Comparative genomics identifies a flagellar and basal body proteome that includes the BBS5 human disease gene.
By Jin Billy Li, J. Gerdes, Courtney J. Haycraft, Yanli Fan, T. Teslovich, H. May-Simera, Haitao Li, O. Blacque, Linya Li, C. C. Leitch and 11 more. Cell, 2004
798 citations recorded by the source corpus.
Subfields: Genetics, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/e7369118202b88e8b874dfc7435d99a8dab9c7b3
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In Genetics
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Citations in the corpus
- Disruption of Bardet-Biedl syndrome ciliary proteins perturbs planar cell polarity in vertebrates (2005, background): “Here we show that mice with mutations in genes involved in Bardet-Biedl syndrome (BBS), a disorder associated with ciliary dysfunctio”
- Insights into Ciliary Genes and Evolution from Multi-Level Phylogenetic Profiling (2017, background): “Most previous studies (Avidor-Reiss et al. 2004; Li et al. 2004, p. 200; Merchant et al. 2007; Hodges et al. 2011) used scoring systems, which can be classified as knowledge-guided methods, to find genes with a phylogenetic profile correlating with the presence-absence of cilia.”
- A core complex of BBS proteins cooperates with the GTPase Rab8 to promote ciliary membrane biogenesis. (2007, positive): “…applied to an evolutionarily diverse set of BBS5 orthologs (Figures S7A and S7B), we were able to extend the 50 amino-acidlong DM16 repeats (Li et al., 2004) to 125 amino-acid-long stretches (Figures 5A and 5B) whose nearest protein fold relatives are the PH-like domains PH-GRAM (Begley et…”
- Proteomic analysis of a eukaryotic cilium (2005, methodology): “For example, by comparing the genomes of ciliated versus nonciliated organisms, Avidor-Reiss et al. (2004) and Li et al. (2004) identified 187 and 688 genes, respectively, that are present in the former but not the latter; these are candidates for encoding flagellar and basal body components.”
- Chemosensation in C. elegans. (2006, background): “elegans cilium structure genes are orthologous to a human polycystic kidney disease gene and multiple human BBS disease genes, whose mutation leads to obesity, mental retardation, and other defects (Ansley et al., 2003; Blacque et al., 2004; Haycraft et al., 2001; Li et al., 2004; Qin et al., 2001).”