Interactome analysis reveals that FAM161A, deficient in recessive retinitis pigmentosa, is a component of the Golgi-centrosomal network.
Lausanne, Switzerland. In Hum Mol Genet, Jul 2015
Notable FAM161A interactors included AKAP9, FIP3, GOLGA3, KIFC3, KLC2, PDE4DIP, NIN and TRIP11.
Sixteen new lung function signals identified through 1000 Genomes Project reference panel imputation.
London, United Kingdom. In Nat Commun, 2014
We identify 14 novel loci (P<5 × 10(-8)) in or near ENSA, RNU5F-1, KCNS3, AK097794, ASTN2, LHX3, CCDC91, TBX3, TRIP11, RIN3, TEKT5, LTBP4, MN1 and AP1S2, and two novel signals at known loci NPNT and GPR126, providing a basis for new understanding of the genetic determinants of these traits and pulmonary diseases in which they are altered.
Golgi Feels Its Own Wound.
Australia. In Adv Wound Care (new Rochelle), 2013
This was achieved by Yadav et al. (2009) through depletion of Golgin-160 or GMAP210 (Golgi microtubule associated protein of 210 kDa), which resulted in fragmentation and dispersal of Golgi without altering secretion kinetics.
Positioning the Golgi apparatus.
Pittsburgh, United States. In Cell, 2004
Ríos et al. (2004) report in this issue that the Golgi protein GMAP-210 is sufficient to confer pericentrosomal positioning and recruits gamma-tubulin and associated microtubule-nucleating ring complex proteins to Golgi membranes.