Ask about this productRelated genes to: FBLN5 antibody
- Gene:
- FBLN5 NIH gene
- Name:
- fibulin 5
- Previous symbol:
- -
- Synonyms:
- EVEC, UP50, DANCE, ARMD3
- Chromosome:
- 14q32.12
- Locus Type:
- gene with protein product
- Date approved:
- 1999-06-25
- Date modifiied:
- 2019-04-23
Related products to: FBLN5 antibody
Related articles to: FBLN5 antibody
- Research to date describes the suprachiasmatic nucleus (SCN) of the hypothalamus as the master pacemaker that synchronizes circadian rhythms in peripheral tissues. However, recent high-impact studies demonstrate that non-SCN tissues can also coordinate rhythms in other peripheral tissues. However, the extent to which the cardiac clock regulates peripheral clocks has not yet been tested. Therefore, we investigated the role of the cardiac clock in modulating extra-cardiac circadian function using a model of cardiac-specific deletion of the core clock protein Bmal1 (Bmal1 cKO). Bmal1 cKO mice demonstrated attenuated day-night differences in skeletal muscle core clock gene expression (Bmal1, Clock, Per1) and circadian expressed metabolic genes (Pdk4, Ppara) as well as impaired day-night muscle grip strength. In the kidney, Bmal1 cKO mice had blunted core clock gene and water balance gene expression (Avp) compared to WT mice. Proteomic analysis of serum identified fibulin 5 (Fbln5) as a potential cardiokine mediating peripheral circadian effects, with rhythmic expression of Fbln5 disrupted in the heart and serum of Bmal1 cKO mice compared to WT. Exogenous treatment of synchronized C2C12 myotubes and human renal cells with rFbln5 disrupted rhythmic clock gene expression. In vivo, supplementation of Fbln5 in the drinking water of healthy wildtype C57Bl6 mice also disrupted kidney muscle rhythms. RNA sequencing data suggested that Fbln5 alters circadian output programs via stress-activated mechanotransduction and metabolic remodeling. Importantly, these changes occur without overt SCN dysfunction. Together, we demonstrate a critical role for the heart in regulating peripheral circadian control through the novel circadian cardiokine Fbln5. - Source: PubMed
Bettadapura Sharanya STangeman David CSatyanarayana Sushumna BRuhmann Madison MBonds Willa JEdwards J HarrisonGupta PoojaYusifov AykhanTodd William DBruns Danielle R - The extracellular matrix (ECM) is crucial in building the extracellular environment and translating extracellular information into biochemical signals that sustain tissue functions. Fibulin-5 (Fbln5) is a multifunctional ECM protein essential for forming elastic fibers and regulating cellular functions by binding to integrins. Although fibulin-5 expression decreases with age in human skin, its functional implications, particularly in epidermal stem cell regulation, remain largely unexplored. Here, we show that the loss of Fbln5 in mice leads to early impairments of epidermal stem cell properties that resemble changes observed during chronological skin aging. Fbln5 deficiency is associated with reduced expression of integrins and other cell junction proteins and decreased YAP activation in epidermal stem cells. Pharmacological inhibition of YAP reduces the fast-cycling stem cell region in mice and downregulates the fast-cycling epidermal stem cell marker SLC1A3 in human primary keratinocytes. At the cellular level, YAP activity and SLC1A3 expression are modulated by cell density, with low-density cultures exhibiting high nuclear YAP and elevated SLC1A3 expression, whereas high-density conditions suppress both. Under high-density conditions, fibulin-5 coating partially restores nuclear YAP localization and increases SLC1A3 expression. Together, these findings suggest that, beyond its structural role in elastic fiber formation, fibulin-5 contributes to the maintenance of epidermal stem cell balance during skin aging by linking extracellular alterations to YAP-dependent intracellular signaling. - Source: PubMed
Fan WenxinIshikawa MizuhoRaja ErnaHegazy Ahmed MDate HinataNgo Yen XuanSato YoshifumiYamagata KazuyaYanagisawa HiromiSada Aiko - Although a range of glomerular diseases profoundly affect glomerulus-associated cells, a comprehensive understanding of their molecular alterations is still lacking. Here, we performed in-depth analysis of glomerular data from mouse models of primary and secondary glomerulopathies and constructed a multi-disease cellular landscape of glomerular cells. We identified a putative subset of proliferative glomerular endothelial cells(gECs) that highly expresses genetic susceptibility genes associated with multiple glomerular diseases. Podocytes exhibited shared injury-associated cell types across different disease models. A podocyte subset highly expressing , , , , , and was predominantly derived from ob/ob mice, whereas another podocyte subset with high expression of , , , , and was mainly observed in adriamycin-induced mice. Mesangial cells shared common injury-related alterations across diseases (high expression of , , , and ), while ob/ob mice exhibited a distinct mesangial cell subset (high expression of and ). In contrast, the gECs displayed similar molecular changes across different diseases without giving rise to disease-specific subtypes. Intercellular ligand-receptor analysis underpins the recruitment of immune cells by injured mesangial cells and podocytes via specific engagement of pairs such as CXCL and MIF, respectively. Our study systematically elucidates the molecular alterations of glomerulus-associated cells across various diseases, providing a foundation and strategic insights for future targeted therapies tailored to specific glomerular disease contexts. - Source: PubMed
Publication date: 2026/02/24
Huang YanLi ShuoLi ShuyingDuan ShuzhongHuang LanWang JingMa LiangyanLiu CeChen Qilin - CMT1H is a rare, autosomal dominant, demyelinating subtype of CMT caused by variants in FBLN5. Symptomatic cranial nerve involvement has never been reported in patients with CMT1H. - Source: PubMed
Koutsis GeorgiosKontogeorgiou ZoiTzempetzis CharalamposRagazos NikolaosEfthymiou EvgeniaKartanou ChrisoulaKoniari ChrysoulaGiagkou NikolaosChatzistefanou KlioVelonakis GeorgiosKaradima GeorgiaZouvelou Vasiliki - Myogenic differentiation is pivotal for muscle development, yet how stress impairs this process remains inadequately understood. Here, we investigated the dynamic regulatory mechanisms of sheep fetal myoblast (SFM) differentiation under normal and dexamethasone (Dex)-induced stress conditions, focusing on integrin-mediated signaling. Transcriptomic analysis identified multiple differentially expressed genes (DEGs). 153 DEGs exhibited up- or downregulation during differentiation, which was reversed by Dex. They were enriched in ECM-receptor interaction, focal adhesion, and the PI3K-Akt pathway. RU486, a glucocorticoid receptor (GR) antagonist, reversed Dex-induced alterations in key gene and protein expression within the FBLN5/Integrin-FAK/Paxillin-Akt-GSK3β cascade and cell cycle-related pathways. Overexpression/interference experiments confirmed that ITGA11 promoted SFM differentiation and rescued Dex-induced suppression through the FAK/Paxillin-Akt-GSK3β pathway. Taken together, stress inhibits SFM differentiation via the transcriptome remodeling and GR-mediated suppression of the ITGA11-FAK/Paxillin-Akt-GSK3β cascade. Our study establishes a framework for elucidating how glucocorticoid-mediated stress inhibits myogenesis and offers insights for controlling stress-induced muscular dysplasia/atrophy and improving meat production/quality in livestock. - Source: PubMed
Publication date: 2026/02/20
Qin JianZhang HaoLi ZhenyueZhang DongjiaoXie YouquanLi JunlingDou MinminCao MingxingYang XuLuo ZiyiWang HejieQin SenDu Rong