COLEC12 antibody - middle region (ARP32484_P050)
- Known as:
- COLEC12 (anti-) - middle region (ARP32484_P050)
- Catalog number:
- arp32484_p050
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- Aviva Systems Biology
- Gene target:
- COLEC12 antibody - middle region (ARP32484_P050)
Related genes to: COLEC12 antibody - middle region (ARP32484_P050)
- Gene:
- COLEC12 NIH gene
- Name:
- collectin subfamily member 12
- Previous symbol:
- -
- Synonyms:
- SRCL, CL-P1, SCARA4
- Chromosome:
- 18p11.32
- Locus Type:
- gene with protein product
- Date approved:
- 2001-12-13
- Date modifiied:
- 2015-11-16
Related products to: COLEC12 antibody - middle region (ARP32484_P050)
Related articles to: COLEC12 antibody - middle region (ARP32484_P050)
- Postbiotics have attracted attention owing to their safety and immunomodulatory effects. The heat-inactivated lactic acid bacterium EF-2001 (EF-2001) is one such postbiotic. Extensive studies on EF-2001 have demonstrated its safety and versatile biological activities, particularly immunomodulatory effects such as anti-inflammatory responses. However, the molecular mechanisms underlying these regulatory processes remain unclear. Here, we investigated phagocytosis and cytokine production of EF-2001 using murine macrophage-like cells, RAW264 cells. After stimulation with EF-2001, phagocytosis was evaluated using flow cytometry and microscopy. Secreted cytokines were evaluated using ELISA. RNA-seq and gene set enrichment analyses were performed to identify candidate receptors. To validate the candidate receptors, the receptor genes were downregulated by siRNA knockdown, followed by Quantitative PCR and immunoblotting to determine knockdown efficacy. The effects of gene silencing on cell function were characterized by flow cytometry and ELISA. A neutralizing antibody was used to confirm knockdown experiments. The intracellular signaling pathways were examined using specific inhibitors of key kinases. EF-2001 was phagocytosed by RAW264 cells with cytokine production, including IL-10, TNF-α, and IL-6, in a dose-dependent manner. Bioinformatic analysis identified , and as candidate receptor genes for phagocytosis by EF-2001. Phagocytosis was significantly reduced by suppressing macrophage scavenger receptor 1 (MSR1) expression. The neutralizing antibody against MSR1 showed similar suppression of phagocytosis. Thus, MSR1 was identified as the primary receptor for EF-2001 recognition and phagocytosis. MSR1 suppression also affects cytokine production, especially that of IL-10. In terms of intracellular signaling pathways, Syk and PI3K inhibition substantially reduced EF-2001 phagocytosis. The inhibition of Syk, PI3K, and MAPKs hampered IL-10 production induced by EF-2001 stimulation. EF-2001 is recognized and phagocytosed primarily via MSR1 in macrophages, accompanied by the induction of IL-10. Syk and PI3K signaling are involved in phagocytosis and IL-10 release, whereas their downstream MAPK pathways predominantly contribute to IL-10 production. Our data provide insights into the immunomodulatory mechanisms through which biotic components interact with macrophages. - Source: PubMed
Publication date: 2026/08/20
Kubota YukiTsuboya TakumiMurakami MarinaUehara ShuichiroSuzuki Shigeo - Inflammatory cardiomyopathy (iCMP) is a leading cause of heart failure, with limited therapeutic options. Excessive cytokine levels are implicated in adverse outcomes, but their pathomechanism in iCMP is poorly understood. We sought to identify key cytokines involved in severe iCMP and elucidate their potential contribution to cardiomyocyte injury. - Source: PubMed
Publication date: 2026/08/30
Suwalski PhillipGolpour AinooshWeiner JanuaryMusigk NicolasBalzer FelixGiesa NiklasAmr AliZyla JoannaGanz PeterSaleem Hafiza NosheenTrebing JohannesSedaghat-Hamedani FarbodMeder BenjaminGold Stefan MEbert AntjeBeule DieterLandmesser UlfHeidecker Bettina - Ischemic cardiomyopathy (ICM) is a condition characterized by inadequate blood supply to the coronary arteries, resulting in myocardial damage and decreased cardiac functionality. This study aimed to identify potential biomarkers and regulatory networks in ICM, providing a foundation for further mechanistic and therapeutic investigations. - Source: PubMed
Publication date: 2026/07/29
Ye XianhuaWu GuoxiangXie JialanWu YanqingChen DaqiuChen YixingXu ShanghuaLuo Shunxiang - Hepatocellular carcinoma (HCC) develops within an immunologically complex tumor microenvironment that is heavily shaped by infiltrating myeloid cells. Immune-based treatment strategies such as atezolizumab plus bevacizumab have shown promising therapeutic benefits, but patients do not experience durable responses. This shortfall motivates current efforts to elucidate signaling programs that sustain pro-tumor myeloid states. Focal adhesion kinase (FAK, encoded by PTK2) integrates adhesion, growth factor, proliferative, and inflammatory signaling, but the contribution of FAK in myeloid cells to HCC has not been tested. In this study, we used human HCC transcriptomic analyses and a myeloid-specific FAK knockout mouse model to investigate the role of myeloid-intrinsic FAK in HCC progression. Analysis of the PRHCCdb single-cell database showed PTK2 expression was detectable in myeloid populations. Higher PTK2 expression in myeloid-rich TCGA-LIHC tumors was associated with a significantly worse overall survival. Further analysis of the NCI-CLARITY single-cell data set localized the strongest FAK-associated transcriptional programs to a monocyte-derived macrophage state marked by VCAN and COLEC12. Specifically, this population demonstrated hypoxia-associated and inflammatory signatures. To test the functional role of FAK in myeloid cells, we generated myeloid-specific FAK knockout (LysMCre;FAK) mice. Deletion of FAK did not alter baseline liver morphology, liver-to-body weight ratio, or proliferation. When challenged with the MET/β-catenin-driven HCC model via hydrodynamic tail vein injection, myeloid-specific FAK deletion did not significantly affect survival, gross tumor burden, or tumor proliferation. However, tumors from the LysMCre;FAK mice showed significantly reduced F4/80 macrophage accumulation compared with FAK controls. These findings indicate that myeloid-specific FAK promotes macrophage accumulation, but its loss alone is insufficient to alter tumor burden, proliferation, or survival in this oncogene-driven HCC model. - Source: PubMed
Publication date: 2026/07/26
Ham EugeneBoedeker KyleKeating Claudia RoseYe RuisongMontalbano FrankieMankaruse SophiaDing XianzhongRennhack Jonathan PQiu Wei - Chronic kidney disease (CKD) is frequently accompanied by reduced muscle strength, metabolic dysregulation, and chronic inflammation. However, the plasma proteomic signatures and underlying biological mechanisms of probable sarcopenia in individuals with CKD remain poorly characterized. This study aimed to systematically characterize the plasma proteomic signatures associated with probable sarcopenia in CKD and explore their potential biological significance. - Source: PubMed
Publication date: 2026/07/15
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