Ask about this productRelated genes to: SCARF1 antibody
- Gene:
- SCARF1 NIH gene
- Name:
- scavenger receptor class F member 1
- Previous symbol:
- -
- Synonyms:
- SREC, KIAA0149, SREC1
- Chromosome:
- 17p13.3
- Locus Type:
- gene with protein product
- Date approved:
- 2002-09-06
- Date modifiied:
- 2017-02-28
Related products to: SCARF1 antibody
Related articles to: SCARF1 antibody
- Systemic lupus erythematosus (SLE) is a complex autoimmune disease known for its heterogeneity in both manifestation and presentation. Recent evidence has increasingly implicated the gut microbiome within immunomodulation and autoimmunity. This study aims to characterize the intestinal inflammation and microbial profile associated with autoimmune diseases, particularly SLE, and to identify unique biomarkers and shared microbial signatures for potential therapeutic measures. Our lab identified scavenger receptor class F, member 1 (SCARF1, SREC-1) as an efferocytosis receptor essential for the clearance of apoptotic debris, and its deficiency results in the development of lupus-like disease. SCARF1 is crucial in immune homeostasis, and defects in efferocytosis lead to inflammation. However, the role of SCARF1 in gut homeostasis remains to be elucidated. To answer our question, we analyzed and compared the metagenomic datasets generated through whole genome shotgun sequencing between our Scarf1 lupus-prone mouse model and healthy counterparts. We found that Scarf1 mice had significantly lengthened intestines, elevated immune cell infiltration, and structural changes in the colon. Microbiome analysis revealed gut dysbiosis, including reduced alpha diversity and increased Firmicute/Bacteroidetes ratio. Notably, beneficial taxa such as Akkermansia muciniphila was absent in Scarf1 mice. Linear regression analysis identified positive associations between lupus disease severity and increased abundances of Alistipes, Lachnospiraceae, and Clostridium. Function analysis of the gut microbiome in Scarf1 mice indicated downregulation of multiple pathways related to cell proliferation. These findings highlight the role of SCARF1 involvement in the gut microbiome and immune regulation in the context of inflammation and SLE. - Source: PubMed
Publication date: 2026/02/11
Shepard Dominique MHahn SabineChitre MonikaNeff HaleyWard Doyle VJadhav NupurRichmond Jillian MRamirez-Ortiz Zaida G - Erythro-myeloid progenitors (EMPs) originate from the haemogenic endothelium in the yolk sac via an endothelial-to-haematopoietic transition (EHT) to generate blood and immune cells that support embryo development. Yet, the transitory nature of EHT and the limited availability of molecular markers have constrained our understanding of the origin, identity, and differentiation dynamics of EMPs. Here, we have refined the annotation of yolk sac haemato-vascular populations in publicly available single-cell RNA sequencing (scRNAseq) datasets from mouse embryos to identify novel molecular markers of haemogenic endothelium and EMPs. By sub-clustering key cell populations followed by pseudotime analysis, we refined cluster annotations and then reconstructed differentiation trajectories. Subsequent differential gene expression analysis between clusters identified novel cell surface markers for haemogenic endothelial cells ( and ) and EMPs (, and ). Further, we have identified candidate signalling and metabolic pathways that may regulate yolk sac haematopoietic emergence and differentiation. The specificity of FXYD5, SCARF1, and FCER1G for haemogenic endothelium and EMPs was validated by immunostaining of the mouse yolk sac. These insights into the transcriptional dynamics in the yolk sac should support future investigation of EHT and haematopoietic differentiation during early mammalian development. - Source: PubMed
Publication date: 2026/01/06
Diez-Pinel GuillermoMuratore AlessandroRuhrberg ChristianaCanu Giovanni - Patients with advanced cardiovascular kidney metabolic syndrome generally face a high risk of cardiovascular complications. Guideline-directed medical therapies (GDMT) are critical for mitigating cardiovascular risk and improving prognosis. However, patients with more advanced kidney disease have frequently been excluded from the foundational cardiovascular outcome trials, leaving clinicians with a paucity of evidence with regards to the cardiovascular benefits and potential risks involved in initiating or maintaining GDMT for cardiovascular diseases in patients with chronic kidney disease stages 4 and 5. Numerous studies have demonstrated a systematic underutilization of GDMT among patients with advanced chronic kidney disease (CKD), likely caused by a combination of clinical inertia and a legitimate fear of potential side-effects such as hyperkalemia and rises in creatinine, which may necessitate repeat laboratory monitoring, dose adjustment, and additional potassium-lowering treatment. In this clinical review, we aim to summarize the accumulating evidence with regards to the use of key cardiovascular drugs among patients with advanced CKD, with an emphasis on GDMT in patients with heart failure, and outline the treatment approach used in our integrated heart-nephrology-diabetes clinic. Since the evidence is not always clear and our patients are generally both older, frailer, and have more multimorbidity than those included in clinical trials, sound clinical judgment, individual patient tolerability as well as shared decision-making are key. We also address the need to continuously align treatment goals with patient preferences across different phases of life and adjusting GDMT in the face of increasing frailty. - Source: PubMed
Publication date: 2025/11/21
Bergen KarinSpaak Jonas - Myotonic dystrophy (DM), the most common adult-onset muscular dystrophy, affects not only motor function and muscle integrity but also leads to debilitating cardiopulmonary, gastrointestinal, and multisystem complications. Central nervous system (CNS) involvement is increasingly recognized, manifesting as impairments in working memory, executive function, sleep regulation, and mood and behavior. These interrelated, multisystemic features contribute to multifaceted symptoms that significantly reduce quality of life for patients and their families. To identify potential biomarkers of CNS disease activity in DM1, we performed the first exploratory cerebrospinal fluid (CSF) proteomic profiling study. - Source: PubMed
Publication date: 2025/11/26
Zafarullah MarwaKamali TaherehHagerman Katharine AGhiglieri LisaDuong TinaWang EricSampson Jacinda BDay John W - Evidence for the microbiome's role in human health and disease has been piling up ever since the human microbiome project. The composition of one's microbiome can have a major effect on one's risk of developing cancer and the nature of how cancer develops. Several estimates suggest the percentage of cancer cases that can be attributed to microorganisms at around 15%. In addition, researchers are still trying to figure out how the microbiota, and the gut microbiota in particular, affects how a patient responds to chemotherapy, immunotherapy, and radiotherapy. In this light, we conducted an in-depth bioinformatics analysis of the gut microbiota- RCCstem cells axis, utilizing python-based programme and enrichment databases to analyses data from many sources, including clinical data, transcription factors, kinases and gene expression profile of RCCstem cells. Five genes, including SLC16A6, CPNE5, AFAP1L1, SCARF1, and NOTCH4, were shown to be shared by the hub gut microbiota and extracellular proteins. Patients with RCCstem cells had a disproportionately high number of certain types of bacteria. In patients expression profile have high CPNE5, AFAP1L1, SCARF1, and NOTCH4 expression. RCCsurvival rates are reduced by roughly 50% due to all of the genes involved. Also, the Actinobacteria and Gammaproteobacteria possible role in renal cancer development via relation to cancer stem cells. The gut microbiota and its components were considered for their possible relevance in the development of RCC. - Source: PubMed
Publication date: 2025/12/09
Alimoradi EhsanHashemnejad Mohammad AminEtemad SarehArabi MaryamBereimipour Ahmad