Ask about this productRelated genes to: CFDP1 Blocking Peptide
- Gene:
- CFDP1 NIH gene
- Name:
- craniofacial development protein 1
- Previous symbol:
- -
- Synonyms:
- BCNT, p97, CP27, SWC5, Yeti, CENP-29
- Chromosome:
- 16q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-12-09
- Date modifiied:
- 2018-06-14
Related products to: CFDP1 Blocking Peptide
Related articles to: CFDP1 Blocking Peptide
- The conserved yeast SWR1 and human SRCAP chromatin remodeling complexes catalyze exchange of nucleosomal histone H2A for H2A.Z, but the underlying mechanism has remained obscure. Here, we show that histone exchange by SRCAP requires the transient activator CFDP1 and resolve nine cryo-electron microscopy structures of the SRCAP-CFDP1 holoenzyme that define the stepwise exchange mechanism. CFDP1 recognizes the conformation of the fully engaged SRCAP-nucleosome complex through interactions with multiple subunits-including direct contact with the ATPase domain-and induces conformational transitions that drive extensive DNA unwrapping, eviction of the H2A-H2B dimer, and insertion of the H2A.Z-H2B dimer, all without necessarily requiring hydrolysis of bound ATP. Collectively, these findings provide unprecedented insight into the mechanism of activator- and nucleotide-driven histone exchange from nucleosomal H2A to H2A.Z. - Source: PubMed
Publication date: 2026/07/31
Park GihoWu CarlLouder Robert K - Acute myocardial infarction (AMI) is one of the leading causes of mortality worldwide. Despite extensive research, only a limited number of genes have been identified as reliable biomarkers for the diagnosis and treatment of AMI. This study aims to identify novel biomarkers and therapeutic targets for AMI by integrating multi-omics data and machine learning. - Source: PubMed
Publication date: 2026/04/13
Wu JiachengYang YuluHuang JianwuLi XuehanMa QianChen HaoWang YaleiLama ErhaQiu ZhihuaZhou Zihua - To elucidate the genetic architecture of blood pressure (BP) and heart rate (HR) during early life and assess their potential relevance to adult health outcomes. - Source: PubMed
Publication date: 2026/04/27
Xie TianAni AlirezaVaez AhmadNolte Ilja MSu ShaoyongIshikuro MamiWang SiqiZhang WenboSoares Ana GoncalvesMotazedi EhsanCalas LucindaRonkainen JustiinaPedersen Casper-Emil TLu XuelingStinson Sara EFelix Janine FStankevic EvelinaWang Carol AThiering ElisabethFernández DietmarCalvo-Serra BeatrizStathopoulou Maria GFore RubyKumar AshishTuhkanen JohannaBilbao Jose RamonIbarluzea JesusIsaacs AaronFonvig Cilius EsmannRivadeneira FernandoLund Morten Asp VonsildHolm Louise Aasvan der Most Peter JRiese HarriëtteNarita AkiraTamiya GenFlexeder ClaudiaWiersma RikstjeArgoty-Pantoja Anna DVinding RebeccaHansen Tine WillumKümler ThomasEstarlich MarisaBustamante MarionaYuan Wen LunBoland-Augé AnneDeleuze Jean-FrançoisPetrelis Alexandros MRifas-Shiman SherylKajantie EeroFernandez-Jimenez NoraSanta-Marina LoretoArts Ilja C WLahti JariStrandberg TimoKull IngerBergström AnnaHivert Marie-FranceBønnelykke KlausKuriyama ShinichiBeilin Lawrence JMori Trevor AHartman Catharina AGrarup NielsThijs CarelRäikkönen KatriMelén ErikOken EmilyVisvikis-Siest SophieGützkow Kristine BGrazuleviciene ReginaHeude BarbaraChatzi LedaVrijheid MartineStandl MarieVrijkotte TanjaPennell Craig EOldehinkel Albertine JHansen TorbenJaddoe Vincent W VHolm Jens-ChristianSebert SylvainTimpson Nicholas JObara TakuWang XiaolingLawlor Deborah ACorpeleijn EvaAhluwalia Tarunveer SSnieder Harold - Genome-wide association studies (GWAS) have identified thousands of non-coding variants associated with complex traits and diseases. However, it remains challenging to pinpoint the causal genes that are regulated by associated genetic variants. Connecting causal non-coding variants with genes can rely on methods that identify direct physical interactions (e.g. chromosome conformation capture) or on probabilistic models that predict regulatory links. These statistical models take advantage of gene expression and chromatin accessibility profiles generated in cells and tissues by bulk or single-cell (sc) methodologies. Here, we tested whether using bulk or sc RNAseq/ATACseq data and corresponding predictive enhancer-to-gene models impact the prioritization of causal GWAS genes. Using non-treated and TNFα-treated human endothelial cells as a well-controlled experimental system, we show that bulk and sc RNAseq/ATACseq profiles are similar and highlight the same biology (e.g. biological pathways). Despite these similarities, we show using GWAS results for coronary artery disease (CAD) and diastolic blood pressure that applying enhancer-to-gene models designed for bulk or sc methodologies can yield differences in terms of captured heritability, fine-mapped variants and linked genes. For instance, at one CAD locus, the bulk-based ABC model predicts a regulatory link with , whereas the sc-based model scE2G prioritizes a different gene (). On the same experimental model, our results indicate that choosing between a bulk or sc approach will influence regulatory link model predictions; this should be considered when planning functional experiments to characterize GWAS discoveries. - Source: PubMed
Publication date: 2026/05/27
Zevounou JenniferLo Ken SinMcGinnis Christopher SSatpathy Ansuman TLettre Guillaume - Microtubule-associated proteins (MAPs) are multifunctional tubulin-binding proteins that contribute to essential aspects of mitotic spindle formation. In the present study, loss of the MAP CFDP1 in mice resulted in gastrulation defects and embryonic lethality at e8.5 due to chromosome segregation spindle defects and loss of K-fiber stability. CFDP1 decreased the association of the nuclear transport protein importin α with the essential spindle assembly factor TPX2, thereby promoting Aurora A kinase activation, microtubule nucleation and spindle assembly. Further defining the CFDP1 mode of action, we identified CFDP1 as a bipartite molecule with an acidic N-terminus that harbors a nuclear localization signal essential for importin α dissociation from TPX2 and a basic C-terminus that interacts with tubulin, co-localizes with the mitotic spindle, and promotes microtubule bundling and polymerization. Together, our studies have established CFDP1 as an essential bipartite MAP involved in chromosomal microtubule nucleation in conjunction with TPX2 and Aurora A while also facilitating nuclear TPX2 activation through importin α dissociation. - Source: PubMed
Publication date: 2026/01/29
Gopinathan GokulLuan XianghongDiekwisch Thomas G H