Ask about this productRelated genes to: OSMR antibody
- Gene:
- OSMR NIH gene
- Name:
- oncostatin M receptor
- Previous symbol:
- -
- Synonyms:
- OSMRB
- Chromosome:
- 5p13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-02-17
- Date modifiied:
- 2018-07-11
Related products to: OSMR antibody
Related articles to: OSMR antibody
- Oncostatin M receptor (OSMR) plays diverse roles in several human malignancies, including brain, breast, and pancreatic cancer. In glioblastoma (GB), OSMR orchestrates a feedforward signaling mechanism with the truncated active mutant of epidermal growth factor receptor (EGFR), the EGFRvIII, and signal transducer and activator of transcription 3 (STAT3) to drive GB progression. Beyond EGFRvIII, OSMR promotes brain tumor stem cell (BTSC) respiration and therapy resistance. The molecular mechanisms underlying OSMR's multifaceted roles remain largely unclear. Here, we systematically mapped the OSMR interactome using Mammalian Membrane Two-Hybrid High-Throughput Screening (MaMTH-HTS). We identified OSMR-specific and OSMR/EGFRvIII-specific high-confidence candidate binding proteins, highlighting OSMR context-dependent functions. Among a subset of common interactors, we uncovered chloride intracellular channel 1 (CLIC1) as a critical regulator of OSMR-STAT3 signaling and the OSMR/EGFRvIII complex. CLIC1 physically associates with OSMR and EGFRvIII and facilitates EGFRvIII packaging into extracellular vesicles (EVs). Genetic deletion of CLIC1 disrupts the OSMR/EGFRvIII interaction, impairs STAT3 activation, reduces EGFRvIII EV content, and slows GB progression. Using whole-cell patch-clamp recordings and a monoclonal antibody that selectively targets transmembrane CLIC1 (tmCLIC1omab), we establish a distinct pharmacologically and biophysically tmCLIC1-mediated current in GB indispensable for sustaining EGFRvIII/STAT3 signaling. Importantly, we show that OSMR is required for maintaining CLIC1-mediated ionic balance at the plasma membrane (PM). Our study uncovers a bidirectional crosstalk between OSMR and tmCLIC1 in GB, essential for fueling its malignant growth. - Source: PubMed
Publication date: 2026/05/23
Mansourabadi Amir HosseinQu DianboCianci FrancescaSnider JamieRandhawa KamaldeepRaco LauraKotlyar MaxAl Ayach MohammadRey GuidoSanghvi ShridharAbovsky MarkSingh HarpreetLuchman H ArteeBurger DylanRak JanuszSoleimani Vahab DJurisica IgorStagljar IgorMazzanti MicheleJahani-Asl Arezu - Primary localized cutaneous amyloidosis (PLCA) is a chronic pruritic dermatological disorder characterized by amyloid deposits in the papillary dermis, significantly impairing patients' quality of life. Although the pathogenesis of PLCA is multifaceted, emerging evidence highlights the pivotal role of dysregulated cytokines, particularly the members of interleukin-6 (IL-6) cytokines family in PLCA. Oncostatin M (OSM) mediates keratinocyte proliferation through the STAT5-KLF7 axis upon OSMRβ engagement. Pathogenic variants in OSMR disrupt receptor dimerization, thereby suppressing signal transduction. These alterations together with cytokine dysregulation concomitantly elevate the expression of AHNAK and suppress that of Bcl-xL, which accelerate keratinocyte differentiation and apoptosis respectively, leading to the thickening of the stratum corneum and amyloid fibril deposition. Furthermore, dysregulated expression of chemokine monocyte chemoattractant protein-1 (MCP-1) by pathogenic variant in IL-31RA reduces monocyte-mediated clearance of amyloid fibrils, thereby promoting their pathological retention. The mechanisms of IL-31-mediated pruritus remain to be elucidated, given the conflicting observations that while some studies report wider cutaneous innervation in FPLCA patients, others demonstrate opposing results in general lichen amyloidosis patients. This review aims to synthesize recent advances in understanding PLCA pathogenesis with a focus on IL-31 and OSM cytokines network dysregulation especially driven by pathogenic variants, and provide critical insights for identifying therapeutic targets and put forward challenges in the future. - Source: PubMed
Publication date: 2026/04/24
Teng YiZhou XingliXiao YueLei KaixinDai LunzhiLi Wei - - Source: PubMed
Publication date: 2026/04/21
Fischer Michael J MReeh Peter W - Blood-brain barrier (BBB) disruption is a major contributor to brain injury following ischemic stroke. However, current endothelial-targeted strategies for BBB protection have shown limited clinical efficacy. Glial cells are essential for maintaining BBB integrity, but the mechanisms underlying glial-mediated BBB dysfunction after ischemic stroke remain poorly defined. Here, we identify microglial oncostatin M (OSM) and astrocytic OSM receptor (OSMR) as critical mediators of BBB disruption following cerebral ischemia-reperfusion. Single-cell RNA sequencing and immunofluorescence analysis revealed selective upregulation of OSMR in astrocytes after transient middle cerebral artery occlusion and reperfusion (MCAO/R) in mice. Astrocyte-specific OSMR knockdown maintained BBB integrity by restoring aquaporin-4 polarity and tight junction protein expression in electron microscopy and dextran leakage assays, thereby reducing infarct volume and improving neurological function. To elucidate the underlying mechanism, cell-cell communication analysis and proximity ligation assays demonstrated a direct and enhanced interaction between microglial OSM and astrocytic OSMR after MCAO/R. Similarly, OSM was markedly upregulated in microglia, and microglia-specific OSM knockout reproduced the protective effects of astrocytic OSMR knockdown, thereby restoring BBB integrity. Collectively, these results support the OSM-OSMR axis as a potential therapeutic target for the preservation of BBB integrity in ischemic stroke. - Source: PubMed
Publication date: 2026/04/10
Li LianxinLi XiangLiu YangyangLi HangDing HaojieLu JinxinCao ChangYuan JinlongChen GangLi Haiying - Oncostatin M (OSM) and its receptor (OSMR) are implicated in chronic inflammatory diseases. The role of OSM in Graves' orbitopathy (GO) pathogenesis remains unclear. Here, we investigated the role of OSM-OSMR signaling in GO pathogenesis and assessed its potential as a therapeutic target. - Source: PubMed
Publication date: 2026/05/24
Park Jeong WooChoi Soo HyunSurl DongheonKo JaesangYoon Jin Sook