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BICC1 encodes an RNA-binding protein that is active in regulating gene expression by modulating protein translation during embryonic development. Additionally we are shipping BICC1 Antibodies (51) and many more products for this protein.
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These results demonstrate that the function of Bicc1 in the kidney is evolutionarily conserved, thus supporting the use of zebrafish as an alternative in vivo model to study the role of mammalian Bicc1 in renal cyst formation.
Results provide some support for the involvement of BICC1 and PCLO in late-life depressive disorders and preliminary evidence that these genetic variants may also influence brain structural volumes
findings identify a role for increased levels of BICC1 in the pathophysiology of depressive behavior
Polymorphisms in intron 2 of BICC1 are associated with its expression and bone (show BEST1 Proteins) mineral density (BMD)
The minor T-allele of BICC1 has a protective role against major depressive disorder and its known structural and functional brain changes.
The nonsense mutation identified in BICC1 and associated with cystic renal dysplasia results in a complete loss of Wnt (show WNT2 Proteins) inhibitory activity. The point mutation in the SAM (show TTN Proteins) domain results in a 22% loss of activity.
Polymerization is a novel disease-relevant mechanism both to stabilize Bicc1 and to present associated mRNAs in specific silencing platforms.
discovered that loss of the Pkd1 (show PKD1 Proteins) gene product, polycystin-1 (PC1 (show PKD1 Proteins)), whose mutation causes human autosomal dominant polycystic kidney disease (ADPKD), downregulates Bicc1 expression in vitro and in vivo
Bicc1 is a novel regulator of osteoblastogenesis and bone mineral density (BMD (show BEST1 Proteins))
Bicc1 KH domains bind the 3' UTRs of AC6 (show ADCY6 Proteins) and PKIa (show PKIA Proteins) mRNAs and cognate miRNA precursors, whereas the SAM (show TTN Proteins) domain loads a silencing complex with AGO2 (show EIF2C2 Proteins). AC6 (show ADCY6 Proteins) and PKIa (show PKIA Proteins) protein levels increase in cystic Bicc1-/- mouse kidneys.
lack of Bicc1 leads to disruption of normal cell-cell junctions.
Data suggest that Bicc1 functions by modulating the expression of polycystin 2 (Pkd2 (show PKD2 Proteins) by antagonizing the repressive activity of the miR-17 microRNA family on the 3'UTR of Pkd2 (show PKD2 Proteins) mRNA.
Binds homoribopolymers in vitro; the third K homology domain is necessary and sufficient for in vitro Bicc1 RNA binding.
Bicc1 and SamCystin interact at the protein level suggesting that they function in a common molecular pathway that when perturbed, is involved in cystogenesis.
Data report that targeted inactivation of BicC randomizes left-right asymmetry by disrupting the planar alignment of motile cilia required for cilia-driven fluid flow, and that BicC can uncouple Dvl2 (show DVL2 Proteins) signaling from the canonical Wnt (show WNT2 Proteins) pathway.
This gene encodes an RNA-binding protein that is active in regulating gene expression by modulating protein translation during embryonic development. Mouse studies identified the corresponding protein to be under strict control during cell differentiation and to be a maternally provided gene product.
bicaudal C homolog 1 (Drosophila)
, bicaudal C homolog 1-like
, bicaudal C homolog 1
, protein bicaudal C homolog 1-like
, protein bicaudal C homolog 1
, juvenile congenital polycystic kidney disease
, polycystic kidney mutation of BALB/c origin