BICC1
- Known as:
- BICC1
- Catalog number:
- Y214450
- Product Quantity:
- 200ul
- Category:
- -
- Supplier:
- ABM
- Gene target:
- BICC1
Related genes to: BICC1
- Gene:
- BICC1 NIH gene
- Name:
- BicC family RNA binding protein 1
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 10q21.1
- Locus Type:
- gene with protein product
- Date approved:
- 2002-10-08
- Date modifiied:
- 2019-04-23
Related products to: BICC1
Related articles to: BICC1
- Oxidative stress-mediated impairment of osteoblast function is a critical pathological basis for the development and progression of various bone metabolic diseases. BicC family RNA binding protein 1 (BICC1) plays important roles in osteoblast function, however, the underlying mechanism remains unclear. This study aimed to investigate the protective role of BICC1 in oxidative stress-induced osteogenic injury and the underlying mechanism. An oxidative injury model was established in MC3T3-E1 cells using 300 µM hydrogen peroxide (HO). Bicc1 over-expressing lentivirus and the pyruvate dehydrogenase kinase isozyme (PDK) inhibitor dichloroacetate (DCA) were used for intervention. The osteoblast differentiation and mitochondrial membrane potential and apoptosis were measured by biochemical analysis and Alizarin Red S staining. RT-qPCR and Western blot were used to detect mRNA and protein levels of key molecules. RNA sequencing was performed to identify core targets and signaling pathways. H₂O₂ treatment significantly suppressed MC3T3-E1 cell viability and osteogenic differentiation, enhanced apoptosis, and up-regulated PDK1 expression as well as pyruvate dehydrogenase complex (PDH) phosphorylation. Bicc1 over-expression markedly alleviated H₂O₂-induced mitochondrial dysfunction and apoptosis, restored osteogenic differentiation, and inhibited the activation of the PDK1/PDH axis. Transcriptomic analysis showed that PDK1 was a key target molecule in Bicc1-regulated apoptosis and oxidative stress responses. Inhibition of PDK1 recapitulates the protective effect of BICC1 to oxidative stress injury in MC3T3-E1 cells. Bicc1 attenuates oxidative stress injury and promotes osteogenic differentiation in MC3T3-E1 cells, and may serve as a potential therapeutic target for osteoporosis. - Source: PubMed
Publication date: 2026/09/08
Liu ZhongshuangChen AijieLi BaoxuLi ShibinHuang WeibinXie QiTao FuchengSu LeyaoZhu KairanLiu QiMa Lin - Genetic variants in the RNA-binding protein bicaudal C1 (BICC1) have been linked to very-early-onset polycystic kidney disease (PKD). This study identifies a crucial integrin-beta1 (ITGB1)-BICC1-polycystin-1 (PC1) complex that regulates F-actin organization and cell adhesion in human kidney cells through the expression of filamin-binding-LIM-protein-1 (FBLIM1). Both and knockout cells exhibit abnormal F-actin structure, increased cell stiffness, decreased adhesion and impaired migration while inhibiting F-actin branching directly triggers cyst formation. Locally, BICC1 interacts with F-actin, ITGB1, and FBLIM1 at focal adhesions. ITGB1 knockdown reduces surface BICC1 expression. In turn, BICC1 stabilizes FBLIM1 by influencing transcript abundance, promoting its local translation, and protecting it from degradation in the presence of PC1. In summary, these findings reveal a novel model of cystogenesis linking BICC1's dual RNA and protein regulatory functions to the maintenance of cytoskeletal and tubular integrity. - Source: PubMed
Publication date: 2026/08/17
Streets Andrew JValluru Manoj KSmith DevonChang LisaBen-Dov Iddo ZWilson Stuart AToseland Christopher POng Albert C M - Autosomal dominant polycystic kidney disease (ADPKD) arises from mutations in polycystin-1/ or polycystin-2/ that induce injury-repair pathways and dysregulate cAMP and Yes-associated protein (YAP) signaling to promote cyst growth. Cystic kidneys with elevated cAMP levels also develop in mouse embryos lacking the BicC family RNA-binding protein 1 (Bicc1). To prevent embryonic lethality, we flanked exon 4 with sites for conditional knockout (cKO) in renal tubules using inducible Pax8-rtTA-driven Cre in adults, or distal segment-specific deletion using Ksp-Cre. Whereas -deficient adult kidneys formed relatively few cysts within six months, distal nephron-specific deletion induced aggressive PKD-like disease. Automated renal tubule and cyst quantification (ARTCyQ), a novel machine-learning pipeline to analyze immunofluorescent stainings, revealed increasing ambiguity in nephron segment identity and activation of ADPKD-related pathways, including YAP signaling. Accordingly, transcriptional profiling revealed overlap with PKD and injury-repair signatures, supporting a role for Bicc1 in polycystin signaling. - Source: PubMed
Publication date: 2026/08/03
Gagnieux CélineBernet FlorianKroese LonaGuiet RomainBurns AllisonCombe RoyHuijbers IvoConstam Daniel BRothé Benjamin - Biliary tract cancers (BTC) pose clinical challenges due to poor chemotherapy response and aggressive disease course. We evaluated patient-derived tumor organoid-based drug sensitivity testing as a tool to guide therapy. In this multicenter study, 26 tumor organoids were successfully derived from 43 patients with BTC and tested with an average of 50 cancer-directed therapies using the Clinical Laboratory Improvement Amendments-certified PARIS assay. Despite most organoids being from late-stage disease, 24/26 (92.3%) exhibited strong sensitivity to one or more targeted agents. Active drugs included inhibitors of EGFR/HER2, MEK, ERK, BCR-ABL and SRC family, mTOR, PI3K, MDM2, BCL2, and BET. Drug sensitivities aligned with known genetic biomarkers but were also observed in cultures lacking them, indicating ex vivo testing can expand actionability beyond genomics. In five cases, results guided therapy; one patient with an FGFR-BICC1 fusion refractory to FGFR inhibitors responded to dasatinib, achieving symptomatic improvement, stable disease, and >8-month survival. - Source: PubMed
Richardson Annie BlairChatterjee PayelRosati RacheleRajewski AlexDiaz Robert LAppleyard Lauren RPereira ShaliniBernard BradyJavle Milind MKing Gentry GDiehl AdamHarris William ProctorRoychowdhury SameekKemp Christopher JGrandori Carla - Bicaudal C Homolog 1 (BICC1) is a conserved RNA-binding protein that, in mammals, has been primarily associated with polycystic kidney disease and renal organogenesis. However, its role in other disease contexts, including cancer, remains poorly understood. In this study, we characterized the BICC1 interactome, with emphasis on its dependence on RNA and the sterile alpha motif (SAM) domain, to identify novel biological processes associated with BICC1 function. Protein complexes were purified from HEK293T cells by co-immunoprecipitation and analyzed by mass spectrometry. Notably, co-immunoprecipitations performed in the presence of RNA yielded a larger number of interacting proteins, with 31 of 71 proteins (~43%) uniquely identified under RNA-preserved conditions, highlighting the critical role of RNA in mediating BICC1 protein-protein interactions. Enriched proteins were predominantly associated with mRNA splicing, the PRMT5 methylosome complex, and membraneless organelles, such as biomolecular condensates. Consistent with these findings, immunofluorescence assays performed on stressed cells revealed the co-localization of BICC1 with stress granule markers. Moreover, BICC1 interactions with PRMT5, STK38, PARP1, and IGF2BP1 were confirmed by immunoblotting. - Source: PubMed
Publication date: 2026/08/07
do Amaral-Prado Heloísa MonteiroMoreira Gabriela AlvesSantos CristianeBosso Fernando HenriqueCiamponi Felipe EduardoBarbosa Guilherme OliveiraBengtson Mario HenriqueMassirer Katlin Brauer