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更新于：2025-01-23

SCARA5

更新于：2025-01-23

基本信息

别名

FLJ23907、MGC45780、NET33

+ [3]

简介

Ferritin receptor that mediates non-transferrin-dependent delivery of iron. Mediates cellular uptake of ferritin-bound iron by stimulating ferritin endocytosis from the cell surface with consequent iron delivery within the cell. Delivery of iron to cells by ferritin is required for the development of specific cell types, suggesting the existence of cell type-specific mechanisms of iron traffic in organogenesis, which alternatively utilize transferrin or non-transferrin iron delivery pathways. Ferritin mediates iron uptake in capsule cells of the developing kidney. Preferentially binds ferritin light chain (FTL) compared to heavy chain (FTH1).

关联

项与 SCARA5 相关的药物

WO2024230638

专利挖掘

靶点

SCARA5

作用机制-

在研机构

上海交通大学医学院附属第九人民医院

原研机构

上海交通大学医学院附属第九人民医院

在研适应症

遗传性眼睛疾病 [+2]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SCARA5 相关的临床结果

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100 项与 SCARA5 相关的转化医学

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0 项与 SCARA5 相关的专利（医药）

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106

项与 SCARA5 相关的文献（医药）

2024-11-01·Pancreatology

The tumor immune microenvironment in resected treatment-naive pancreatic cancer patients with long-term survival

Article

作者: Doukas, Michael ; van Eijck, Casper W F ; Vietsch, Eveline E ; Heij, Lara R ; Alonso, Lola ; Groot Koerkamp, Bas ; Wiltberger, Georg ; Verheij, Maaike ; van ’t Land, Freek R. ; Malats, Núria ; Stubbs, Andrew ; van 't Land, Freek R ; Ju, Jie ; Heij, Lara R. ; van Eijck, Casper H J ; van Eijck, Casper H.J. ; Vietsch, Eveline E. ; Li, Yunlei ; van Eijck, Casper W.F. ; Lila, Karishma

BACKGROUNDPancreatic ductal adenocarcinoma (PDAC) is one of the most lethal cancers worldwide. Presently, only a fraction of patients undergo successful surgical resection, the most effective treatment. Enhancing treatment strategies necessitates a deep comprehension of the factors underlying extended survival after surgical resection in patients.METHODSThis study aims to identify the important factors of PDAC patients' long-term survival with metatranscriptomics and multiplex immunofluorescence (IF) staining analyses. Specifically, differences in tumor immune microenvironment (TIME) were investigated between treatment-naïve PDAC short-term survivors (STS, overall survival <6 months) and long-term survivors (LTS, overall survival >5 years).RESULTSAs a result, we detected 589 over-expressed genes, including HOXB9, CDA, and HOXB8, and 507 under-expressed genes, including AMY2B, SCARA5, and SLC2A2 in LTS. Most of the Reactome overbiological pathways enriched in our data were over-expressed in LTS, such as RHO GTPase Effectors and Cell Cycle Checkpoints. Eleven microbiomes significantly differed between LTS and STS, including Sphingopyxis and Capnocytophaga. Importantly, we demonstrate that the TIME profile with an increased abundance of memory B cells and the reduction of M0 and pro-tumoral M2 macrophages are associated with a good prognosis in PDAC.CONCLUSIONSIn this study, we delved into the TIME with metatranscriptomics and IF staining analyses to understand the prerequisite of prolonged survival in PDAC patients. In LTS, several biological pathways were overexpressed, and specific microbiomes were identified. Furthermore, apparent differences in driven immune factors were found that provide valuable insights into developing new treatment strategies.

2024-07-01·Diabetes/Metabolism Research and Reviews

Associations between multiple neurological biomarkers and distal sensorimotor polyneuropathy: KORA F4/FF4 study

Article

作者: Roden, Michael ; Bönhof, Gidon J. ; Strom, Alexander ; Peters, Annette ; Maalmi, Haifa ; Heier, Margit ; Ziegler, Dan ; Herder, Christian ; Rathmann, Wolfgang ; Thorand, Barbara ; Morrison, Helen ; Koenig, Wolfgang

AbstractAimsThe aim of this study was to assess associations between neurological biomarkers and distal sensorimotor polyneuropathy (DSPN).Materials and MethodsCross‐sectional analyses were based on 1032 participants aged 61–82 years from the population‐based KORA F4 survey, 177 of whom had DSPN at baseline. The prevalence of type 2 diabetes was 20%. Prospective analyses used data from 505 participants without DSPN at baseline, of whom 125 had developed DSPN until the KORA FF4 survey. DSPN was defined based on the examination part of the Michigan Neuropathy Screening Instrument. Serum levels of neurological biomarkers were measured using proximity extension assay technology. Associations between 88 biomarkers and prevalent or incident DSPN were estimated using Poisson regression with robust error variance and are expressed as risk ratios (RR) and 95% CI per 1‐SD increase. Results were adjusted for multiple confounders and multiple testing using the Benjamini–Hochberg procedure.ResultsHigher serum levels of CTSC (cathepsin C; RR [95% CI] 1.23 (1.08; 1.39), pB‐H = 0.044) and PDGFRα (platelet‐derived growth factor receptor A; RR [95% CI] 1.21 (1.08; 1.35), pB‐H = 0.044) were associated with prevalent DSPN in the total study sample. CDH3, JAM‐B, LAYN, RGMA and SCARA5 were positively associated with DSPN in the diabetes subgroup, whereas GCP5 was positively associated with DSPN in people without diabetes (all pB‐H for interaction <0.05). None of the biomarkers showed an association with incident DSPN (all pB‐H>0.05).ConclusionsThis study identified multiple novel associations between neurological biomarkers and prevalent DSPN, which may be attributable to functions of these proteins in neuroinflammation, neural development and myelination.

2024-07-01·Journal of Molecular and Cellular Cardiology

Knockdown of LncRNA Lcn2-204 alleviates sepsis-induced myocardial injury by regulation of iron overload and ferroptosis

Article

作者: Qin, Hongqian ; Huang, Yuhui ; Li, Wentao ; Li, Lu ; Kang, Pinfang ; Cheng, Zhipeng ; Wang, Rui ; Ye, Hongwei ; Lu, Na ; Gao, Qin ; Li, Yuping ; Li, Zhenghong

Ferroptosis is an iron-dependent programmed cell death form resulting from lipid peroxidation damage, it plays a key role in organ damage and tumor development from various causes. Sepsis leads to severe host response after infection with high mortality. The long non-coding RNAs (LncRNAs) are involved in different pathophysiological mechanisms of multiple diseases. Here, we used cecal ligation and puncture (CLP) operation to mimic sepsis induced myocardial injury (SIMI) in mouse model, and LncRNAs and mRNAs were profiled by Arraystar mouse LncRNA Array V3.0. Based on the microarray results, 552 LncRNAs and 520 mRNAs were differentially expressed in the sham and CLP groups, among them, LncRNA Lcn2-204 was the highest differentially expressed up-regulated LncRNA. Iron metabolism disorder was involved in SIMI by bioinformatics analysis, meanwhile, myocardial iron content and lipocalin-2 (Lcn2) protein expressions were increased. The CNC network comprised 137 positive interactions and 138 negative interactions. Bioinformatics analysis showed several iron-related terms were enriched and six genes (Scara5, Tfrc, Lcn2, Cp, Clic5, Ank1) were closely associated with iron metabolism. Then, we constructed knockdown LncRNA Lcn2-204 targeting myocardium and found that it ameliorated cardiac injury in mouse sepsis model through modulating iron overload and ferroptosis. In addition, we found that LncRNA Lcn2-204 was involved in the regulation of Lcn2 expression in septic myocardial injury. Based on these findings, we conclude that iron overload and ferroptosis are the key mechanisms leading to myocardial injury in sepsis, knockdown of LncRNA Lcn2-204 plays the cardioprotective effect through inhibition of iron overload, ferroptosis and Lcn2 expression. It may provide a novel therapeutic approach to ameliorate sepsis-induced myocardial injury.

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