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anti-Mouse (Murine) CRB2 Antibodies:
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cells with high apical CRB2 are basally extruded from the epiblast by neighbouring cells with high levels of apical myosin.
CRB2 is required for maintenance of the apical polarity complex during development of the cortex and regulation of cell division, and that loss of CRB2 results in cortical abnormalities
Our study identified CRB2 as the member of the CRB protein family that is present together with the rest of the components of the Crumbs complex in the RPE apico-lateral cell membrane.
Here we show that mouse POGLUT1 modifies NOTCH1 in vivo; however, the essential role of POGLUT1 in gastrulation is due to POGLUT1-dependent glycosylation of EGF repeats in the apical polarity protein CRUMBS2
Study showed that CRB1 and CRB2 in human retinas have an opposite pattern of expression in Muller glia and photoreceptor cells compared with mouse retinas, and that Crb2 influences the severity of the murine Crb1-linked retinal dystrophies.
Data suggest that short-term loss of CRB2 in adult mouse photoreceptors, but not in Muller glial cells, causes sporadic loss of adhesion between photoreceptors and Muller cells
These findings suggest that CRB1 and CRB2 suppress late progenitor pool expansion by regulating multiple proliferative signaling pathways.
loss of CRB2 in the developing retina results in retinal disorganization and subsequent degeneration without major changes in the transcriptome of the retina.
data suggest an essential role for CRB2 in proper lamination of the photoreceptor layer and suppression of proliferation of late-born retinal progenitor cells
Data show the deletion of Pals1 leads to the disruption of the apical localization of Crb polarity complex proteins Crb1, Crb2 and Crb3 in retinal progenitors and the adult retina.
Deficiency in Crumbs homolog 2 (Crb2) affects gastrulation and results in embryonic lethality in mice.
demonstrate that Crb2 overexpression under self-renewing conditions increases glycogen synthase kinase (GSK)-3beta inhibition
Case Report: steroid-resistant nephrotic syndrome caused by a novel Crumbs homolog 2 mutation.
These findings demonstrate that Crb2 abnormalities caused by these mutations are the mechanism of steroid-resistant nephrotic syndrome
Clinically, CRB2 should be assessed when ciliopathy is suspected, especially in Ashkenazi Jews, where we found that p.N800K carrier frequency is 1 of 64. Patients harboring CRB2 mutations should be tested for the complete range of ciliopathy manifestations.
Additional sequence variants in genes involved in kidney development were found in patients with CRB2-related syndrome, suggesting that these variants may modify the phenotype.
We demonstrate that CRB2 mutations result in loss of function and therefore constitute causative mutations leading to Nephrotic syndrome in humans.
The three families with six affected individuals present compelling evidence for the role of CRB2 in human disease, with a phenotype comprising severe, congenital neurological and renal involvement.
results suggest that CRB2 functions as an inhibitory binding protein that is involved in the formation of a mature but inactive pool of the gamma-secretase complex
The CRB2 gene encodes a transmembrane protein (1285 aa) and a secreted protein (1176 aa). The transmembrane isoform consists of 14 extracellular EGF-like domains, 3 extracellular laminin G-like domains, and a Crb cytoplasmic tail domain.
This study shows that CRB2 sequence variants are not a common cause of autosomal recessive RP and LCA.
Using X-ray crystallography and NMR spectroscopy, we show that, despite low amino acid sequence conservation, both 53BP1 and Crb2 contain tandem tudor domains that interact with histone H4 specifically dimethylated at Lys20 (H4-K20me2).
overexpression of human CRB1 and related isoforms, CRB2 and CRB3, had no effect on the levels of presenilin complex components, on NCT maturation or on PS endoproteolysis
Mutations in crb2a affect cilia length in a subset of tissues accompanied by accumulation of other Crumbs proteins in the ciliary compartment.
This study show that the undifferentiated CNS expresses Crb1, Crb2a, and Crb2b in distinct spatial and temporal patterns.
oko meduzy (crb2a) locus encodes a crumbs gene homolog, essential for the proper apico-basal polarity of neural tube epithelia
It was demonstrated that the extracellular domains of Crb2a and Crb2b mediate a cell-cell adhesion function, which plays an essential role in maintaining the integrity of the photoreceptor layer.
Study shows that the FERM protein Mosaic Eyes (Moe) is a novel regulatory component of the Crumbs complex and coimmunoprecipitates with Ome/Crb2a and Nok (Pals1) from adult eye and in vitro interaction experiments suggest these interactions are direct.
May play a role in polarized cells morphogenesis.
crumbs-like protein 2
, protein crumbs homolog 2
, crumbs family member 2
, crumbs homolog 2
, crumbs homolog 2a
, oko meduzy