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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 (show RPE Antibodies) apico-lateral cell membrane.
Here we show that mouse POGLUT1 (show POGLUT1 Antibodies) modifies NOTCH1 (show NOTCH1 Antibodies) in vivo; however, the essential role of POGLUT1 (show POGLUT1 Antibodies) in gastrulation is due to POGLUT1 (show POGLUT1 Antibodies)-dependent glycosylation of EGF (show EGF Antibodies) repeats in the apical polarity protein CRUMBS2
Study showed that CRB1 (show CRB1 Antibodies) 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 (show CRB1 Antibodies)-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 (show CRB1 Antibodies) 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 (show MPP5 Antibodies) leads to the disruption of the apical localization of Crb polarity complex proteins Crb1 (show CRB1 Antibodies), Crb2 and Crb3 (show CRB3 Antibodies) in retinal progenitors and the adult retina.
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 (show CLTA Antibodies).
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).
May play a role in polarized cells morphogenesis.
crumbs-like protein 2
, protein crumbs homolog 2