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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.


Pallid, BLOC-1, p-A, PLDN
The protein encoded by this gene may play a role in intracellular vesicle trafficking. It interacts with Syntaxin 13 which mediates intracellular membrane fusion. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: DTNBP1, HPS, CAN, HAD, tyrosinase
Papers on Pallid
BLOC-1 Brings Together the Actin and Microtubule Cytoskeletons to Generate Recycling Endosomes.
Raposo et al., Paris, France. In Curr Biol, Feb 2016
We show that recycling endosome biogenesis requires the protein complex BLOC-1.
Rab9A is required for delivery of cargo from recycling endosomes to melanosomes.
Setty et al., Bengaluru, India. In Pigment Cell Melanoma Res, Jan 2016
Biogenesis of melanosomes is regulated by BLOC-1, -2, -3, or AP-1, -3 complexes, which mediate cargo transport from recycling endosomes to melanosomes.
Effects of Seismic Air Guns on Pallid Sturgeon and Paddlefish.
Young et al., College Park, United States. In Adv Exp Med Biol, Dec 2015
Pallid sturgeon and paddlefish were placed at different distances from a seismic air gun array to determine the potential effects on mortality and nonauditory body tissues from the sound from a single shot.
A Genome-wide Scan for Selective Sweeps in Racing Horses.
Kim et al., Seoul, South Korea. In Asian-australas J Anim Sci, Nov 2015
Neighboring genes around RALGAP2 included insulinoma-associated 1 (INSM1), pallid (PLDN), and Ras and Rab interactor 2 (RIN2) genes have similar roles in signal trafficking, suggesting that a co-evolving gene cluster located on the chromosome 22 is under strong artificial selection in racehorses.
Recognition deficits in mice carrying mutations of genes encoding BLOC-1 subunits pallidin or dysbindin.
Karlsgodt et al., Hempstead, United States. In Genes Brain Behav, Nov 2015
Dysbindin protein levels are lower in mice with null mutations in pallidin, another gene in the BLOC-1, and pallidin levels are lower in mice with null mutations in the dysbindin gene, suggesting that multiple subunit proteins must be present to form a functional oligomeric complex.
Clinical, laboratory and molecular signs of immunodeficiency in patients with partial oculo-cutaneous albinism.
Badolato et al., Brescia, Italy. In Orphanet J Rare Dis, 2012
Recently, a new subtype, HPS9, was defined in patients presenting with immunodeficiency and oculocutaneous albinism, associated with mutations in the pallidin-encoding gene, PLDN.Hypopigmentation together with recurrent childhood bacterial or viral infections suggests syndromic albinism.
Cell biology of the BLOC-1 complex subunit dysbindin, a schizophrenia susceptibility gene.
Faundez et al., Atlanta, United States. In Mol Neurobiol, 2011
Here, we discuss phylogenetically conserved dysbindin molecular interactions that define its contribution to the assembly of the biogenesis of lysosome-related organelles complex-1 (BLOC-1).
Functional interactions between OCA2 and the protein complexes BLOC-1, BLOC-2, and AP-3 inferred from epistatic analyses of mouse coat pigmentation.
Dell'angelica et al., Los Angeles, United States. In Pigment Cell Melanoma Res, 2011
Data suggest functional links between OCA2 and the BLOC-1, BLOC-2, and AP-3 protein complexes involved in melanosome biogenesis.
Dysbindin-containing complexes and their proposed functions in brain: from zero to (too) many in a decade.
Dell'Angelica et al., Los Angeles, United States. In Asn Neuro, 2010
In tissues other than brain and in non-neuronal cell types, the protein has been characterized as a stable component of a multi-subunit complex, named BLOC-1 (biogenesis of lysosome-related organelles complex-1), which has been implicated in intracellular protein trafficking and the biogenesis of specialized organelles of the endosomal-lysosomal system.
Slc15a4, AP-3, and Hermansky-Pudlak syndrome proteins are required for Toll-like receptor signaling in plasmacytoid dendritic cells.
Beutler et al., Los Angeles, United States. In Proc Natl Acad Sci U S A, 2010
The identification of the feeble mutation led to our subsequent observations that AP-3, as well as the BLOC-1 and BLOC-2 are essential for plasmacytoid dendritic cells signaling through TLR7 and TLR9.
Hermansky-Pudlak protein complexes, AP-3 and BLOC-1, differentially regulate presynaptic composition in the striatum and hippocampus.
Faundez et al., Atlanta, United States. In J Neurosci, 2010
This study demonstrated that Loss-of-function alleles of BLOC-1, Pldn(pa/pa), and Muted(mu/mu) revealed that this complex acts as a brain-region-specific regulator of AP-3.
Physiological factors that regulate skin pigmentation.
Hearing et al., Nagoya, Japan. In Biofactors, 2009
Enzymatic components of melanosomes include tyrosinase, tyrosinase-related protein 1, and dopachrome tautomerase, which depend on the functions of OA1, P, MATP, ATP7A, and BLOC-1 to synthesize eumelanins and pheomelanins.
Palladin is a dynamic actin-associated protein in podocytes.
European Renal cDNA Bank Consortium et al., Greifswald, Germany. In Kidney Int, 2009
palladin is expressed in podocytes and plays an important role in actin dynamics.
The sandy (sdy) mouse: a dysbindin-1 mutant relevant to schizophrenia research.
Talbot, Philadelphia, United States. In Prog Brain Res, 2008
This null protein mutation (Dtnbp1(sdy)) leads to an absence of dysbindin-1 in homozygotes, as well as reductions in several direct and indirect binding partners of dysbindin-1 that contribute to the protein assembly known as BLOC-1.
Cell-specific ATP7A transport sustains copper-dependent tyrosinase activity in melanosomes.
Marks et al., Philadelphia, United States. In Nature, 2008
Copper is supplied to melanosomes by ATP7A, a cohort of which localizes to melanosomes in a biogenesis of lysosome-related organelles complex-1 (BLOC-1)-dependent manner.
Hermansky-Pudlak syndrome type 7 (HPS-7) results from mutant dysbindin, a member of the biogenesis of lysosome-related organelles complex 1 (BLOC-1).
Swank et al., Buffalo, United States. In Nat Genet, 2003
We also show that dysbindin is a component of the biogenesis of lysosome-related organelles complex 1 (BLOC-1; refs.
Biogenesis of lysosome-related organelles complex 3 (BLOC-3): a complex containing the Hermansky-Pudlak syndrome (HPS) proteins HPS1 and HPS4.
Dell'Angelica et al., Los Angeles, United States. In Proc Natl Acad Sci U S A, 2003
The coat-color phenotype of young homozygous double-mutant mice deficient in subunits of BLOC-3 (HPS1) and BLOC-1 (pallidin) was indistinguishable from that of BLOC-1 single mutants.
The pallid gene encodes a novel, syntaxin 13-interacting protein involved in platelet storage pool deficiency.
Gitschier et al., San Francisco, United States. In Nat Genet, 1999
Pallid (pa) is 1 of 13 platelet storage pool deficiency (SPD) mouse mutants.
The murine pallid mutation is a platelet storage pool disease associated with the protein 4.2 (pallidin) gene.
Lux et al., Boston, United States. In Nat Genet, 1992
Pallid is one of 12 independent murine mutations with a prolonged bleeding time that are models for human platelet storage pool deficiencies in which several intracellular organelles are abnormal.
Repeated Homing Exhibited by a Female Pallid Bat.
Cockrum et al., In Science, 1962
A pallid bat (Antrozous pallidus) returned home from eight consecutive releases from six distinctly different directions and from distances ranging from 21 to 68 miles.
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