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LYST encodes a protein that regulates intracellular protein trafficking in endosomes, and may be involved in pigmentation. Additionally we are shipping LYST Kits (4) and and many more products for this protein.
Showing 4 out of 4 products:
Human Monoclonal LYST Primary Antibody for ELISA - ABIN514402
Sánchez-Guiu, Antón, García-Barberá, Navarro-Fernández, Martínez, Fuster, Couselo, Ortuño, Vicente, Rivera, Lozano: Chediak-Higashi syndrome: description of two novel homozygous missense mutations causing divergent clinical phenotype. in European journal of haematology 2013
Effects of LYST mutations in Chediak-Higashi syndrome show that LYST is involved in regulation of natural killer cell lytic activity, from lytic granule size to polarization and exocytosis, as well as endolysosomal compartment identity.
Lack of LYST during endolysosomal biogenesis leads to the formation of enlarged hybrid organelles and blocks the terminal maturation of lytic granules into secretory granules.
Lysosome degradation and traffcking of cargo via autophagy, endocytosis or retrograde transport are not affected by LYST depletion.
involved in the regulation of phospholipase D (show PLD Antibodies) activity
present an AR-HSP family with cerebellar ataxia (show USP14 Antibodies) and neuropathy with a novel homozygous missense mutation in the lysosomal trafficking regulator (LYST) gene. LYST is known as the causative gene for Chediak-Higashi syndrome.
this is the first report of a severe early-onset Chediak-Higashi syndrome (CHS0 with a homozygous LYST/CHS1 missense mutation.
gene sequencing of all exons of the lysosome trafficking regulator (CHS1/LYST) gene and revealed a nonsense mutation in exon 5 (c.925C>T, p.R309X).
R1836X mutation in the LYST gene is associated with Chediak Higashi syndrome.
The Chediak-Higashi protein interacts with SNARE (show NAPA Antibodies) complex and signal transduction proteins.
results suggest that the Beige protein interacts with at least two different partners and that the Beige protein affects cellular events, such as nuclear PtdIns(4,5)P2 localization, in addition to lysosome size
results identify an association between oxidative damage to lipid membranes and the severity of Lyst-mutant phenotypes, revealing a new mechanism that contributes to pathophysiology involving LYST
the Lyst(Ing3618 )allele could represent a new model for adult Chediak-Higashi syndrome with neurological impairment
Apolipoprotein E (ApoE (show APOE Antibodies))-deficient beige mice have markedly reduced development of atherosclerotic lesions when fed a chow diet; expression of the beige mutation in all cell types involved in lesion development contributes to atheroprotection.
The upregulation of LYST/Beige in infected cells functions as a host innate response to limit parasite growth.
These results demonstrated that mutation of the Lyst gene can produce ocular features of human XFS (show FST Antibodies) (exfoliation syndrome) and suggested that LYST or LYST-interacting genes may contribute to XFS (show FST Antibodies).
This gene encodes a protein that regulates intracellular protein trafficking in endosomes, and may be involved in pigmentation. Mutations in this gene are associated with Chediak-Higashi syndrome, a lysosomal storage disorder. Alternative splicing results in multiple transcript variants, though the full-length nature of some of these variants has not been determined.
lysosomal trafficking regulator
, lysosomal-trafficking regulator-like
, Chediak-Higashi syndrome 1
, beige homolog
, lysosomal-trafficking regulator
, CHS1 homolog