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The RP2 locus has been implicated as one cause of X-linked retinitis pigmentosa. Additionally we are shipping RP2 Proteins (1) and many more products for this protein.
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maternal rp2 mRNA is essential for successful embryonic development and thus contributes to egg developmental competence
Knockout of RP2 decreases GRK1 (show GRK1 ELISA Kits) and rod transducin (show GNAT1 ELISA Kits) subunits and leads to photoreceptor degeneration in zebrafish
Results suggest that RP2 plays a key role in photoreceptor development and maintenance in zebrafish
Zebrafish RP2 is widely expressed throughout development. ZFRP2 knockdown caused retinal degeneration in zebrafish.
The ability of the restored RP2 protein level to reverse the observed cellular phenotypes in cells lacking RP2 indicates that translational read-through could be clinically beneficial for patients.
ellipsometric measurements of naRP2 demonstrated that its particular affinity for saturated phospholipids can be explained by its larger extent of insertion in this phospholipid monolayer compared to that in polyunsaturated phospholipid monolayers.
The methylation state of CpG sites close to the RP2 core promoter (GAAA)n repeat serves as a proxy measurement of X-chromosome inactivation in human and non-human primates.
A novel frameshift mutation in RP2 was detected. This mutation was located in exon 2 of the RP2 gene: a nucleotide C was inserted at 111 (c.111insC, Fig. 1A), which caused a protein translation frameshift
Direct sequencing of RPGR and RP2 allowed for identification of a disease-causing mutation in 21 families. Of these "adRP" families 19 had RPGR mutations, and two had RP2 mutations.
Based on our findings, we suggest that RPGR (show RPGR ELISA Kits) should be considered as a first tier gene for screening isolated males with retinal degeneration.
data support a role for RP2 in facilitating the membrane association and traffic of Gbeta1, potentially prior to the formation of the obligate Gbeta:Ggamma heterodimer; combined with other recent evidence, this suggests that RP2 may co-operate with Arl3 and its effectors in the cilia-associated traffic of G proteins
The localization of RP2 to basal bodies and cilia in photoreceptors and kidney cells has linked RP2 dysfunction with ciliopathies.
Data demonstrate that Importin (show KPNA4 ELISA Kits) beta2 is necessary for localization of retinitis pigmentosa 2 (RP2) to the primary cilium, and identify two distinct binding sites of RP2, which interact independently with Importin (show KPNA4 ELISA Kits) beta2.
An identifiable phenotype for RP2-X-linked retinitis pigmentosa aids in clinical diagnosis and targeted genetic screening.
we first performed detailed characterization of the Rp2-knockout (Rp2-KO) mice and observed early-onset cone dysfunction
Our studies suggest that RP2 contributes to the maintenance of photoreceptor function and that cone opsin mislocalization represents an early step in XLRP caused by RP2 mutations.
We propose that RP2 regulation of Arl3 is important for maintaining Golgi cohesion, facilitating the transport and docking of vesicles and thereby carrying proteins to the base of the photoreceptor connecting cilium for transport to the outer segment.
The RP2 locus has been implicated as one cause of X-linked retinitis pigmentosa. The predicted gene product shows homology with human cofactor C, a protein involved in the ultimate step of beta-tubulin folding. Progressive retinal degeneration may therefore be due to the accumulation of incorrectly-folded photoreceptor or neuron-specific tubulin isoforms followed by progressive cell death
, retinitis pigmentosa 2 (X-linked recessive)
, XRP2 protein
, XRP2-like protein
, protein XRP2-like
, retinitis pigmentosa 2 homolog