TTC25 Deficiency Results in Defects of the Outer Dynein Arm Docking Machinery and Primary Ciliary Dyskinesia with Left-Right Body Asymmetry Randomization.

doi:10.1016/j.ajhg.2016.06.014

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Article

TTC25 Deficiency Results in Defects of the Outer Dynein Arm Docking Machinery and Primary Ciliary Dyskinesia with Left-Right Body Asymmetry Randomization.

American journal of human genetics - 4 Aug 2016

Wallmeier Julia, Shiratori Hidetaka, Dougherty Gerard W, Edelbusch Christine, Hjeij Rim, Loges Niki T, Menchen Tabea, Olbrich Heike, Pennekamp Petra, Raidt Johanna, Werner Claudius, Minegishi Katsura, Shinohara Kyosuke, Asai Yasuko, Takaoka Katsuyoshi, Lee Chanjae, Griese Matthias, Memari Yasin, Durbin Richard, Kolb-Kokocinski Anja, Sauer Sascha, Wallingford John B, Hamada Hiroshi, Omran Heymut

Abstract excerpt

Multiprotein complexes referred to as outer dynein arms (ODAs) develop the main mechanical force to generate the ciliary and flagellar beat. ODA defects are the most common cause of primary ciliary dyskinesia (PCD), a congenital disorder of ciliary beating, characterized by recurrent infections of the upper and lower airways, as well as by progressive lung failure and randomization of left-right body asymmetry....

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PMID: 27486780
DOI: 10.1016/j.ajhg.2016.06.014
PMCID: PMC4974089

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

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TTC25 Deficiency Results in Defects of the Outer Dynein Arm Docking Machinery and Primary Ciliary Dyskinesia with Left-Right Body Asymmetry Randomization.PMID 27486780Read ↗

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