Retinoschisin 1 (RS1) ELISA Kits

RS1 encodes an extracellular protein that plays a crucial role in the cellular organization of the retina. Additionally we are shipping Retinoschisin 1 Antibodies (17) and Retinoschisin 1 Proteins (7) and many more products for this protein.

list all ELISA KIts Gene Name GeneID UniProt
RS1 6247 O15537
RS1 20147 Q9Z1L4
Anti-Rat RS1 RS1 100125595  
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Top Retinoschisin 1 ELISA Kits at

Showing 2 out of 7 products:

Catalog No. Reactivity Sensitivity Range Images Quantity Delivery Price Details
Human 0.057 ng/mL 0.15 ng/mL - 10 ng/mL 96 Tests 13 to 16 Days
Mouse 0.2 ng/mL n/a   96 Tests 15 to 18 Days

Top referenced Retinoschisin 1 ELISA Kits

  1. Human RS1 ELISA Kit for Sandwich ELISA - ABIN423926 : Delgado, del Pozo-Rodríguez, Solinís, Avilés-Triqueros, Weber, Fernández, Gascón: Dextran and protamine-based solid lipid nanoparticles as potential vectors for the treatment of X-linked juvenile retinoschisis. in Human gene therapy 2012 (PubMed)
    Show all 5 Pubmed References

More ELISA Kits for Retinoschisin 1 Interaction Partners

Human Retinoschisin 1 (RS1) interaction partners

  1. Full-field electroretinography recordings showed extinguished rod and cone responses. Diagnostic-genetic testing revealed a hemizygous missense mutation in the RS1 gene (c.305G > A; p.Arg102Gln) was identified.

  2. A novel RS1 (Xp22.2) mutation was detected (413C > A) resulting in a Thr138Asn substitution in an Irish pedigree of X-linked Retinoschisis. Protein modelling demonstrated a change in higher order protein folding that is likely pathogenic.

  3. The central foveal thickness varies during daytime hours in patients with XLRS. This finding may explain the inconsistent and heterogeneous responses to treatment with CAIs and necessitate standardization of measurement times in treatment trials for XLRS as well as in the routine ophthalmic evaluation of these patients.

  4. molecular detail such as the precise localization of mutant protein in the cell as well as its ability to assemble into a functionally active oligomer might largely influence disease severity among XLRS patients

  5. These results establish that extracellular delivery of RS1 rescues the structural and functional deficits in the Rs1h knockout mouse model and that this ex vivo gene therapy approach can inhibit progression of disease.

  6. Taken together, RS1 mutation was found to segregate with retinoschisis phenotype while none of the other identified variations were co-segregating with the systemic defects. Hereby, we infer that the multisystemic defects harbored by the patient are a rare coexistence of XLRS, developmental delay, sensorineural hearing loss, and reduced axial tone reported for the first time in the literature.

  7. Results suggest a regulatory effect of retinoschisin on Na/K-ATPase signaling and localization, whereas Na/K-ATPase-dysregulation caused by retinoschisin deficiency could represent an initial step in XLRS pathogenesis.

  8. these findings support distinct mechanisms of pathology for two classes of X-linked retinoschisis -associated mutations in the retinoschisin assembly.

  9. A novel RS1 (97delT) mutation was identified in a Taiwanese family with X-linked retinoschisis (XLRS). This finding expands the RS1 mutation spectrum and may help to further understand the molecular pathogenesis of XLRS.

  10. Clinical and genetic characterization of affected homozygous females in XLRS affords the rare opportunity to explore the molecular mechanisms of XLRS and the manifestation of these mutations as disease in humans.

  11. A novel RS1 (304C > T) mutation in a Taiwanese family with X-linked retinoschisis.

  12. We identified a novel causative mutation of RS1 in a Chinese family with X-linked juvenile retinoschisis.

  13. the disease and p.Arg197Cys mutation of RS1 gene was identified

  14. X-linked retinoschisis despite striking differences in phenotypic presentation in affected subjects, homozygosity of one affected female, and seemingly dominant inheritance in three subsequent generations because of multiple consanguinity.

  15. Sequencing of the RS1 gene identified 16 mutations, nine of which were novel.

  16. Severe RS1 missense changes were associated with a lower ERG b/a ratio than were mild changes in X-linked retinoschisis suggesting the effect of the mutations on protein structure influenced the retinal dysfunction.

  17. Two novel exonic deletions within the RS1 gene locus, are reported.

  18. There is profound phenotypic variability in patients with XLRS. Nonsense, splice-site, or frame-shifting mutations in RS1 consistently caused electronegative bright-flash ERG, delayed flicker response, and abnormal PERG

  19. Four novel RS1 gene mutations have been described in male Polish patients with X-linked juvenile retinoschisis.

  20. aggregation propensity in the RS1 C110Y mutant is dependent upon the formation of suitable aggregating substrates for propagation of aggregation and not directly related to or determined by overall structural instability

Mouse (Murine) Retinoschisin 1 (RS1) interaction partners

  1. Results suggest a regulatory effect of retinoschisin on Na/K-ATPase signaling and localization, whereas Na/K-ATPase-dysregulation caused by retinoschisin deficiency could represent an initial step in XLRS pathogenesis.

  2. retinoschisin is a novel regulator of MAP kinase signalling and exerts an anti-apoptotic effect on retinal cells.

  3. Based on this structure, we propose that RS1 couples neighboring membranes together through octamer-octamer contacts, perhaps modulated by interactions with other membrane components.

  4. Changes in Rs1-knockout mice were associated with age related alterations in photoreceptor morphology and transcription factor expression that suggest delayed photoreceptor maturation.

  5. Time line analysis after short-term treatment with dorzolamide failed to show short-, intermediate-, or long-term evidence of structural improvement in Rs1h(-/y) mice.

  6. The results of this study demonstrated that loss of Rs1 gene function has a significant impact on the expression of photoreceptor transcription factor network genes, and morphological and functional defects in young (P21) Rs1-KO mice.

  7. RS1 is needed for preservation of synaptic structures but not synaptogenesis in retinoschisis model.

  8. Data suggest that a CpG island enhancer and two CBRs may act in a combinatorial fashion to fine-tune RS1 transcript levels in the retina.

  9. Retinoschisin, the protein involved in the pathogenesis of X-linked juvenile retinoschisis, membrane association is severely impaired in the absence of ATP1A3 and ATP1B2.

  10. Upon Rs1 adsorption, phosphatidylserine and phosphatidylserine-containing mixed lipid bilayers underwent fast and extensive reorganization.

  11. Inactivation of Rs1h suggests a role of retinoschisin in retinal cell layer organization and synaptic structure

  12. After synthesis and secretion by the photoreceptors, retinoschisin [Xlrs1] reaches the surface of retinal cells and mediates interactions/adhesion between photoreceptor, bipolar, and Muller cells

  13. Mimics structural features of human X-linked juvenile retinoschisis. Knockout results in electronegative ERG waveform characteristic of human retinoschisis and implicates synaptic transmission deficit in the absence of retinoschisin protein.

  14. We have generated and characterized a mutant mouse line that was produced using ENU-based mutagenesis. The 44TNJ pedigree manifests with photoreceptor dysfunction and concurrent structural and functional aberrations at the post-receptoral level.

  15. analysis of two mature isoforms of retinoschisin in murine retina

  16. photoreceptor degeneration in the Rs1h(-/Y) mouse is due to apoptotic events peaking around postnatal day 18. Cell death is accompanied by increased expression of initiator and inflammatory caspases but not by downstream effector caspases.

  17. Retinoschisin protein(RS) is expressed in the pinealocytes but not in interstitial glial cells. The lack of structural abnormalities in the RS1(-/Y) mice suggests that RS serves a different function in the pineal gland than in the retina.

  18. These results demonstrate that RS1H has functional significance in the morphology and function of the synapse between photoreceptors and second-order neurons.

  19. confirmed the co-localization of retinoschisin with Na/K ATPase and SARM1 in photoreceptors and bipolar cells of retina tissue

  20. These results indicate that activated microglia from degenerating retinae express high levels of Dap12 and PU.1, and PU.1 controls the myeloid-specific regulation of Dap12 directly.

Retinoschisin 1 (RS1) Antigen Profile

Antigen Summary

This gene encodes an extracellular protein that plays a crucial role in the cellular organization of the retina. The encoded protein is assembled and secreted from photoreceptors and bipolar cells as a homo-oligomeric protein complex. Mutations in this gene are responsible for X-linked retinoschisis, a common, early-onset macular degeneration in males that results in a splitting of the inner layers of the retina and severe loss in vision.

Gene names and symbols associated with Retinoschisin 1 (RS1) ELISA Kits

  • retinoschisin 1 (RS1) antibody
  • retinoschisin 1 S homeolog (rs1.S) antibody
  • retinoschisin 1 (rs1) antibody
  • retinoschisis (X-linked, juvenile) 1 (human) (Rs1) antibody
  • retinoschisin 1a (rs1a) antibody
  • retinoschisin 1 (Rs1) antibody
  • RS antibody
  • rs1 antibody
  • Rs1h antibody
  • tmgc1 antibody
  • Xlrs1 antibody
  • zgc:92703 antibody

Protein level used designations for Retinoschisin 1 (RS1) ELISA Kits

X-linked juvenile retinoschisis protein , retinoschisin , retinoschisis (X-linked, juvenile) 1 , retinoschisin 1 , retinoschisin-like , X-linked juvenile retinoschisis protein homolog , retinoschisis 1 homolog

6247 Homo sapiens
491762 Canis lupus familiaris
615193 Bos taurus
748866 Pan troglodytes
779332 Xenopus laevis
100124900 Xenopus (Silurana) tropicalis
100126075 Oryctolagus cuniculus
100127441 Sus scrofa
100423325 Macaca mulatta
20147 Mus musculus
445044 Danio rerio
100125595 Rattus norvegicus
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