ANO5
- Known as:
- ANO5
- Catalog number:
- 001671A
- Product Quantity:
- 250ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- ANO5
Related genes to: ANO5
- Gene:
- ANO5 NIH gene
- Name:
- anoctamin 5
- Previous symbol:
- TMEM16E, LGMD2L
- Synonyms:
- GDD1
- Chromosome:
- 11p14.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-04-07
- Date modifiied:
- 2019-04-23
Related products to: ANO5
Related articles to: ANO5
- Malignant hyperthermia (MH) is a life-threatening pharmacogenetic disorder of skeletal muscle primarily associated with pathogenic variants in ; however, a substantial proportion of MH-susceptible individuals lack identifiable variants in known genes. This study aimed to identify novel genetic contributors in Ca-induced Ca release (CICR)-positive patients without variants and to evaluate their functional relevance. - Source: PubMed
Publication date: 2026/08/20
Miyoshi HirotsuguOtsuki SachikoKido KenshiroSumii AyakoIkeda TsuyoshiXia GuoqiangNoda YukoIshii TomomiKamiya SatoshiNarasaki SoshiYeh Huei-MingChen Pei-LungIchihara YasukoMukaida KeikoTsutsumi Yasuo M - Rhabdomyolysis is a potentially life-threatening condition that can result from genetic causes. Despite that, little is known about the genetic underpinnings behind monogenic rhabdomyolysis in Brazil. - Source: PubMed
Publication date: 2026/08/13
Martins Aldrin PedrozaMartinez Alberto Rolim MuroNucci AnamarliFrança Júnior Marcondes Cavalcante - In the 5th edition World Health Organisation (WHO) classification of head and neck tumours, lesions that are distinctive in the jaws for reasons of presentation, behaviour or molecular changes are separated from the bone tumour classification and listed with head and neck tumours in a section on odontogenic and maxillofacial bone tumours. The molecular characterisation of these lesions has advanced recently and this narrative review discusses critically the genetic alterations in the odontogenic tumours that form bone/cementum (variable findings), giant cell-rich lesions of the jaws (sporadic giant cell granulomas with mutually exclusive TRPV4, KRAS or FGFR1 mutations, brown tumours with KRAS mutations and cherubism with SH3BP2 mutations), and bone cysts (aneurysmal bone cyst with USP6 rearrangements and simple bone cyst lacking NFATC2 rearrangement). Additionally, fibro-osseous lesions are discussed, with fibrous dysplasia harbouring GNAS mutations, familial florid cemento-osseous dysplasia, familial gigantiform cementoma and gnathodiaphyseal dysplasia sharing ANO5 mutations and psammomatoid ossifying fibroma showing SATB2 rearrangements. In most cases the changes support the current classification, but areas of uncertainty are described and differences between jaw lesions and similar lesions elsewhere in the skeleton are highlighted. - Source: PubMed
Publication date: 2026/06/19
Guimarães Letícia MartinsOdell Edward WGomes Carolina Cavalieri - Atherosclerosis (AS) is a widespread cardiovascular disorder that constitutes a major contributor to global morbidity and mortality, thereby imposing significant economic burdens on healthcare systems worldwide. Efferocytosis, the phagocytic removal of apoptotic cells, serves as a fundamental mechanism for maintaining tissue homeostasis during normal physiological function and for restoring equilibrium following pathological insults. - Source: PubMed
Publication date: 2026/05/26
Qian JintaoZhang JunhaoWang JiahuiXu SuyuYu LiKong ChuiyuZhou Qing - Osteoporosis is driven by a pathological imbalance in bone remodeling, with osteoclast hyperactivation being a primary driver of bone loss. However, the intrinsic signaling nodes that govern osteoclast survival and function remain poorly understood. While loss-of-function mutations in Anoctamin 5 (Ano5) are associated with genetic skeletal disorders, its precise involvement in metabolic osteoporosis remains elusive. In this study, we utilized an Ano5-deficient ovariectomized (OVX) mouse model to investigate the role of Ano5 in bone homeostasis. We found that genetic depletion of Ano5 significantly attenuated the osteoporotic phenotype in OVX mice, evidenced by preserved bone microarchitecture, enhanced biomechanical properties, and suppressed bone resorptive activity. Mechanistically, Ano5-deficient osteoclasts exhibited classical hallmarks of ferroptosis, including the accumulation of the lipid peroxidation end-product malondialdehyde (MDA), elevated reactive oxygen species (ROS), and a notable upregulation of the key lipid metabolic enzyme ACSL4 at the protein level. Importantly, the impaired osteoclastogenesis observed in Ano5-deficient cells was effectively rescued by pharmacological inhibition of either ferroptosis (via Ferrostatin-1) or ACSL4 activity (via Rosiglitazone), which restored TRAP-positive osteoclast numbers, F-actin ring formation, and the expression of resorptive markers such as CTSK. Our findings identify Ano5 as a critical regulator of bone remodeling that modulates osteoclastogenesis through the ACSL4-dependent ferroptosis pathway. This study not only uncovers a previously unrecognized molecular axis in bone cell biology but also highlights the Ano5-ACSL4-ferroptosis axis as a potential therapeutic target for the treatment of osteoporosis. - Source: PubMed
Publication date: 2026/05/28
Zhang MingyueXu HuichongSun KaiwenZhang ShuaiWang ShengnanLin LiqiLi HongyuHu Ying