtype (79%), followed by amyloid A (AA) (11%), and the rare subtypes included amyloid leukocyte cell-derived chemotactic factor-2 (3.2%); amyloid transthyretin wild-type (1.6%); amyloid apolipoprotein C-II (1.6%); amyloid fibrinogen (1.6%); and amyloid gelsolin amyloidosis (1.6%). Patients with AA amyloidosis were younger than those with other subtypes. The classic histological patterns of common and rare amyloid subtypes, as described in the literature, were replicated in our cohort. Interstitial fibrosis and tubular atrophy had a strong correlation with baseline eGFR and were important prognostic factors for SRI. Nephrotic-range proteinuria showed a trend towards SRI, but amyloid subtype (AL vs AA vs other) did not stratify outcome. Most AL amyloidosis cases (69%) were confirmed to be monoclonal gammopathy of undetermined significance, with a smaller proportion showing an underlying haematological malignancy. All patients with AA subtype had an underlying chronic inflammatory disease condition. We demonstrate classic histopathological features of common and rare subtypes of renal amyloidosis in an Australian cohort. Histological markers at biopsy, indicative of chronic renal damage, have value as prognostic factors. - Source: PubMed
Publication date: 2026/07/03
Loh Jonathon W JGangadharan Komala MuralikrishnaLow Gary K KRobinson CarolFadaee Shannon BLee Adrian Y SNankivell Brian JViswanathan Seethalakshmi - Familial chylomicronemia syndrome (FCS) is a rare autosomal recessive disorder characterized by severe hypertriglyceridemia (sHTG) due to variants in canonical genes (LPL [lipoprotein lipase], APOA5, APOC2, GPIHBP1, and LMF1); its genotype distribution in Latin America remains scarcely reported. Given limited access to genetic testing and frequent negative results in clinically consistent cases, clinical scores and lipid ratios have been proposed to predict FCS. - Source: PubMed
Publication date: 2026/07/10
Fariña GregorioSleiman AmiraAlonso RodrigoGutiérrez Restrepo JonhayroSpagnuolo CamilaAgudelo Valencia NataliaGonzález Moore JosefinaSánchez Peñarete DianaSchvarzman NadiaGonzález Alejandro RománMonsalve ClaudiaCuevas AdaMelnik Luciana YennyCastaño Ceballos Pablo AlbertoLavalle Cobo AugustoEsteban Eduardo OsvaldoAimone DanielCastellanos Pinedo AlejandroNogueira Juan PatricioBerg Gabriela - Depression is a prevalent but underdiagnosed comorbidity in type 2 diabetes mellitus (T2DM), intensifying disease burden and complicating metabolic management. Reliable biomarkers for early detection remain limited. This study aimed to identify serum protein signatures associated with depression in individuals with T2DM using an untargeted proteomic approach. Methods Serum samples from healthy controls, T2DM patients, and T2DM patients with comorbid depression (n = 6 per group) were analyzed using LC-MS/MS-based untargeted proteomics (total n = 18). Differential protein abundance was assessed using MetaboAnalyst 6.0. Protein-protein interaction networks and pathway enrichment analyses were conducted using the STRING database. Candidate markers were further validated by ELISA in an independent cohort of healthy controls (n = 30), T2DM (n = 30), and T2DM with depression (n = 30). Diagnostic performance was evaluated using receiver operating characteristic (ROC) curves. Results LC-MS/MS identified 242 serum proteins, of which 12 were significantly dysregulated among the groups. Nine proteins showed unique alterations in the T2DM-depression group. STRING analysis highlighted ST18 as a central regulatory protein. ELISA validation confirmed significant elevation of LRG1, APOC2, and ST18 in T2DM with depression compared to controls and T2DM without depression. Among these, ST18 demonstrated the highest diagnostic accuracy, yielding the greatest area under the ROC curve. Conclusion Untargeted proteomic profiling revealed distinct serum protein alterations in T2DM patients with comorbid depression. ST18 emerged as a robust and specific biomarker, suggesting its potential involvement in the molecular interplay between metabolic dysregulation and depressive pathology. Larger, longitudinal studies are required to validate its predictive utility and clarify its role in T2DM-associated depression. - Source: PubMed
Publication date: 2026/07/23
Singh JiyaBandyopadhyay SabyasachiSen AtanuKant RaviDas AnindyaSaha Sarama