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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 Proteins (3) and many more products for this protein.
Showing 10 out of 57 products:
Human Polyclonal BICC1 Primary Antibody for WB - ABIN1944768
Ota, Suzuki, Nishikawa, Otsuki, Sugiyama, Irie, Wakamatsu, Hayashi, Sato, Nagai, Kimura, Makita, Sekine, Obayashi, Nishi, Shibahara, Tanaka, Ishii, Yamamoto, Saito, Kawai, Isono, Nakamura, Nagahari et al.: Complete sequencing and characterization of 21,243 full-length human cDNAs. ... in Nature genetics 2003
Show all 3 Pubmed References
Human Polyclonal BICC1 Primary Antibody for IHC (p), WB - ABIN390954
Grupe, Li, Rowland, Nowotny, Hinrichs, Smemo, Kauwe, Maxwell, Cherny, Doil, Tacey, van Luchene, Myers, Wavrant-De Vrièze, Kaleem, Hollingworth, Jehu, Foy, Archer, Hamilton, Holmans, Morris, Catanese et al.: A scan of chromosome 10 identifies a novel locus showing strong association with late-onset Alzheimer disease. ... in American journal of human genetics 2005
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The authors demonstrate that OFD1 (show OFD1 Antibodies) cooperates with the mRNA binding protein Bicc1 to functionally control the protein synthesis machinery at the centrosome where also the PIC and eIF4F (show EIF4A2 Antibodies) components were shown to localize in mammalian cells.
genetic variants in BICC1 and RASGRF1 are closely associated with high myopia, which appears to be a potential candidate for high myopia in Chinese Han population.
Our findings suggested rs17648524 (intronic RBFOX1 gene) and rs7084402 (7.5kb 5' of the BICC1 gene) showed gender-specific associations with high myopia in the Han Chinese.
Suggest allelic changes in the regulation of the BICC1 gene in amygdala neurones may contribute to mood disorders.
Results provide some support for the involvement of BICC1 and PCLO (show PCLO Antibodies) 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 Antibodies) 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 Antibodies) inhibitory activity. The point mutation in the SAM (show TTN Antibodies) 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 Antibodies) gene product, polycystin-1 (PC1 (show PKD1 Antibodies)), 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 Antibodies))
Bicc1 KH domains bind the 3' UTRs of AC6 (show ADCY6 Antibodies) and PKIa (show PKIA Antibodies) mRNAs and cognate miRNA precursors, whereas the SAM (show TTN Antibodies) domain loads a silencing complex with AGO2 (show EIF2C2 Antibodies). AC6 (show ADCY6 Antibodies) and PKIa (show PKIA Antibodies) 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 Antibodies) by antagonizing the repressive activity of the miR-17 microRNA family on the 3'UTR (show UTS2R Antibodies) of Pkd2 (show PKD2 Antibodies) mRNA.
Binds homoribopolymers in vitro; the third K homology domain is necessary and sufficient for in vitro Bicc1 RNA binding.
Bicc1 and SamCystin (show ANKS6 Antibodies) 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 Antibodies) signaling from the canonical Wnt (show WNT2 Antibodies) pathway.
Bicc1 has a role in mRNA target-specific translation repression related to its biological role in the maternally controlled stages of vertebrate embryogenesis
Repression by Bic-C required its N-terminal domain, comprised of multiple hnRNP-K (show HNRNPK Antibodies)-homolog motifs, for specific binding to relevant control elements within the cripto-1 (show TDGF1 Antibodies) mRNA and a functionally separable C-terminal translation repression domain.
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.
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.
, protein bicaudal C homolog 1
, juvenile congenital polycystic kidney disease
, polycystic kidney mutation of BALB/c origin
, bicaudal C homolog 1 (Drosophila)
, protein bicaudal C homolog 1-B
, bicaudal C homolog 1-like
, bicaudal C homolog 1
, protein bicaudal C homolog 1-like