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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 BICC1 Proteins (3) and many more products for this protein.
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 (show PCLO ELISA Kits) 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 ELISA Kits) 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 ELISA Kits) inhibitory activity. The point mutation in the SAM (show TTN ELISA Kits) 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 ELISA Kits) gene product, polycystin-1 (PC1 (show PKD1 ELISA Kits)), 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 ELISA Kits))
Bicc1 KH domains bind the 3' UTRs of AC6 (show ADCY6 ELISA Kits) and PKIa (show PKIA ELISA Kits) mRNAs and cognate miRNA precursors, whereas the SAM (show TTN ELISA Kits) domain loads a silencing complex with AGO2 (show EIF2C2 ELISA Kits). AC6 (show ADCY6 ELISA Kits) and PKIa (show PKIA ELISA Kits) 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 ELISA Kits) by antagonizing the repressive activity of the miR-17 microRNA family on the 3'UTR (show UTS2R ELISA Kits) of Pkd2 (show PKD2 ELISA Kits) 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 ELISA Kits) signaling from the canonical Wnt (show WNT2 ELISA Kits) 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