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SEC24 family, member D

The protein encoded by this gene is a member of the SEC24 subfamily of the SEC23/SEC24 family, which is involved in vesicle trafficking. The encoded protein has similarity to yeast Sec24p component of COPII. COPII is the coat protein complex responsible for vesicle budding from the ER. This gene product is implicated in the shaping of the vesicle, and also in cargo selection and concentration. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: CAN, V1a, Rdl, HAD, ACID
Papers on Sec24D
TECPR2 Cooperates with LC3C to Regulate COPII-Dependent ER Export.
Behrends et al., Frankfurt am Main, Germany. In Mol Cell, Nov 2015
Here, we show that TECPR2 associates with several trafficking components, among them the COPII coat protein SEC24D.
Mutations in SEC24D, encoding a component of the COPII machinery, cause a syndromic form of osteogenesis imperfecta.
Netzer et al., Köln, Germany. In Am J Hum Genet, Apr 2015
As a result of a whole-exome sequencing study, we report three mutant alleles in SEC24D, a gene encoding a component of the COPII complex involved in protein export from the ER: the truncating mutation c.613C>T (p.Gln205(∗)) and the missense mutations c.3044C>T (p.Ser1015Phe, located in a cargo-binding pocket) and c.2933A>C (p.Gln978Pro, located in the gelsolin-like domain).
Yip1A, a novel host factor for the activation of the IRE1 pathway of the unfolded protein response during Brucella infection.
Murata et al., Tokyo, Japan. In Plos Pathog, Mar 2015
First, during Brucella infection, the IRE1 pathway, but not the PERK and ATF6 pathways, of the unfolded protein response (UPR) was activated in a time-dependent manner, and the COPII vesicle components Sar1, Sec23, and Sec24D were upregulated.
Molecular basis of the dominant negative effect of a glycine transporter 2 mutation associated with hyperekplexia.
López-Corcuera et al., Madrid, Spain. In J Biol Chem, Feb 2015
We show that the presence of an arginine rather than serine 512 provoked transporter misfolding, enhanced association to the ER-chaperone calnexin, altered association with the coat-protein complex II component Sec24D, and thereby impeded ER exit.
Accelerating novel candidate gene discovery in neurogenetic disorders via whole-exome sequencing of prescreened multiplex consanguineous families.
Alkuraya et al., Riyadh, Saudi Arabia. In Cell Rep, Feb 2015
This prescreening step led to the identification of 69 recessive genes not previously associated with disease, of which 33 are here described (SPDL1, TUBA3E, INO80, NID1, TSEN15, DMBX1, CLHC1, C12orf4, WDR93, ST7, MATN4, SEC24D, PCDHB4, PTPN23, TAF6, TBCK, FAM177A1, KIAA1109, MTSS1L, XIRP1, KCTD3, CHAF1B, ARV1, ISCA2, PTRH2, GEMIN4, MYOCD, PDPR, DPH1, NUP107, TMEM92, EPB41L4A, and FAM120AOS).
ERp29 regulates epithelial sodium channel functional expression by promoting channel cleavage.
Rubenstein et al., Philadelphia, United States. In Am J Physiol Cell Physiol, 2014
Instead, ERp29 appeared to promote the interaction of β-ENaC with the Sec24D cargo recognition component of the coat complex II ER exit machinery.
Modulation of the secretory pathway rescues zebrafish polycystic kidney disease pathology.
Drummond et al., Seattle, United States. In J Am Soc Nephrol, 2014
sec24D knockdown prevented dorsal axis curvature and kidney cystogenesis in polycystin 2 morphants.
Mammalian COPII coat component SEC24C is required for embryonic development in mice.
Ginsburg et al., In J Biol Chem, 2014
The embryonic lethality resulting from loss of SEC24C occurs considerably later than the lethality previously observed in SEC24D deficiency; it is clearly distinct from the restricted neural tube phenotype of Sec24b null embryos and the mild hypocholesterolemic phenotype of adult Sec24a null mice.
Axonal targeting of the serotonin transporter in cultured rat dorsal raphe neurons is specified by SEC24C-dependent export from the endoplasmic reticulum.
Freissmuth et al., Dublin, Ireland. In J Neurosci, 2014
(3) The overexpression of dominant-negative SEC24C-D(796)V/D(797)N (but not of the corresponding SEC24D mutant) redirected both endogenous SERT and heterologously expressed yellow fluorescent protein-SERT from axons to the somatodendritic region.
A new class of endoplasmic reticulum export signal PhiXPhiXPhi for transmembrane proteins and its selective interaction with Sec24C.
Inaba et al., Sapporo, Japan. In J Biol Chem, 2013
Co-transfection of Sec24C-AAA, in which the residues (895)LIL(897) (the binding site for another ER export signal motif IXM on Sec24C and Sec24D) were mutated to (895)AAA(897), specifically increased ER retention of the AE1-Ly49E chimera.
Switching the clientele: a lysine residing in the C terminus of the serotonin transporter specifies its preference for the coat protein complex II component SEC24C.
Freissmuth et al., Vienna, Austria. In J Biol Chem, 2013
The closely related transporters for noradrenaline and dopamine depend on SEC24D.
Disruption of the Sec24d gene results in early embryonic lethality in the mouse.
Ginsburg et al., Baltimore, United States. In Plos One, 2012
We now report characterization of mice with targeted disruption of Sec24d.
Hsp70 promotes epithelial sodium channel functional expression by increasing its association with coat complex II and its exit from endoplasmic reticulum.
Rubenstein et al., Philadelphia, United States. In J Biol Chem, 2012
Instead, Hsp70 overexpression increased the association of ENaC with the Sec24D cargo recognition component of coat complex II, which carries protein cargo from the endoplasmic reticulum to the Golgi.
Pharmacological chaperoning of nicotinic acetylcholine receptors reduces the endoplasmic reticulum stress response.
Lester et al., Pasadena, United States. In Mol Pharmacol, 2012
Each of these four manipulations increased Sec24D-enhanced green fluorescent protein fluorescence of condensed ER exit sites and attenuated translocation of ATF6-enhanced green fluorescent protein to the nucleus.
A triple arg motif mediates α(2B)-adrenergic receptor interaction with Sec24C/D and export.
Wu et al., New Orleans, United States. In Traffic, 2012
A triple arg motif mediates alpha(2B)-adrenergic receptor interaction with Sec24C/D and export
Characterizing functional α6β2 nicotinic acetylcholine receptors in vitro: mutant β2 subunits improve membrane expression, and fluorescent proteins reveal responsive cells.
Lester et al., Pasadena, United States. In Biochem Pharmacol, 2011
We dramatically increased chances of detecting functional α6-eGFPβ2 nAChRs by (i) introducing two endoplasmic reticulum (ER) export-enhancing mutations into β2 subunits, and (ii) choosing cells with abundant Sec24D-mCherry-labeled ER exit sites.
Mutations in the carboxyl-terminal SEC24 binding motif of the serotonin transporter impair folding of the transporter.
Kudlacek et al., Vienna, Austria. In J Biol Chem, 2011
Mutations in the carboxyl-terminal SEC24 binding motif of the serotonin transporter impair folding of the transporter
Concentrative export from the endoplasmic reticulum of the gamma-aminobutyric acid transporter 1 requires binding to SEC24D.
Sitte et al., Vienna, Austria. In J Biol Chem, 2007
concentrative endoplasmic reticulum-export is contingent on a direct interaction of GAT1 with Sec24D.
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