Ask about this productRelated genes to: Rbm3 Blocking Peptide
- Gene:
- RBM3 NIH gene
- Name:
- RNA binding motif protein 3
- Previous symbol:
- -
- Synonyms:
- IS1-RNPL
- Chromosome:
- Xp11.23
- Locus Type:
- gene with protein product
- Date approved:
- 1995-08-29
- Date modifiied:
- 2017-12-06
Related products to: Rbm3 Blocking Peptide
Related articles to: Rbm3 Blocking Peptide
- As a non-coding RNA (lncRNA), the RNA component of mitochondrial RNA processing endoribonuclease (RMRP) is implicated in ribosome biogenesis. In recent years, its role in the neurodegenerative system has been reported; however, the molecular mechanism underlying RMRP-mediated neuroprotective effects remains elusive. In the present study, we identified that RMRP expression is regulated by the RNA-binding protein RBM3. The overexpression of RBM3 significantly upregulated RMRP transcription in SH-SY5Y neural cells, whereas RBM3 knockdown led to a marked reduction in RMRP expression. Furthermore, RNA Immunoprecipitation (RIP) assays confirmed the potential interaction between RMRP and RBM3. We then investigated the functional significance of RMRP regulated by RBM3 in Parkinson's disease (PD) cell models. Exogenous overexpression of RMRP strongly attenuated cytotoxicity induced by neurotoxins rotenone (ROT) and MPP in SH-SY5Y cells, as evidenced by decreased levels of cleaved poly ADP-ribose polymerase 1 (PARP1) and enhanced cell viability. Given that RBM3 exerts robust neuroprotective effects by accelerating global protein synthesis (GPS), we hypothesized that RMRP is a key mediator of RBM3-conferred neuroprotection. Consistent with this hypothesis, RMRP overexpression enhanced the activity of eukaryotic elongation factor 2 (eEF2), a hallmark of cellular GPS. Its stimulatory effect on GPS was further validated using a puromycin incorporation assay. Collectively, our data reveal that RMRP acts as a novel effector of RBM3 in stimulating cellular GPS and conferring neuroprotective effects in SH-SY5Y cells, providing a new therapeutic target for PD. - Source: PubMed
Publication date: 2026/07/28
Ma ShuangpingLiu XiantingXie YimingHan YuxuanWang NingLi ShenxueCheng BinfengJu FeiWang Lei - In this study, we evaluated the effect of a previous exposure of in vitro produced blastocysts to hypothermia (33°C) on their further cryotolerance. In Experiment 1, embryos were exposed to hypothermia for either 6 or 12 h on day 5 or 6 of development, and the blastocyst rates and kinetics were evaluated. In Experiment 2, the transcriptome of embryos exposed to hypothermia on either day 5 or 6 for 12 h was assessed. In Experiment 3, embryos were exposed to hypothermia for 12 h on day 6, vitrified-warmed, and their re-expansion, apoptotic index, and total cell number were assessed. Results showed that hypothermia had no effect on blastocyst rate but reduced the percentage of hatched blastocysts when applied for 12 h. Moreover, hypothermia was associated with changes in the transcriptional profile, particularly in embryos exposed on day 6, including increased expression of the cold-shock-related transcripts RBM3 and CIRBP. Finally, hypothermia on day 6 did not improve embryo re-expansion after cryopreservation but did reduce apoptosis in the surviving embryos. Our results provide insight into transcriptomic responses associated with mild hypothermia in bovine embryos and support the hypothesis that hormetic-like responses may contribute to improved embryo quality after cryopreservation. - Source: PubMed
Pantoja Luciano CGarcia Pereira-Junior Sérgio ARodrigues Izamara S RRodrigues Aryadne de LimaHomobono Bruno PSantos Simone S DCosta Nathália NCordeiro Marcela SSousa Alysson OChiaratti Marcos RMiranda Moysés Dos Santos - The cold-stress hormone fibroblast growth factor 21 (FGF21) induces a broad spectrum of neuroprotective effects, including a blunting effect on α-II-spectrin breakdown product 145 (SBDP145) levels in models of hypoxia-ischemia (HI). Here, we studied the impact of FGF21 dosing on cell survival and on SBDP145 levels in normothermic male/female cortical neurons in an oxygen-glucose deprivation (OGD) injury model of necrosis. We also explored the impact of FGF21 dosing on cold-shock proteins RNA-binding motif 3 (RBM3) and cold-induced RNA-binding protein (CIRBP) in the OGD injury model. FGF21 concentrations ≥ 100 ng/mL attenuated postinsult increases in SBDP145 levels but had no effect on acute (24 h) or delayed (48-72 h) neuronal survival at normothermia. Further, FGF21 treatment at the highest dose tested (10 µg/mL) induced a sparing effect on postinsult RBM3 levels. This prompted follow-up studies to test if combination therapy with FGF21 and therapeutic hypothermia (TH)-induced synergistic benefits on cell survival. Only intraischemic TH increased 24-h cell survival in our model. FGF21 had no effect on cell survival when combined with intraischemic or posttreatment TH. Finally, we verified that necrosis was the primary mechanism of cell death induced by OGD injury in our model. Pretreatment with calpain inhibitors decreased markers of necrosis, but increased markers of autophagy/apoptosis, and had no effect on 24-h cell survival. In contrast, pretreatment with NMDA receptor antagonist MK801 robustly increased 24-h cell survival. In summary, FGF21 posttreatment (≥ 100 ng/mL) primarily alleviated α-II-spectrin disruption in an OGD model of excitotoxicity-induced necrosis. - Source: PubMed
Publication date: 2026/07/01
Snyder KaraGorse KierstenC Jackson Travis - Microglia are key regulators of neuroinflammation and neuronal survival after ischemic stroke. Emerging single-cell, transcriptomic, and metabolic studies show that ischemia induces rapid microglial reprogramming toward pro-inflammatory states that exacerbate neuronal death, oxidative stress, blood-brain barrier (BBB) disruption, and white-matter injury. Multiple pathways, including TLR4/NF-κB, NLRP3 inflammasome activation, Notch1-JAK/STAT signaling, epigenetic modulators such as HDAC3 and METTL14, and metabolic shifts involving AMPK/mTOR/HIF1α, collectively shape post-stroke microglial polarization. High-altitude hypoxia elicits similar inflammatory responses, activating microglia through RAGE-MAPK/NFκB signaling, CX3CL1/CX3CR1-dependent synaptic pruning, mitochondrial dysfunction, and lactate-mediated chromatin changes, highlighting hypoxia as a convergent driver of neuroinflammation. Modulating microglial activity, therefore, represents a promising therapeutic strategy. A wide range of natural compounds (e.g., curcumin, acteoside, astagaloside IV, artemisinin), synthetic agents (e.g., DBZ, resolvin D1), and cellular/molecular cellular interventions (e.g., rhFGF21, S100A9 inhibition, RBM3 induction) have shown efficacy in reducing inflammation, preserving BBB integrity, improving mitochondrial function, and promoting M2-like reparative phenotypes in preclinical models. Advances in understanding microglial subtypes, including CH25H, OASL, CD11c, and antioxidant Prdx1-enriched populations, further highlight their dynamic roles across injury and repair. This review presents current insights into microglial signalling, epigenetic and metabolic regulation, and therapeutic targeting in ischemic stroke, integrating parallel insights from high-altitude hypoxia. Together, these prospectives illuminate microglia as crucial mediators of neurovascular injury and recovery, and highlight opportunities for translating microglia-directed therapies into clinical interventions. - Source: PubMed
Publication date: 2026/05/06
Khan ShafaSultan ArmiyaSadik MohdAshraf Mohammad Zahid - -Aminobutyric acid (GABA) is the principal inhibitory neurotransmitter in the central nervous system and is involved in the development of neural tissue as well as the regulation of its functions. Meanwhile, GABA has also been demonstrated to confer multiple physiological benefits, including alleviating stress and improving metabolic homeostasis. This study investigated GABA effects on proliferation, differentiation, and temperature stress protection of bovine skeletal muscle satellite cells (BSCs). - Source: PubMed
Publication date: 2026/04/14
Manzoor AbidNaseem SajidaFu ZhiqiRuan ChaohuiLiu XuYan ChunriChoi SeonghoLi Xiangzi