Ask about this productRelated genes to: RBPMS Blocking Peptide
- Gene:
- RBPMS NIH gene
- Name:
- RNA binding protein, mRNA processing factor
- Previous symbol:
- -
- Synonyms:
- HERMES
- Chromosome:
- 8p12
- Locus Type:
- gene with protein product
- Date approved:
- 2003-02-25
- Date modifiied:
- 2018-01-04
Related products to: RBPMS Blocking Peptide
Related articles to: RBPMS Blocking Peptide
- To compare diazoxide (DZ), an ATP-sensitive potassium channel opener and latanoprost free acid (LFA), the active metabolite of the prostaglandin analogue latanoprost, a first-line agent for intraocular pressure (IOP) reduction in patients with glaucoma, on IOP, retinal ganglion cell (RGC) density, retinal morphology, and glial cell activation in the DBA/2J mouse model of pigment dispersion glaucoma. - Source: PubMed
Publication date: 2026/08/15
Niknam ParvinOmer Mohammed EAnderson Kjersten JRinkoski Tommy ARoy Chowdhury UttioRoddy Gavin W - Glaucoma is a neurodegenerative eye disease characterized by progressive loss of retinal ganglion cells (RGCs), resulting in irreversible vision loss. Previous work demonstrated that irbesartan, an angiotensin II type I receptor blocker, promotes RGC survival in rat retinal explants. This study extends these findings to ex vivo mouse explants, in vivo optic nerve crush model, and transcriptomic analysis to identify associated pathways. Retinal explants from C57BL/6 mice were cultured for 4 days with irbesartan (10 μmol/L), vehicle, or angiotensin II (2 μmol/L). RGC survival was assessed by βIII-tubulin and RNA-binding protein with multiple splicing (RBPMS) immunostaining; superoxide and mitochondrial density were measured using dihydroethidium and MitoTracker Red CMXRos. Mice received vehicle or irbesartan (10 μmol/L) eye drops for 7 days after optic nerve crush to assess RGC survival. Irbesartan enhanced RGC survival in explants (1.5-fold and 4-fold; P = 0.0138 and 0.000129) and in vivo (1.7-fold; P = 0.0045). Irbesartan reduced dihydroethidium intensity (P < 0.0072) and preserved mitochondrial labeling at day 2 (P = 0.02). RNA sequencing revealed differential expression of electron transport chain genes (eg, Cox4i2 and Ndufa12), with gene set enrichment analysis showing enrichment of proinflammatory pathways in vehicle-treated explants and neuronal/metabolic pathways with irbesartan. In conclusion, irbesartan reduces oxidative stress and modulates mitochondrial and inflammatory pathways, potentially supporting RGC survival, thus providing insights relevant to glaucoma and optic neuropathies involving RGC degeneration. - Source: PubMed
Publication date: 2026/08/11
Pattamatta UshasreeLiang Yichuan GSundaram RaviQin MelanieCarnt NicoleMarcus AdrianWhite Andrew - This study evaluated the neuroprotective effects of inhibiting the pro-apoptotic molecule Bim (Bcl-2-interacting mediator of cell death) in retinal ganglion cells (RGCs). A mouse optic nerve crush (ONC) model was used to induce RGC degeneration. Bim expression and RGC survival were assessed by immunohistochemistry, RNA-binding protein with multiple splicing (RBPMS) immunofluorescence, and histologic analyses. Following intravitreal injection of adeno-associated virus serotype 2-shBim, retinal structure and visual function were evaluated by optical coherence tomography, flash visual-evoked potentials, and flash electroretinography. Optic nerve axons were assessed by cholera toxin subunit B-555 anterograde tracing. Primary dorsal root ganglion neurons were used to examine the effects of Bim manipulation on axon growth. RNA sequencing, real-time quantitative PCR, and pharmacologic modulation of Drd1 signaling were performed to investigate associated molecular changes. ONC induced marked up-regulation of Bim expression accompanied by substantial RGC loss. Adeno-associated virus serotype 2-shBim treatment reduced Bim expression, preserved retinal structure, increased RGC survival, partially improved visual function, and enhanced axonal preservation after injury. In dorsal root ganglion cultures, Bim knockdown promoted axon elongation, whereas Bim overexpression suppressed axon growth. Transcriptomic analysis identified significant up-regulation of Drd1 following Bim inhibition, which was confirmed by real-time quantitative PCR. Pharmacologic activation of DRD1 enhanced axon growth, whereas DRD1 blockade attenuated this effect. Taken together, these findings indicate that Bim inhibition is associated with enhanced RGC survival and axonal preservation after ONC, with Drd1-related signaling potentially contributing to these effects. - Source: PubMed
Publication date: 2026/08/07
Cheng ZhenhaoWu LinglingQu YilunZhang ChuyueYe ZiLi ZhaohuiChen Xiaoniao - To investigate the role of BCL-2-interacting mediator of cell death (), a pro-apoptotic molecule, in retinal ganglion cell (RGC) injury after optic nerve crush (ONC), and to analyze its association with changes in the expression of inflammation-related genes. This was an experimental study. The study was conducted from January 2025 to December 2025. Healthy male mice aged 6-8 weeks were randomly divided into four groups: control, ONC, AAV2-scramble, and AAV2-shBim, with 6 mice in each group. The control group received no intervention, the ONC group underwent ONC only, the AAV2-scramble group received intravitreal injection of AAV2-mediated scrambled negative control sequence after ONC, and the AAV2-shBim group received intravitreal injection of AAV2-mediated short hairpin RNA targeting the gene after ONC. Immunohistochemical staining was used to detect the protein expression of Bim, complement component 3 (C3), and lipocalin 2 (Lcn2). Hematoxylin-eosin (HE) staining was used to observe retinal structural changes. Retinal flat-mount immunofluorescence staining was used to assess RGC survival. Optical coherence tomography (OCT) was used to measure ganglion cell complex (GCC) thickness. Flash visual evoked potential (F-VEP) and flash electroretinography (F-ERG) were used to evaluate visual electrophysiological function. RNA sequencing was performed to analyze retinal transcriptomic changes after knockdown. Quantitative real-time PCR (qPCR) was used to validate inflammation-related differentially expressed genes. Independent-sample -test and one-way analysis of variance were used for statistical analysis. The proportions of Bim-positive RGCs in the peripheral and central retina were 0.56±0.06 and 0.63±0.06 in the ONC group, respectively, both of which were higher than those in the control group (0.00±0.00) (=21.60, 24.61; both <0.001). The numbers of RNA-binding protein with multiple splicing(RBPMS)-positive RGCs in the peripheral and central retina were 74.2±4.4 and 118.5±8.0 in the ONC group, respectively, both of which were lower than those in the control group (222.7±6.0 and 325.0±6.5, respectively) (=48.94, 48.88; both <0.001). Significant differences were observed among the four groups in ganglion cell complex thickness, the number of TUJ1-positive RGCs, F-VEP N2-P2 amplitude, and F-ERG b-wave amplitude (=57.42, 1 216.78, 467.88, 423.76; all <0.001). In the AAV2-shBim group, ganglion cell complex thickness, the number of TUJ1-positive RGCs, F-VEP N2-P2 amplitude, and F-ERG b-wave amplitude were 54.64±2.61 μm, 242.8±13.1, 11.13±0.80 μV, and 318.00±25.14 μV, respectively, all of which were higher than those in the ONC group [(44.29±1.95) μm, 140.0±5.3, (3.43±0.48) μV, and (190.68±25.50) μV, respectively] (all <0.001). RNA sequencing showed that the expression levels of the inflammation-related genes , , , , , and were lower in the AAV2-shBim group than in the ONC group (=10.21, 12.02, 8.98, 12.19, 7.33, 9.41; all <0.001), and the quantitative polymerase chain reaction results were consistent with the RNA sequencing results. The C3-positive cell rates in the central and peripheral retina were 0.11±0.04 and 0.08±0.02 in the AAV2-shBim group, respectively, both of which were lower than those in the ONC group (0.64±0.06 and 0.57±0.05, respectively) (=18.63, 21.04; both <0.001). The Lcn2-positive cell rates in the central and peripheral retina were 0.08±0.03 and 0.09±0.02 in the AAV2-shBim group, respectively, both of which were lower than those in the ONC group (0.55±0.06 and 0.48±0.07, respectively) (=17.19, 12.38; both <0.001). expression is upregulated after ONC. AAV2-mediated knockdown alleviates RGC loss, retinal structural damage, and visual electrophysiological dysfunction, accompanied by downregulation of inflammation-related gene expression. - Source: PubMed
Cheng Z HChen X NLi Z H - To investigate the changes in the neurovascular unit (NVU) of the retina in rats following optic nerve (ON) injury, and to explore the translational implications for traumatic optic neuropathy (TON). - Source: PubMed
Publication date: 2026/06/09
Wu QiongWang HuiLiu HongJuanZhang LuyinWei Qiping