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)
- 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
Yan CuiLin LiyuWu Zilun - Collectin Subfamily Member 12 (COLEC12), a C-type lectin family member with collagen-like and carbohydrate recognition domains, remains poorly characterized in pancreatic cancer (PC). COLEC12 expression was analyzed by bioinformatics and immunohistochemistry. Functional assays (CCK-8, colony formation, EdU, flow cytometry, Transwell) and a xenograft model were used to assess its tumor-promoting effects. Mechanistically, transcriptome sequencing, Western blotting, co-immunoprecipitation (Co-IP), molecular docking, truncation mutant mapping, cycloheximide (CHX) chase assay, and ubiquitination assays were performed. The Cancer Genome Atlas (TCGA) data were used for immune infiltration analysis, and quantitative real-time PCR (qRT-PCR) was used to examine the role of COLEC12 in macrophage polarization. Chemosensitivity to gemcitabine and 5-fluorouracil (5-FU) was also evaluated. COLEC12 was upregulated in PC and promoted cell proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT), while suppressing apoptosis. Mechanistically, COLEC12 directly bound to TGF-β1 via its collagen-like domain, as demonstrated using truncation mutants. CHX chase assays revealed that COLEC12 overexpression delayed TGF-β1 degradation, and ubiquitination assays showed that COLEC12 knockdown increased TGF-β1 ubiquitination, indicating that COLEC12 stabilizes TGF-β1 by suppressing its ubiquitin-proteasome degradation, thereby sustaining activation of the TGF-β/Smad pathway. Furthermore, COLEC12 expression positively correlated with immune cell infiltration levels in TCGA data, and qRT-PCR revealed that COLEC12 expression in PC cells promotes M2 polarization of co-cultured macrophages. Knockdown of COLEC12 increased the sensitivity of PC cells to gemcitabine and 5‑FU. This study reveals, for the first time, the tumor-promoting function of COLEC12 in PC and highlights its potential as a therapeutic target in PC. - Source: PubMed
Publication date: 2026/06/19
Feng XinXu JianYang QingqingRen YiChen HuizhuJiang Zheng - Lung cancer, especially small-cell lung cancer (SCLC), is a widespread and deadly disease often detected at advanced stages, resulting in low five-year survival rates. This study aims to identify new genetic targets to enhance understanding of the genetic drivers of SCLC progression. - Source: PubMed
Publication date: 2026/03/21
Liu HailinQu FangyuanZhou GuangyaoCui YuechenYan BoZhang LianminLi ChenguangZhang ZhenfaQin TingtingZhang Qiangzhe