Ask about this productRelated genes to: STOML3 antibody
- Gene:
- STOML3 NIH gene
- Name:
- stomatin like 3
- Previous symbol:
- -
- Synonyms:
- SRO, Epb7.2l
- Chromosome:
- 13q13.2
- Locus Type:
- gene with protein product
- Date approved:
- 2002-11-11
- Date modifiied:
- 2015-12-01
Related products to: STOML3 antibody
Related articles to: STOML3 antibody
- The microtubule-stabilizing drug paclitaxel remains the standard of care for various solid malignancies but frequently leads to chemotherapy-induced peripheral neuropathy (CIPN). CIPN is a leading cause for premature treatment termination and a significantly reduced quality of life in long-term cancer survivors. The molecular mechanisms of neuro-axonal degeneration, neuroinflammation, and pain in patients treated with paclitaxel remain incompletely understood, and there are currently no predictive biomarkers or preventive treatments. We used human iPSC-derived sensory neurons exposed to paclitaxel to comprehensively model the pathophysiology of CIPN. Neurotoxicity was assessed over time using viability assays and sequential RNA sequencing, as well as deep proteome and lipidomic analyses. We observed a time and dose-dependent decline of cell viability at clinically relevant paclitaxel doses. Sequential RNA sequencing defined JUN as an early immediate gene, followed by the overexpression of genes of the neuronal stress response (e.g., ARID5A, WEE1, DUSP16, GADD45A), neuronal injury and apoptotic pathways (e.g., ATF3, HRK, BBC3 [PUMA], BCL2L11 [BIM], CASP3), neuroinflammation and nociception (CALCB, MMP10, IL31RA, CYSLTR2, C3AR1, TNFRSF12A) and neuronal transduction (e.g., CAMK2A, STOML3, PIRT), while key enzymes of lipid biosynthesis were markedly downregulated (e.g., LSS, HMGCS1, HMGCR, DHCR24). Deep proteome analyses following 48 h of exposure to 100 nM paclitaxel revealed a strong correlation of differentially expressed RNA with proteins, and a marked degradation of essential axonal transport proteins such as kinesins, stathmins, and scaffold proteins. Consistent with the downregulation of rate-limiting enzymes of lipid biosynthesis, lipidome analysis confirmed deregulation of neuronal lipid homeostasis. In summary, paclitaxel induces transcriptomic and proteomic signatures of the neuronal stress response, neuroinflammation, nociception, and disturbed metabolism. These may explain, in part, the clinical phenotype of sensory loss, hypersensitivity, and neuropathic pain frequently observed in patients suffering from CIPN, but constitute pharmacologically addressable targets. - Source: PubMed
Publication date: 2026/02/10
Schinke ChristianMaierhof Smilla KHew LoisFernandez Vallone ValeriaFrahm SilkeTelugu Narasimha SwamyDiecke SebastianIvanov AndranikKovács RichardBeule DieterKirchner MarieluiseMertins PhilippBrüning UlrikeKirwan Jennifer AStachelscheid HaraldEndres MatthiasHuehnchen PetraBoehmerle Wolfgang - Mammalian olfactory epithelium (OE) undergoes consistent self-renewal throughout life. In OE homeostasis, globose basal cells (GBCs) contribute to the generation of olfactory sensory neurons (OSNs) to replace old ones. Chitinase-like 4 (Chil4), a chitinase-like protein expressed in supporting cells, plays a critical role in OE regeneration, while its role in tissue homeostasis is still elusive. Here, we found that Chil4 is upregulated in the aged OE. Deletion of Chil4 leads to a reduction in the number of GBCs and immature OSNs (iOSNs). Chil4 GBCs show attenuation in cell cycle progression and an aberrant expression pattern of cell-cycle-related genes such as Cdk1. Chil4 deletion causes loss of a specific subcluster of GAP43 iOSNs expressing Cebpb, Nqo1 and low level of mature OSN (mOSN) marker Stoml3 (iOSN_CeStNq), potentially suggesting a transitional state between immature and mature neurons. Chil4 knockout induces inflammatory activation in Iba1 microglia (MG)-like cells in the OE. Chil4 downregulation in aged organoids reduced the number of mature sensory neurons, suggesting a necessary role of Chil4 in maintaining neuronal generation in the aged OE. Collectively, these observations reveal a previously unidentified function of Chil4, establishing the cellular mechanism underlying OE homeostasis. - Source: PubMed
Publication date: 2025/05/19
Wu TingtingLi WeihaoZhuang LiujingLiu JinxiaWang PingGu YeLiu YongliangYu Yiqun - Allergic conjunctivitis (AC) is a common inflammatory condition characterized by immune dysregulation in response to environmental allergens. Despite extensive research into general allergic mechanisms, the specific immunological features of the ocular mucosal microenvironment remain poorly understood. Investigating immune-related mRNAs and LncRNAs may provide insights into the mechanisms underlying AC and potential novel targets for therapeutic intervention. - Source: PubMed
Publication date: 2025/05/08
Zhang HongZhang HongyuLeng QingZheng Ya Juan - Nerve regeneration is associated with the plasticity of sensory neurons such that even muscle afferents directed to the skin form mechanosensitive receptive fields appropriate for the new target. STOML3 is an essential mechanotransduction component in many cutaneous mechanoreceptors. Here, we asked whether STOML3 is required for functional and anatomical plasticity following peripheral nerve regeneration. We used a cross-anastomosis model adapted to the mouse, in which the medial gastrocnemius nerve was redirected to innervate hairy skin previously occupied by the sural nerve. We recorded from muscle afferents innervating the skin and found that in wild-type mice their receptive properties were largely identical to normal skin mechanoreceptors. However, in mice lacking STOML3, muscle afferents largely failed to form functional mechanosensitive receptive fields, despite making anatomically appropriate endings in the skin. Our tracing experiments demonstrated that muscle afferents from both wild-type and stoml3 mutant mice display remarkable anatomical plasticity, forming new somatotopically appropriate synaptic terminals in the region of the dorsal horn representing the sural nerve territory. The dramatic reduction in stimulus-evoked activity from the cross-anastomosed gastrocnemius nerve in stoml3 mutant mice did not prevent central anatomical plasticity. Our results have identified a molecular factor required for functional plasticity following peripheral nerve injury. - Source: PubMed
Publication date: 2025/03/31
Haseleu JuliaWalcher JanLewin Gary R - This study aimed to clarify the roles and underlying mechanisms of luteolin in the progression of cerebral ischemia/reperfusion injury (CIRI). - Source: PubMed
Publication date: 2024/11/04
Yu FeiWang GuangxueChen XingyiZhang YanfeiYang ChengHu HuiWei Liang