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1.
正Published online:14 March 2014óScience China Press and Springer-Verlag Berlin Heidelberg 2014Erratum to:Chin.Sci.Bull.(2014)59(5–6):528–532DOI 10.1007/s11434-013-0060-1In the original publication of this paper,the first name and the last name of the first author has been documented 相似文献
2.
Functional diversification of closely related ARF-GEFs in protein secretion and recycling 总被引:1,自引:0,他引:1
Richter S Geldner N Schrader J Wolters H Stierhof YD Rios G Koncz C Robinson DG Jürgens G 《Nature》2007,448(7152):488-492
Guanine-nucleotide exchange factors on ADP-ribosylation factor GTPases (ARF-GEFs) regulate vesicle formation in time and space by activating ARF substrates on distinct donor membranes. Mammalian GBF1 (ref. 2) and yeast Gea1/2 (ref. 3) ARF-GEFs act at Golgi membranes, regulating COPI-coated vesicle formation. In contrast, their Arabidopsis thaliana homologue GNOM (GN) is required for endosomal recycling, playing an important part in development. This difference indicates an evolutionary divergence of trafficking pathways between animals and plants, and raised the question of how endoplasmic reticulum-Golgi transport is regulated in plants. Here we demonstrate that the closest homologue of GNOM in Arabidopsis, GNOM-LIKE1 (GNL1; NM_123312; At5g39500), performs this ancestral function. GNL1 localizes to and acts primarily at Golgi stacks, regulating COPI-coated vesicle formation. Surprisingly, GNOM can functionally substitute for GNL1, but not vice versa. Our results suggest that large ARF-GEFs of the GBF1 class perform a conserved role in endoplasmic reticulum-Golgi trafficking and secretion, which is done by GNL1 and GNOM in Arabidopsis, whereas GNOM has evolved to perform an additional plant-specific function of recycling from endosomes to the plasma membrane. Duplication and diversification of ARF-GEFs in plants contrasts with the evolution of entirely new classes of ARF-GEFs for endosomal trafficking in animals, which illustrates the independent evolution of complex endosomal pathways in the two kingdoms. 相似文献
3.
Sayer JA Otto EA O'Toole JF Nurnberg G Kennedy MA Becker C Hennies HC Helou J Attanasio M Fausett BV Utsch B Khanna H Liu Y Drummond I Kawakami I Kusakabe T Tsuda M Ma L Lee H Larson RG Allen SJ Wilkinson CJ Nigg EA Shou C Lillo C Williams DS Hoppe B Kemper MJ Neuhaus T Parisi MA Glass IA Petry M Kispert A Gloy J Ganner A Walz G Zhu X Goldman D Nurnberg P Swaroop A Leroux MR Hildebrandt F 《Nature genetics》2006,38(6):674-681
4.
Terhi Vihervaara Riikka-Liisa Uronen Gerd Wohlfahrt Ingemar Björkhem Elina Ikonen Vesa M. Olkkonen 《Cellular and molecular life sciences : CMLS》2011,68(3):537-551
ORP1L is an oxysterol binding homologue that regulates late endosome (LE) positioning. We show that ORP1L binds several oxysterols
and cholesterol, and characterize a mutant, ORP1L Δ560–563, defective in oxysterol binding. While wild-type ORP1L clusters
LE, ORP1L Δ560–563 induces LE scattering, which is reversed by disruption of the endoplasmic reticulum (ER) targeting FFAT
motif, suggesting that it is due to enhanced LE–ER interactions. Endosome motility is reduced upon overexpression of ORP1L.
Both wild-type ORP1L and the Δ560–563 mutant induce the recruitment of both dynactin and kinesin-2 on LE. Most of the LE decorated
by overexpressed ORP1L fail to accept endocytosed dextran or EGF, and the transfected cells display defective degradation
of internalized EGF. ORP1L silencing in macrophage foam cells enhances endosome motility and results in inhibition of [3H]cholesterol efflux to apolipoprotein A-I. These data demonstrate that LE motility and functions in both protein and lipid
transport are regulated by ORP1L. 相似文献
5.
Nitric oxide stimulates human neural progenitor cell migration via cGMP-mediated signal transduction
Tegenge MA Rockel TD Fritsche E Bicker G 《Cellular and molecular life sciences : CMLS》2011,68(12):2089-2099
Neuronal migration is one of the most critical processes during early brain development. The gaseous messenger nitric oxide
(NO) has been shown to modulate neuronal and glial migration in various experimental models. Here, we analyze a potential
role for NO signaling in the migration of fetal human neural progenitor cells. Cells migrate out of cultured neurospheres
and differentiate into both neuronal and glial cells. The neurosphere cultures express neuronal nitric oxide synthase and
soluble guanylyl cyclase that produces cGMP upon activation with NO. By employing small bioactive enzyme activators and inhibitors
in both gain and loss of function experiments, we show NO/cGMP signaling as a positive regulator of migration in neurosphere
cultures of early developing human brain cells. Since NO signaling regulates cell movements from developing insects to mammalian
nervous systems, this transduction pathway may have evolutionary conserved functions. 相似文献
6.
Lubka-Pathak M Shah AA Gallozzi M Müller M Zimmermann U Löwenheim H Pfister M Knipper M Blin N Schimmang T 《Cellular and molecular life sciences : CMLS》2011,68(16):2739-2749
Introduction
Tff3 peptide exerts important functions in cytoprotection and restitution of the gastrointestinal (GI) tract epithelia. Moreover, its presence in the rodent inner ear and involvement in the hearing process was demonstrated recently. However, its role in the auditory system still remains elusive. Our previous results showed a deterioration of hearing with age in Tff3-deficient animals.Results
Present detailed analysis of auditory brain stem response (ABR) measurements and immunohistochemical study of selected functional proteins indicated a normal function and phenotype of the cochlea in Tff3 mutants. However, a microarray-based screening of tissue derived from the auditory central nervous system revealed an alteration of securin (Pttg1) and serpina3n expression between wild-type and Tff3 knock-out animals. This was confirmed by qRT-PCR, immunostaining and western blots.Conclusions
We found highly down-regulated Pttg1 and up-regulated serpina3n expression as a consequence of genetically deleting Tff3 in mice, indicating a potential role of these factors during the development of presbyacusis. 相似文献7.
Ann-Karin Haas Gunnar Kleinau Inna Hoyer Susanne Neumann Jens Furkert Claudia Rutz Ralf Schülein Marvin C. Gershengorn Gerd Krause 《Cellular and molecular life sciences : CMLS》2011,68(1):159-167
The thyrotropin receptor (TSHR) exhibits elevated cAMP signaling in the basal state and becomes fully activated by thyrotropin.
Previously we presented evidence that small-molecule ligands act allosterically within the transmembrane region in contrast
to the orthosteric extracellular hormone-binding sites. Our goal in this study was to identify positions that surround the
allosteric pocket and that are sensitive for inactivation of TSHR. Homology modeling combined with site-directed mutagenesis
and functional characterization revealed seven mutants located in the allosteric binding site that led to a decrease of basal
cAMP signaling activity. The majority of these silencing mutations, which constrain the TSHR in an inactive conformation,
are found in two clusters when mapped onto the 3D structural model. We suggest that the amino acid positions identified herein
are indicating locations where small-molecule antagonists, both neutral antagonists and inverse agonists, might interfere
with active TSHR conformations. 相似文献
8.
Heterozygous missense mutations in BSCL2 are associated with distal hereditary motor neuropathy and Silver syndrome 总被引:6,自引:0,他引:6
Windpassinger C Auer-Grumbach M Irobi J Patel H Petek E Hörl G Malli R Reed JA Dierick I Verpoorten N Warner TT Proukakis C Van den Bergh P Verellen C Van Maldergem L Merlini L De Jonghe P Timmerman V Crosby AH Wagner K 《Nature genetics》2004,36(3):271-276
Distal hereditary motor neuropathy (dHMN) or distal spinal muscular atrophy (OMIM #182960) is a heterogeneous group of disorders characterized by an almost exclusive degeneration of motor nerve fibers, predominantly in the distal part of the limbs. Silver syndrome (OMIM #270685) is a rare form of hereditary spastic paraparesis mapped to chromosome 11q12-q14 (SPG17) in which spasticity of the legs is accompanied by amyotrophy of the hands and occasionally also the lower limbs. Silver syndrome and most forms of dHMN are autosomal dominantly inherited with incomplete penetrance and a broad variability in clinical expression. A genome-wide scan in an Austrian family with dHMN-V (ref. 4) showed linkage to the locus SPG17, which was confirmed in 16 additional families with a phenotype characteristic of dHMN or Silver syndrome. After refining the critical region to 1 Mb, we sequenced the gene Berardinelli-Seip congenital lipodystrophy (BSCL2) and identified two heterozygous missense mutations resulting in the amino acid substitutions N88S and S90L. Null mutations in BSCL2, which encodes the protein seipin, were previously shown to be associated with autosomal recessive Berardinelli-Seip congenital lipodystrophy (OMIM #269700). We show that seipin is an integral membrane protein of the endoplasmic reticulum (ER). The amino acid substitutions N88S and S90L affect glycosylation of seipin and result in aggregate formation leading to neurodegeneration. 相似文献
9.
10.
Homology of a 150K cytoplasmic dynein-associated polypeptide with the Drosophila gene Glued 总被引:26,自引:0,他引:26
E L Holzbaur J A Hammarback B M Paschal N G Kravit K K Pfister R B Vallee 《Nature》1991,351(6327):579-583
Cytoplasmic dynein is a microtubule-activated ATPase which produces force towards the minus ends of microtubules. It is thought to be responsible for retrograde axonal transport and other aspects of organelle motility and may have a role in the poleward movement of mitotic chromosomes. Cytoplasmic dynein is an oligomeric complex of two catalytic heavy chains and a number of accessory subunits. We now report the cloning and sequencing of a complementary DNA for one of these species, a cytoplasmic dynein-associated polypeptide of relative molecular mass 150,000 (Mr 150K). A full-length cDNA was found to contain an open reading frame of 4.0 kilobases, which is predicted to encode a polypeptide of Mr 145K. It has extensive homology with the product of the Drosophila gene Glued, which encodes a polypeptide of Mr 148K. The Glued mutation is dominant, with pleiotropic developmental defects in heterozygotes and an embryonic lethal phenotype in homozygotes. As dominant mutations may involve disruption of normal protein-protein interactions, the Glued mutation should provide insight into the mode of action of cytoplasmic dynein in vivo. 相似文献