Results 121 to 130 of about 709 (136)
Cryo-EM structures of the human endolysosomal TRPML3 channel in three distinct states [PDF]
Nature Structural and Molecular Biology, 2017 TRPML3 channels are mainly localized to endolysosomes and play a critical role in the endocytic pathway. Their dysfunction causes deafness and pigmentation defects in mice. TRPML3 activity is inhibited by low endolysosomal pH. Here we present cryo-electron microscopy (cryo-EM) structures of human TRPML3 in the closed, agonist-activated, and low-pH ...
Qi Jia, Xueming Li, Jian Yang
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Expression and vesicular localization of mouse Trpml3 in stria vascularis, hair cells, and vomeronasal and olfactory receptor neurons [PDF]
Journal of Comparative Neurology, 2011 TRPML3 is a member of the mucolipin branch of the transient receptor potential cation channel family. A dominant missense mutation in Trpml3 (also known as Mcoln3) causes deafness and vestibular impairment characterized by stereocilia disorganization, hair cell loss, and endocochlear potential reduction.
Jaime García-Añoveros
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Constitutive Activity of TRPML2 and TRPML3 Channels versus Activation by Low Extracellular Sodium and Small Molecules [PDF]
Journal of Biological Chemistry, 2012 The transient receptor potential channels TRPML2 and TRPML3 (MCOLN2 and MCOLN3) are nonselective cation channels. They are widely expressed in mammals. However, little is known about their physiological function(s) and activation mechanism(s). TRPML3 can be activated or rather de-inhibited by exposing it first to sodium-free extracellular solution and ...
Christian Grimm +2 more
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The TRPML3 Channel: From Gene to Function
2010TRPML3 is a transient receptor potential (TRP) channel that is encoded by the mucolipin 3 gene (MCOLN3), a member of the small mucolipin gene family. Mcoln3 shows a broad expression pattern in embryonic and adult tissues that includes differentiated cells of skin and inner ear.
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Biochimica et Biophysica Acta (BBA) - Molecular Cell Research
TNBC remains the most aggressive and therapy-resistant type of breast cancer, for which efficient targeted therapies have not been developed yet. Here, we identified TRPML3 (ML3) as a potential therapeutic target in TNBC. Our data showed that ML3 is significantly upregulated in TNBC cells compared with nontumorigenic control cells.
Gabriela Maria De Abreu, Gomes +10 more
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TNBC remains the most aggressive and therapy-resistant type of breast cancer, for which efficient targeted therapies have not been developed yet. Here, we identified TRPML3 (ML3) as a potential therapeutic target in TNBC. Our data showed that ML3 is significantly upregulated in TNBC cells compared with nontumorigenic control cells.
Gabriela Maria De Abreu, Gomes +10 more
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American Journal of Respiratory and Critical Care Medicine
Abstract Introduction Lysosomes have recently gained prominence as pivotal signaling hubs implicated in drug resistance within cancer cells. However, the precise role of Transient receptor potential mucolipin 3 (TRPML3), an endo-lysosomal Ca2+-permeable channel known to regulate lysosomal ...
S -h Yang, M Kim, M Kim
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Abstract Introduction Lysosomes have recently gained prominence as pivotal signaling hubs implicated in drug resistance within cancer cells. However, the precise role of Transient receptor potential mucolipin 3 (TRPML3), an endo-lysosomal Ca2+-permeable channel known to regulate lysosomal ...
S -h Yang, M Kim, M Kim
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ABSTRACT Autophagy is a conserved pro-survival pathway for delivering misfolded proteins and damaged organelles to lysosomes for degradation and protein homeostasis. Anomaly in autophagy leads to aberrant protein aggregation in neuronal cells, which is a common etiology of neurodegenerative disorders.
Sushanth Adusumilli +3 more
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Sushanth Adusumilli +3 more
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The intracellular Ca2+channel TRPML3 is a PI3P effector that regulates autophagosome biogenesis
Proceedings of the National Academy of Sciences of the United States of America, 2022Hyun Jin Kim +2 more
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The Ca2+ Channel TRPML3 Regulates Membrane Trafficking and Autophagy
Traffic, 2009Hyun Jin Kim, Shmuel Muallem, Insuk So
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