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
- - Source: PubMed
Publication date: 2026/02/20
Xing YuanxinFan RongJiang XiuzhenZhu WenshuaiJing FuboMa XiaoliWang YunshanJia Yanfei - Pork is a major source of animal protein for humans, and as living standards have improved, consumer demand has shifted from quantity to quality. Amino acid and fatty acid compositions determine the nutritional value and flavor of pork. However, the genetic mechanisms underlying variation in these parameters have not been fully elucidated. In this study, we quantified 17 amino acids and 42 fatty acids in the muscle from three crossbred pig populations, namely Yorkshire × Tibetan (YT), Yorkshire × Neijiang (YN), and Duroc × Tibetan (DT). YT and YN pigs exhibited higher amino acid concentrations, while DT pigs showed elevated fatty acid levels. Subsequently, whole-genome resequencing of 73 pigs identified 24,125,658 high-quality SNPs, among which 146 were significantly associated with fatty acid traits, leading to the identification of 19 candidate genes linked to palmitic acid (i.e., , and ), oleic acid (i.e., , and ), and total fatty acids (i.e., ). Functional annotation revealed that these candidate genes participate primarily in pathways related to lipid metabolism, glucose homeostasis, and energy balance. The identified SNPs and candidate genes provide valuable insights into the genetic architecture of the fatty acid composition in pork and may serve as molecular targets for improving meat quality through breeding. - Source: PubMed
Publication date: 2026/01/29
Tang JieLiang YanAn RuiLuo GanTao XuanLiu PengliangGu Yiren - Autosomal-dominant polycystic kidney disease (ADPKD) is primarily of adult-onset and caused by pathogenic variants in or . Yet, disease expression is highly variable and includes very early-onset PKD presentations in utero or infancy. In animal models, the RNA-binding molecule Bicc1 has been shown to play a crucial role in the pathogenesis of PKD. To study the interaction between BICC1, PKD1, and PKD2, we combined biochemical approaches, knockout studies in mice and genetic engineered human kidney cells carrying variants, as well as genetic studies in a large ADPKD cohort. We first demonstrated that BICC1 physically binds to the proteins Polycystin-1 and -2 encoded by and via distinct protein domains. Furthermore, PKD was aggravated in loss-of-function studies in and mouse models, resulting in more severe disease when was depleted in conjunction with . Finally, in a large human patient cohort, we identified a sibling pair with a homozygous variant and patients with very early onset PKD (VEO-PKD) that exhibited compound heterozygosity of in conjunction with variants. Genome editing demonstrated that these variants were hypomorphic in nature and impacted disease-relevant signaling pathways. These findings support the hypothesis that BICC1 cooperates functionally with PKD1 and PKD2, and that variants may aggravate PKD severity, highlighting RNA metabolism as an important new concept for disease modification in ADPKD. - Source: PubMed
Publication date: 2026/02/12
Tran UyenStreets Andrew JSmith DevonDecker EvaKirschfink AnnemarieIzem LahoucineHassey Jessie MRutland BrianaValluru Manoj KBräsen Jan HinrichOtt ElisabethEpting DanielEisenberger TobiasOng Albert C MBergmann CarstenWessely Oliver - The use of reversible fibroblast growth factor receptor 2 (FGFR) inhibitors leads to the emergence of "undruggable" FGFR2 kinase domain mutations, hampering sequential treatment strategies. Lirafugratinib and futibatinib are irreversible FGFR inhibitors with the most promising clinical activity against FGFR2-driven tumors. - Source: PubMed
Facchinetti FrancescoHollebecque AntoineBarbé RémyJang Dong ManAlonso-De-Castro BeatrizBrayé FlorianeBigot LudovicNobre CatlineDa Silva AliceMéteau MélissandreDelavigne MathisSoares MiguelItaliano AntoineRodriguez JulietaMosele FernandaBeshiri KristiDucreux MichelBoilève AliceNikolaev SergeyAlonso-Garcia InmaculadaVasseur DamienSmolenschi CristinaBourien HéloiseCotteret SophieSamaniego JulietteBernard ElsaNicotra ClaudioNgo-Camus MaudNakazawa SeshiruTselikas LambrosBadoual CécileAndré FabriceEck Michael JOlaussen Ken ALoriot YohannFriboulet Luc - Bicaudal C1 (Bicc1) encodes an RNA-binding protein critical for many organ development and epithelial tissue homeostasis. Bicc1 null mutations have been shown to lead to the development of polycystic kidney disease (PKD) and death at an early prenatal stage. To elucidate the tissue-specific functions of Bicc1, we engineered two independent conditional knockout (cKO) mouse lines targeting distinct exonic regions of the gene. The first line was generated using a traditional embryonic stem (ES) cell-based approach, wherein loxP sites were inserted flanking exon 4 (E4), enabling Cre-mediated excision of a functionally essential coding region. The second line was created using CRISPR/Cas9 genome editing, introducing loxP sites around both exon 4 and exon 5 (E4-5) in a double-step zygote injection strategy. Both alleles were validated by PCR genotyping, sequencing, and functional recombination was confirmed via a tissue-specific Cre driver. These independent cKO models provide a robust platform for dissecting the role of Bicc1 in specific tissues and developmental stages, and offer new avenues for studying the mechanistic basis of PKD and other Bicc1-related pathologies. - Source: PubMed
Liu Chia-FengLeon StevenHerrig IsabellaWessely OliverTang W H Wilson