FIS1 antibody Polyclonal Antibodies Primary antibodies
- Known as:
- FIS1 (anti-) Polyclonal Antibodies Primary antibodies
- Catalog number:
- orb101186
- Product Quantity:
- 100
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- FIS1 antibody Polyclonal Antibodies Primary antibodies
Related genes to: FIS1 antibody Polyclonal Antibodies Primary antibodies
- Gene:
- FIS1 NIH gene
- Name:
- fission, mitochondrial 1
- Previous symbol:
- TTC11
- Synonyms:
- CGI-135, H_NH0132A01.6, Fis1
- Chromosome:
- 7q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 2003-07-09
- Date modifiied:
- 2017-03-08
Related products to: FIS1 antibody Polyclonal Antibodies Primary antibodies
Related articles to: FIS1 antibody Polyclonal Antibodies Primary antibodies
- Neuroimmune dysregulation, characterized by microglial overactivation and imbalances in mitochondrial dynamics within the central nervous system represents a core pathological mechanism in postoperative cognitive dysfunction (POCD). This study investigated the neuroinflammation-mitochondrial interaction through the establishment of in vivo and in vitro models using lipopolysaccharide (LPS). Findings indicated that LPS-induced microglial overactivation was associated with marked upregulation of mitochondrial fission proteins, including phosphorylated Drp1 at Ser616, mitochondrial Drp1, and Fis1, along with downregulation of mitofusin-2. These alterations promoted mitochondrial fragmentation in hippocampal neurons, which subsequently led to mitochondrial membrane potential depolarization, adenosine triphosphate depletion, and excessive production of reactive oxygen species. This cascade further activated the intrinsic apoptotic pathway via Bax/Bcl-2 imbalance and caspase-9/3 activation. Conversely, administration of the Drp1 inhibitor Mdivi-1 reduced microglial activation, attenuated inflammatory cytokine levels, restored mitochondrial network integrity and function, inhibited neuronal apoptosis, and ameliorated LPS-induced spatial memory impairment in behavioral assays. These findings indicate that microglial activation-induced mitochondrial fission plays a pivotal role in inflammation-related cognitive impairment. Moreover, they highlight mitochondrial fission as a promising therapeutic target for intervention in POCD. - Source: PubMed
Publication date: 2026/06/06
Chen Meng-JieNing Jia-QiLiu Jia-XiLuo Jian-ShengYan Ru-YuYang Yu-XuanLi XiangDing Ling-Ling - Osteoarthritis (OA) is a prevalent degenerative joint disease accompanied by increased number of senescent chondrocytes. Mitochondrial dysfunction is a well-established hallmark of chondrocyte senescence in OA pathogenesis. Sterile α and Toll/Interleukin-1 Receptor motif-containing 1 (SARM1), known to drive mitochondrial impairment in various cell types, has not been thoroughly investigated in the context of chondrocyte aging or OA. - Source: PubMed
Publication date: 2026/06/02
Gu YuZhao Xin-HaoXing Bai-ZhouWu BiaoPeng RongLi Chang-QingLv HaiLu Hua-Ding - Vascular dementia (VaD) is associated with chronic cerebral hypoperfusion, oxidative stress, mitochondrial dysfunction, and hippocampal neuronal senescence. Citronellal (CT) ameliorates cognitive impairment in 2VO-induced VaD rats. CT improved spatial learning and working memory, reduced in vivo oxidative stress, restored hippocampal dendritic spine density, upregulated hippocampal myelin basic protein (MBP), and decreased P-p53, p21, and SA-β-gal. CT also restored mitochondrial membrane potential and reduced Drp1/FIS1 expression. Mechanistically, CT suppressed TRPM2 and restored NMDAR1; TRPM2 deficiency weakened CT-mediated NMDAR1 regulation. These findings suggest that CT ameliorates VaD-related cognitive impairment by inhibiting hippocampal aging through TRPM2/NMDAR-associated oxidative stress-mitochondrial pathways. - Source: PubMed
Publication date: 2026/06/01
Fu Zhan-ZhouNiu Qian-QianZhang Chun-RuiWang Hui-DanLi Xi-YueLi Cheng-ZhiLi PengWang Qian-Qian - Endothelial dysfunction plays a key role in the development of diabetic cardiomyopathy (DCM), but the underlying mechanisms of endothelial dysfunction remain to be elucidated. Recent studies have revealed that dysregulated mitochondrial dynamics contributes to the development of cardiac microvascular dysfunction. Fission-1 (FIS1), a key effector of mitochondrial fission, functions as an outer mitochondrial membrane adapter that recruits dynamin-related protein-1 (Drp1) from the cytosol to the outer mitochondrial membrane for activating mitochondrial fission. The present study screened a library targeting deubiquitinases, and identified the regulatory role of USP33 on FIS1-dependent mitochondrial fission. We found USP33 silencing elevated FIS1 protein expression and resulted in excessive mitochondrial fission in endothelial cells, which in turn impaired mitochondrial function and worsen endothelial and cardiovascular dysfunction in DCM. Mechanistically, USP33 interacted with FIS1 at the TPR2 domain and promoted FIS1 degradation via lysosomal degradation. Further studies revealed that USP33 stabilized autophagy-related 7 (ATG7) at protein level by blocking K63-linked ubiquitination of human ATG7 at K48 (mouse K44) site. This process led to lysosomal degradation of FIS1 via ATG7-mediated autophagy. In summary, our findings reveal that USP33 plays a critical role in endothelial dysfunction in DCM and demonstrate that ATG7-FIS1 pathway acts as one of the potential downstream mechanisms. - Source: PubMed
Publication date: 2026/05/30
Chen YuqiongSun XiangyuLi XinyanGuan BoYan XiaopeiHuang ChaoZhang NannanMao WenjunTian YuanChen ChaoLu YaoLi Su - Atrial fibrillation (AF) is a common clinical arrhythmia associated with mitochondrial dysfunction, oxidative stress, and atrial fibrosis. Mitochondrial-derived peptides (MDPs), including humanin (HN) and MOTS-c, exhibit cytoprotective properties, but their role in AF remains largely unknown. This study aimed to investigate the expression of HN and MOTS-c in AF patients and to evaluate their therapeutic potential and underlying mechanisms in an AngII-induced mouse model and primary cardiac cells. HN and MOTS-c expression in human atrial tissues was analyzed using public GEO data, immunohistochemistry, and immunofluorescence. Plasma levels were measured in a matched cohort (39 AF patients, 39 sinus rhythm controls). Murine AF models (male C57BL/6J mice, = 36) and primary rat cardiomyocytes and fibroblasts were exposed to angiotensin II (AngII) with or without treatment with HNG (an HN analogue) or MOTS-c. HN and MOTS-c were significantly downregulated in human AF atrial tissue, and their levels inversely correlated with fibrosis extent. Plasma MOTS-c was decreased in AF patients and inversely correlated with NT-proBNP. In vivo, HNG or MOTS-c treatment reduced AF inducibility and attenuated AngII-induced atrial fibrosis and hypertrophy. Peptide treatment was associated with improved mitochondrial ultrastructure, reduced mitochondrial fission proteins (Drp1, Fis1), and lower pro-inflammatory cytokines (IL-1β, IL-6) in mouse atria. In primary cardiomyocytes, both peptides mitigated AngII-induced oxidative stress. In fibroblasts, they directly inhibited AngII-induced activation, proliferation, and migration. Exploratory RNA-seq suggested that HNG predominantly affects cell adhesion pathways, while MOTS-c acts on metabolic processes. Downregulation of HN and MOTS-c in human AF is associated with disease severity. In murine models, HNG or MOTS-c administration attenuates atrial fibrosis and mitochondrial dysfunction and reduces AF inducibility. These findings suggest that MDPs may represent a novel therapeutic avenue for AF, although further validation with larger cohorts and mechanistic studies are required. - Source: PubMed
Publication date: 2026/05/05
Liao YingyingXu JieJiao YuhengSun XinxinGao MingkuiDing YagangCai DihuiShen YinyinZhou XiaohuiHan Wei