Results 111 to 120 of about 709 (136)
Life and Death of Sensory Hair Cells Expressing Constitutively Active TRPML3 [PDF]
Journal of Biological Chemistry, 2009 The varitint-waddler mutation A419P renders TRPML3 constitutively active, resulting in cationic overload, particularly in sustained influx of Ca(2+). TRPML3 is expressed by inner ear sensory hair cells, and we were intrigued by the fact that hair cells are able to cope with expressing the TRPML3(A419P) isoform for weeks before they ultimately die.
Christian Grimm, Stefan Heller
exaly +20 more sources
Small Molecule Activators of TRPML3 [PDF]
Chemistry and Biology, 2010 We conducted a high-throughput screen for small molecule activators of the TRPML3 ion channel, which, when mutated, causes deafness and pigmentation defects. Cheminformatics analyses of the 53 identified and confirmed compounds revealed nine different chemical scaffolds and 20 singletons.
Bifeng Pan +2 more
exaly +4 more sources
Handbook of Experimental Pharmacology, 2014 TRPML3 belongs to the MCOLN (TRPML) subfamily of transient receptor potential (TRP) channels comprising three genes in mammals. Since the discovery of the pain sensing, capsaicin- and heat-activated vanilloid receptor (TRPV1), TRP channels have been found to be involved in regulating almost all kinds of our sensory modalities. Thus, TRP channel members
Christian Grimm +2 more
exaly +4 more sources
Journal of Physiology, 2008 TRPML3 (mucolipin‐3) belongs to one of the transient‐receptor‐potential (TRP) ion channel families. Mutations in the Trpml3 gene cause disorganization of the stereociliary hair bundle, structural aberrations in outer and inner hair cells and stria vascularis defects, leading to deafness in the varitint‐waddler (Va) mouse.
Richard Goodyear, Konrad Noben-Trauth
exaly +5 more sources
Lysosomal Localization of TRPML3 Depends on TRPML2 and the Mucolipidosis-associated Protein TRPML1 [PDF]
Journal of Biological Chemistry, 2006 Mucolipidosis type IV is an autosomal recessive lysosomal storage disorder characterized by severe neurodegeneration, achlorhydria, and visual impairments such as corneal opacity and strabismus. The disease arises due to mutations in a group 2 transient receptor potential (TRP)-related cation channel, TRPML1.
Craig Montell, Kartik Venkatachalam
exaly +3 more sources
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Biochemical and Biophysical Research Communications, 2014
TRPML3 is a Ca(2+) permeable cation channel expressed in multiple intracellular compartments. Although TRPML3 is implicated in autophagy, how TRPML3 can regulate autophagy is not understood. To search interacting proteins with TRPML3 in autophagy, we performed split-ubiquitin membrane yeast two-hybrid (MY2H) screening with TRPML3-loop as a bait and ...
Hyun Jin Kim
exaly +3 more sources
TRPML3 is a Ca(2+) permeable cation channel expressed in multiple intracellular compartments. Although TRPML3 is implicated in autophagy, how TRPML3 can regulate autophagy is not understood. To search interacting proteins with TRPML3 in autophagy, we performed split-ubiquitin membrane yeast two-hybrid (MY2H) screening with TRPML3-loop as a bait and ...
Hyun Jin Kim
exaly +3 more sources