PMID-sentid	Pub_year	Sent_text	comp_official_name	comp_offset	protein_name	organism	prot_offset
32989250-3	2020	In addition, lysosomal damage triggers LC3 recruitment on lysosomes, where lipidated LC3 interacts with the lysosomal calcium channel TRPML1, facilitating calcium efflux essential for TFEB activation.	Calcium	118-125	mucolipin 1	Mus musculus	134-140
32989250-3	2020	In addition, lysosomal damage triggers LC3 recruitment on lysosomes, where lipidated LC3 interacts with the lysosomal calcium channel TRPML1, facilitating calcium efflux essential for TFEB activation.	Calcium	155-162	mucolipin 1	Mus musculus	134-140
32586947-10	2020	Despite our previous finding of diminished accumulation of the ferritin-bound iron in the Mcoln1 -/- brain, we report no significant changes in expression of the cytosolic iron reporters, suggesting that iron-handling deficits in MLIV occur in the lysosomes and do not involve broad iron deficiency.	Iron	78-82	mucolipin 1	Mus musculus	90-96
32366951-7	2021	Mechanistically we found that TFEB regulates the secretion of truncated mutant tau lacking MTBR and this process is dependent on the lysosomal calcium channel TRPML1.	Calcium	143-150	mucolipin 1	Mus musculus	159-165
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	0-45	mucolipin 1	Mus musculus	257-263
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	NAADP	47-52	mucolipin 1	Mus musculus	257-263
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	Calcium	88-95	mucolipin 1	Mus musculus	257-263
32676502-1	2020	Nicotinic acid adenine dinucleotide phosphate (NAADP) is a second messenger that evokes calcium release from intracellular organelles by the engagement of calcium release channels, including members of the Transient Receptor Potential (TRP) family, such as TRPML1, the (structurally) related Two Pore Channel type 1 (TPC1) and TPC2 channels as well as Ryanodine Receptors type 1 (RYR1; Guse, 2012).	Calcium	155-162	mucolipin 1	Mus musculus	257-263
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	gadolinium chloride	195-200	mucolipin 1	Mus musculus	437-443
32138242-3	2020	In Mcoln1-/- mice, we found that a high dose of vitamin D (Vit D; 500,000 IU/kg/day) resulted in increased AMC compared to their wild-type littermates, which was accompanied by significant downregulation of SM22-alpha and upregulation of RUNX2 and osteopontin in the arterial media, indicating a phenotypic switch to osteogenic.	Vitamin D	48-57	mucolipin 1	Mus musculus	3-9
32138242-8	2020	All these data indicate that the Mcoln1 gene deletion in mice leads to abnormal lysosome positioning and increased sEV secretion, which may contribute to the arterial stiffness during the development of AMC.	7-amino-4-methylcoumarin	203-206	mucolipin 1	Mus musculus	33-39
31974459-3	2020	As a key lysosomal Ca2+ channel, Transient Receptor Potential Mucolipin-1 (TRPML1) regulates lysosomal exocytosis and subsequent phagosome biogenesis, thereby promoting phagocytosis of large extracellular particles.	Calcium	19-23	mucolipin 1	Mus musculus	33-73
31974459-3	2020	As a key lysosomal Ca2+ channel, Transient Receptor Potential Mucolipin-1 (TRPML1) regulates lysosomal exocytosis and subsequent phagosome biogenesis, thereby promoting phagocytosis of large extracellular particles.	Calcium	19-23	mucolipin 1	Mus musculus	75-81
31974459-4	2020	Recently, we have suggested that TRPML1-mediated lysosomal exocytosis is essentially dependent on lysosomal big conductance Ca2+-activated potassium (BK) channel.	Calcium	124-128	mucolipin 1	Mus musculus	33-39
31974459-4	2020	Recently, we have suggested that TRPML1-mediated lysosomal exocytosis is essentially dependent on lysosomal big conductance Ca2+-activated potassium (BK) channel.	Potassium	139-148	mucolipin 1	Mus musculus	33-39
31687088-7	2019	Lycorine attenuated oxidized transient receptor potential cation channel, mucolipin subfamily (TRPML1) by reducing mitochondrial reactive oxygen species (mROS) and decreased transcription factor EB (TFEB) nuclear translocation.	Oxygen	138-144	mucolipin 1	Mus musculus	95-101
31268777-7	2019	Pharmacologically, it was found that TRPML1 channel activity was remarkably attenuated by the AC inhibitor carmofur.	carmofur	107-115	mucolipin 1	Mus musculus	37-43
31268777-8	2019	Sphingosine, as an AC product, was demonstrated to induce TRPML1-mediated Ca2+ release, which was inhibited by a TRPML1 blocker, verapamil.	Sphingosine	0-11	mucolipin 1	Mus musculus	58-64
31268777-8	2019	Sphingosine, as an AC product, was demonstrated to induce TRPML1-mediated Ca2+ release, which was inhibited by a TRPML1 blocker, verapamil.	Sphingosine	0-11	mucolipin 1	Mus musculus	113-119
31268777-8	2019	Sphingosine, as an AC product, was demonstrated to induce TRPML1-mediated Ca2+ release, which was inhibited by a TRPML1 blocker, verapamil.	Verapamil	129-138	mucolipin 1	Mus musculus	58-64
31268777-8	2019	Sphingosine, as an AC product, was demonstrated to induce TRPML1-mediated Ca2+ release, which was inhibited by a TRPML1 blocker, verapamil.	Verapamil	129-138	mucolipin 1	Mus musculus	113-119
31268777-9	2019	Using a Port-a-Patch planar patch-clamp system, we found that AC-associated sphingolipids, sphingomyelin, ceramide, and sphingosine had different effects on TRPML1 channel activity in podocytes.	Sphingolipids	76-89	mucolipin 1	Mus musculus	157-163
31268777-9	2019	Using a Port-a-Patch planar patch-clamp system, we found that AC-associated sphingolipids, sphingomyelin, ceramide, and sphingosine had different effects on TRPML1 channel activity in podocytes.	Sphingomyelins	91-104	mucolipin 1	Mus musculus	157-163
31268777-9	2019	Using a Port-a-Patch planar patch-clamp system, we found that AC-associated sphingolipids, sphingomyelin, ceramide, and sphingosine had different effects on TRPML1 channel activity in podocytes.	Ceramides	106-114	mucolipin 1	Mus musculus	157-163
31268777-9	2019	Using a Port-a-Patch planar patch-clamp system, we found that AC-associated sphingolipids, sphingomyelin, ceramide, and sphingosine had different effects on TRPML1 channel activity in podocytes.	Sphingosine	120-131	mucolipin 1	Mus musculus	157-163
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	Hydrogen Peroxide	29-33	mucolipin 1	Mus musculus	437-443
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	Hydrogen Peroxide	29-33	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	Hydrogen Peroxide	29-33	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	Hydrogen Peroxide	29-33	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	Hydrogen Peroxide	29-33	mucolipin 1	Mus musculus	461-467
31317194-9	2019	Luteal cell degeneration and impaired mitochondrial functions can both contribute to progesterone deficiency in the Mcoln1-/- mice.	Progesterone	85-97	mucolipin 1	Mus musculus	116-122
30917721-5	2019	MCOLN1 is regulated by phosphoinositide kinase PIKFYVE and its product PtdIns(3,5)P2, which is also decreased in RC-deficiency.	phosphatidylinositol 3,5-diphosphate	71-84	mucolipin 1	Mus musculus	0-6
30917721-7	2019	Building on these data and the literature, we propose that downregulation of the AMPK-PIKFYVE-PtdIns(3,5)P2-MCOLN1 pathway causes lysosomal Ca2+ accumulation and impaired lysosomal catabolism.	phosphatidylinositol 3,5-diphosphate	94-107	mucolipin 1	Mus musculus	108-114
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	gadolinium chloride	195-200	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	gadolinium chloride	195-200	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	gadolinium chloride	195-200	mucolipin 1	Mus musculus	461-467
31060676-3	2019	Results After treatment with H2O2,the expression of caspase-1 protein and NLRP3 mRNA in BV2 cells was increased,and IL-1beta protein in BV2 cells was significantly increased after treatment with GdCl3(P=0.0036).After treatment with CA-074Me,the doses of NLRP3 mRNA(P=0.037),caspase-1(P=0.021),and IL-1beta(P= 0.036)were significantly reduced.Cells in the H2O2 group and H2O2+GdCl3 group grew more slowly.The expressions of CTSB mRNA and TRPML1 mRNA,or CTSB and TRPML1 proteins in BV2 cells in the treatment group with 200 mumol/L of H2O2 concentration were similar.H2O2-induced CTSB protein expression was inhibited after silencing TRPML1 gene.The changes of other cathepsins were not affected for the different concentration of H2O2.In the BV2 cells treated with TRPML1 gene silencing,the expression of CTSB protein was significantly reduced and the difference was statistically significant(P=0.021)between the H2O2 +siRNA treatment group and the H2O2 treatment group.<b>Conclusion</b> CTSB regulates the activation of NLRP3 inflammasome in the oxidative stress model of microglia cells,probably mediated by calcium channel protein TRPML1.	gadolinium chloride	195-200	mucolipin 1	Mus musculus	461-467
29771310-9	2018	Fingolimod promotes cytokine homeostasis, down-regulates signaling within the PI3K/Akt and MAPK pathways and restores the lysosomal compartment in Mcoln1-/- astrocytes.	Fingolimod Hydrochloride	0-10	mucolipin 1	Mus musculus	147-153
29030399-0	2018	Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation.	Calcium	17-24	mucolipin 1	Mus musculus	51-57
29030399-1	2018	The transient receptor potential cation channel mucolipin 1 (TRPML1) channel is a conduit for lysosomal calcium efflux, and channel activity may be affected by lysosomal contents.	Calcium	104-111	mucolipin 1	Mus musculus	61-67
29030399-3	2018	This study asks whether stimulation of TRPML1 can release lysosomal calcium in RPE cells and whether such release is affected by lysosomal accumulations.	Calcium	68-75	mucolipin 1	Mus musculus	39-45
29062301-0	2017	Curcumin Exerts Effects on the Pathophysiology of Alzheimer"s Disease by Regulating PI(3,5)P2 and Transient Receptor Potential Mucolipin-1 Expression.	Curcumin	0-8	mucolipin 1	Mus musculus	98-138
29062301-1	2017	BACKGROUND: To validate our speculation that curcumin may ameliorate Alzheimer"s disease (AD) pathogenesis by regulating PI(3,5)P2 and transient receptor potential mucolipin-1 (TRPML1) expression levels.	Curcumin	45-53	mucolipin 1	Mus musculus	135-175
29062301-1	2017	BACKGROUND: To validate our speculation that curcumin may ameliorate Alzheimer"s disease (AD) pathogenesis by regulating PI(3,5)P2 and transient receptor potential mucolipin-1 (TRPML1) expression levels.	Curcumin	45-53	mucolipin 1	Mus musculus	177-183
29062301-13	2017	Western blotting results also showed that TRPML1 was upregulated and mTOR/S6K signaling pathway was activated and markers of the autophagy-lysosomal system were downregulated after curcumin use in Abeta1-42-treated HT-22 cells.	Curcumin	181-189	mucolipin 1	Mus musculus	42-48
29062301-14	2017	Knockdown of PI (3,5)P2 or TRPML1 increased the protein levels of markers of the autophagy-lysosomal system after curcumin use in Abeta1-42-treated HT-22 cells, inhibited mTOR/S6K signaling pathway, increased the protein levels of markers of the autophagy-lysosomal system after curcumin use in APP/PS1 mice.	Curcumin	114-122	mucolipin 1	Mus musculus	27-33
29062301-14	2017	Knockdown of PI (3,5)P2 or TRPML1 increased the protein levels of markers of the autophagy-lysosomal system after curcumin use in Abeta1-42-treated HT-22 cells, inhibited mTOR/S6K signaling pathway, increased the protein levels of markers of the autophagy-lysosomal system after curcumin use in APP/PS1 mice.	Curcumin	279-287	mucolipin 1	Mus musculus	27-33
29062301-15	2017	Besides, knockdown of PI(3,5)P2 or TRPML1 reversed the protective role of curcumin on memory and recognition impairments in mice with APP/PS1 transgenes.	Curcumin	74-82	mucolipin 1	Mus musculus	35-41
29062301-16	2017	CONCLUSION: To some extent, it suggested that the effects of curcumin on AD pathogenesis were, at least partially, associated with PI(3,5)P2 and TRPML1 expression levels.	Curcumin	61-69	mucolipin 1	Mus musculus	145-151
28610891-3	2017	The disease results from mutations in the gene encoding mucolipin-1, a transient receptor potential channel believed to play a key role in lysosomal calcium egress.	Calcium	149-156	mucolipin 1	Mus musculus	56-67
28610891-4	2017	Loss of mucolipin-1 and subsequent defects lead to a host of cellular aberrations, including accumulation of glycosphingolipids (GSLs) in neurons and other cell types, microgliosis and, as reported here, cerebellar Purkinje cell loss.	Glycosphingolipids	109-127	mucolipin 1	Mus musculus	8-19
28610891-4	2017	Loss of mucolipin-1 and subsequent defects lead to a host of cellular aberrations, including accumulation of glycosphingolipids (GSLs) in neurons and other cell types, microgliosis and, as reported here, cerebellar Purkinje cell loss.	Glycosphingolipids	129-133	mucolipin 1	Mus musculus	8-19
26682800-6	2016	Preliminary exploration of synaptic vesicle size, spontaneous mEPSCs, and glutamate secretion in neurons provided further evidence for enhanced exocytosis that was rescued by re-expression of TRPML1 in neurons.	Glutamic Acid	74-83	mucolipin 1	Mus musculus	192-198
29131026-12	2017	TRPML1 overexpression or treatment with the mTOR activator propranolol also attenuated the Abeta1-42-inhibited mTOR/S6K signalling pathway and the Abeta1-42-induced ALR-related protein expression levels.	Propranolol	59-70	mucolipin 1	Mus musculus	0-6
25266962-7	2014	Moreover, different from the insect TRPML, mouse TRPML1 was readily activated by ML-SA1 independent of PI(3,5)P2.	phosphatidylinositol 3,5-diphosphate	103-112	mucolipin 1	Mus musculus	49-55
26398942-8	2015	We observed reduced Perls" staining in Mcoln1(-/-) brain, indicating lower levels of ferric iron.	ferric sulfate	85-96	mucolipin 1	Mus musculus	39-45
21111738-1	2011	BACKGROUND & AIMS: Mutations in TRPML1, a lysosomal Ca(2+)-permeable TRP channel, lead to mucolipidosis type IV, a neurodegenerative lysosomal storage disease.	Adenosine Monophosphate	12-15	mucolipin 1	Mus musculus	36-42
23283937-6	2013	When CAMs were treated with TRP-ML1 siRNA, FasL-induced interactions between the lysosomes and SR were substantially blocked.	cams	5-9	mucolipin 1	Mus musculus	28-35
23283937-8	2013	These results suggest that TRP-ML1 channel-mediated lysosomal Ca(2+) bursts upon FasL stimulation promote lysosome trafficking and interactions with the SR, leading to apoptosis of CAMs via a Ca(2+)-dependent mechanism.	cams	181-185	mucolipin 1	Mus musculus	27-34
23993788-5	2013	Using time-lapse confocal imaging and direct patch clamping of phagosomal membranes, we found that particle binding induces lysosomal PI(3,5)P2 elevation to trigger TRPML1-mediated lysosomal Ca2+ release specifically at the site of uptake, rapidly delivering TRPML1-resident lysosomal membranes to nascent phagosomes via lysosomal exocytosis.	phosphatidylinositol 3,5-diphosphate	134-143	mucolipin 1	Mus musculus	165-171
23993788-5	2013	Using time-lapse confocal imaging and direct patch clamping of phagosomal membranes, we found that particle binding induces lysosomal PI(3,5)P2 elevation to trigger TRPML1-mediated lysosomal Ca2+ release specifically at the site of uptake, rapidly delivering TRPML1-resident lysosomal membranes to nascent phagosomes via lysosomal exocytosis.	phosphatidylinositol 3,5-diphosphate	134-143	mucolipin 1	Mus musculus	259-265
21111738-6	2011	RESULTS: Trpml1 is expressed by parietal cells and localizes predominantly to the lysosomes; it was dynamically palmitoylated and dephosphorylated in vivo following histamine stimulation of acid secretion.	Histamine	165-174	mucolipin 1	Mus musculus	9-15
21111738-7	2011	Trpml1-null mice had significant impairments in basal and histamine-stimulated gastric acid secretion and markedly reduced levels of the gastric proton pump.	Histamine	58-67	mucolipin 1	Mus musculus	0-6
16517607-2	2006	Mutations in ML1 result in mucolipidosis type IV, a lysosomal storage disease characterized by the intracellular accumulation of enlarged vacuolar structures containing phospholipids, sphingolipids, and mucopolysaccharides.	Glycosaminoglycans	203-222	mucolipin 1	Mus musculus	13-16
18048323-5	2007	Proline substitutions in TM5 of other TRP channels revealed that TRPML1, TRPML2, TRPV5, and TRPV6 display a similar susceptibility at comparable positions, whereas other TRP channels were not affected.	Proline	0-7	mucolipin 1	Mus musculus	65-71
16517607-2	2006	Mutations in ML1 result in mucolipidosis type IV, a lysosomal storage disease characterized by the intracellular accumulation of enlarged vacuolar structures containing phospholipids, sphingolipids, and mucopolysaccharides.	Phospholipids	169-182	mucolipin 1	Mus musculus	13-16
20802798-4	2010	Both PI(3,5)P(2)-deficient cells and cells that lack TRPML1 exhibited enlarged endolysosomes/vacuoles and trafficking defects in the late endocytic pathway.	phosphatidylinositol 3,5-diphosphate	5-16	mucolipin 1	Mus musculus	53-59
20802798-5	2010	We find that the enlarged vacuole phenotype observed in PI(3,5)P(2)-deficient mouse fibroblasts is suppressed by overexpression of TRPML1.	phosphatidylinositol 3,5-diphosphate	56-67	mucolipin 1	Mus musculus	131-137
20802798-6	2010	Notably, this PI(3,5)P(2)-dependent regulation of TRPML1 is evolutionarily conserved.	(3,5)p(2)	16-25	mucolipin 1	Mus musculus	50-56
19763610-10	2009	Conversely, significant upregulation of TRPML2sv transcripts was observed when primary mouse lymphoid cells were treated with nicotinic acid adenine dinucleotide phosphate, or N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide, both known activators of TRPML1.	NAADP	126-171	mucolipin 1	Mus musculus	263-269
19763610-10	2009	Conversely, significant upregulation of TRPML2sv transcripts was observed when primary mouse lymphoid cells were treated with nicotinic acid adenine dinucleotide phosphate, or N-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide, both known activators of TRPML1.	n-(2-[p-bromocinnamylamino]ethyl)-5-isoquinoline sulfonamide	176-236	mucolipin 1	Mus musculus	263-269
16517607-2	2006	Mutations in ML1 result in mucolipidosis type IV, a lysosomal storage disease characterized by the intracellular accumulation of enlarged vacuolar structures containing phospholipids, sphingolipids, and mucopolysaccharides.	Sphingolipids	184-197	mucolipin 1	Mus musculus	13-16
34617321-5	2021	Moreover, melatonin restored mitophagy by improving mitophagosome-lysosome fusion via Mcoln1, and thus, ameliorated mitochondrial functions, attenuated Abeta pathology, and improved cognition.	Melatonin	10-19	mucolipin 1	Mus musculus	86-92
34669246-7	2021	Trehalose upregulated p-GSK3beta ser9, TFEB and TRPML1, ADAM10, OST48, ERalpha and induced TFEB nuclear translocation in hippocampus, elevated IDE and ERbeta in cortex, while reduced p-tau ser396&404, CDK5, cathepsin B and GFAP in hippocampus.	Trehalose	0-9	mucolipin 1	Mus musculus	48-54
35486730-3	2022	These organelles undergo exclusive retrograde transport in axons, with occasional pauses triggered by regulated calcium efflux from agonist-evoked transient receptor potential cation channel mucolipin subfamily member 1 (TRPML1) channels-an effect greatly exaggerated by exogenous agonist mucolipin synthetic agonist 1 (ML-SA1).	Calcium	112-119	mucolipin 1	Mus musculus	221-227
34686351-2	2021	Here, we report that mucolipin TRP channel 1 (TRPML1), a lysosomal Ca2+ and Zn2+ release channel that regulates multiple aspects of lysosome function, is dramatically upregulated in metastatic melanoma cells compared with normal cells.	Zinc	76-80	mucolipin 1	Mus musculus	46-52
34686351-5	2021	While pharmacological inhibition or genetic silencing of TRPML1 in metastatic melanoma cells prevents such cell death, overexpression of TRPML1 in normal cells confers ML-SA vulnerability.	ml-sa	168-173	mucolipin 1	Mus musculus	137-143
35491864-5	2022	We found that MCOLN1 is activated secondary to reactive oxygen species (ROS) elevation following I/R, which in turn induces the release of lysosomal zinc into the cytosol.	Reactive Oxygen Species	47-70	mucolipin 1	Mus musculus	14-20
35491864-5	2022	We found that MCOLN1 is activated secondary to reactive oxygen species (ROS) elevation following I/R, which in turn induces the release of lysosomal zinc into the cytosol.	Reactive Oxygen Species	72-75	mucolipin 1	Mus musculus	14-20
35491864-7	2022	Furthermore, we discovered that the MCOLN1-mediated inhibition of autophagy induced by I/R impairs mitochondrial function, which results in further detrimental ROS release that directly contributes to cardiomyocyte death.	Reactive Oxygen Species	160-163	mucolipin 1	Mus musculus	36-42
35491864-9	2022	Therefore, targeting MCOLN1 represents a novel therapeutic strategy to protect against myocardial I/R injury.Abbreviations: I/R: ischemia-reperfusion; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCOLN1/TRPML1: mucolipin TRP cation channel 1; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1.	Reactive Oxygen Species	259-262	mucolipin 1	Mus musculus	21-27
35491864-9	2022	Therefore, targeting MCOLN1 represents a novel therapeutic strategy to protect against myocardial I/R injury.Abbreviations: I/R: ischemia-reperfusion; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; MCOLN1/TRPML1: mucolipin TRP cation channel 1; ROS: reactive oxygen species; SQSTM1/p62: sequestosome 1.	Reactive Oxygen Species	264-287	mucolipin 1	Mus musculus	21-27
35095492-12	2021	Calcium imaging results suggested that BK might regulate the autophagy pathway from TRPML1.	Calcium	0-7	mucolipin 1	Mus musculus	84-90
35099830-0	2022	LAMTOR1 inhibition of TRPML1-dependent lysosomal calcium release regulates dendritic lysosome trafficking and hippocampal neuronal function.	Calcium	49-56	mucolipin 1	Mus musculus	22-28
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	Triethylenephosphoramide	243-246	mucolipin 1	Mus musculus	72-78
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	Triethylenephosphoramide	243-246	mucolipin 1	Mus musculus	199-205
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	phosphatidylinositol 3,5-diphosphate	255-264	mucolipin 1	Mus musculus	72-78
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	phosphatidylinositol 3,5-diphosphate	255-264	mucolipin 1	Mus musculus	199-205
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	phosphatidylinositol 3,5-diphosphate	283-292	mucolipin 1	Mus musculus	72-78
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	phosphatidylinositol 3,5-diphosphate	283-292	mucolipin 1	Mus musculus	199-205
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	Sirolimus	309-318	mucolipin 1	Mus musculus	72-78
35131932-5	2022	To reveal the structural basis underlying the synergistic activation of TRPML1 by PI(3,5)P2 and rapamycin, we determined the high-resolution cryoelectron microscopy (cryo-EM) structures of the mouse TRPML1 channel in various states, including apo closed, PI(3,5)P2-bound closed, and PI(3,5)P2/temsirolimus (a rapamycin analog)-bound open states.	Sirolimus	309-318	mucolipin 1	Mus musculus	199-205
35389129-8	2022	As a result, the inhibited myocardial autophagic flux induced by TRPML1 disrupted mitochondria turnover and resulted in mass accumulation of damaged mitochondria and further ROS release, which directly led to cardiomyocyte death.	ros	174-177	mucolipin 1	Mus musculus	65-71
35389129-10	2022	In summary, our study demonstrates that secondary to ROS elevation, activation of TRPML1 results in autophagy inhibition in the cardiomyocytes subjected to I/R, which directly leads to cardiomyocyte death by disrupting mitochondria turnover.	ros	53-56	mucolipin 1	Mus musculus	82-88
34030116-7	2021	By GCaMP3 Ca2+ imaging, we confirmed the inhibition of TRPML1 channel activity by Hcy which was remarkably ameliorated by catalase and gp91 ds-tat peptide.	Homocysteine	82-85	mucolipin 1	Mus musculus	55-61
34030116-10	2021	Moreover, we found that hydrogen peroxide (H2O2) mimicked the effect of Hcy on TRPML1 channel activity, lysosome-MVB interaction, and exosome secretion in podocytes.	Hydrogen Peroxide	24-41	mucolipin 1	Mus musculus	79-85
34030116-0	2021	Regulation of TRPML1 channel activity and inflammatory exosome release by endogenously produced reactive oxygen species in mouse podocytes.	Reactive Oxygen Species	96-119	mucolipin 1	Mus musculus	14-20
34030116-10	2021	Moreover, we found that hydrogen peroxide (H2O2) mimicked the effect of Hcy on TRPML1 channel activity, lysosome-MVB interaction, and exosome secretion in podocytes.	Hydrogen Peroxide	43-47	mucolipin 1	Mus musculus	79-85
34030116-10	2021	Moreover, we found that hydrogen peroxide (H2O2) mimicked the effect of Hcy on TRPML1 channel activity, lysosome-MVB interaction, and exosome secretion in podocytes.	Homocysteine	72-75	mucolipin 1	Mus musculus	79-85
34030116-11	2021	Based on these results, we conclude that endogenously produced ROS importantly contributes to inflammatory exosome secretion from podocytes through inhibition of TRPML1 channel activity, which may contribute to the initiation of glomerular inflammation during hHcy.	Reactive Oxygen Species	63-66	mucolipin 1	Mus musculus	162-168
32070194-6	2021	The lysosomal Ca2+ channel protein MCOLN1/TRPML1 (mucolipin 1) regulates lysosomal-plasma membrane fusion and its overexpression increased, while inhibition blocked FA efflux.	Calcium	14-18	mucolipin 1	Mus musculus	35-41
32070194-6	2021	The lysosomal Ca2+ channel protein MCOLN1/TRPML1 (mucolipin 1) regulates lysosomal-plasma membrane fusion and its overexpression increased, while inhibition blocked FA efflux.	Calcium	14-18	mucolipin 1	Mus musculus	42-48
32070194-6	2021	The lysosomal Ca2+ channel protein MCOLN1/TRPML1 (mucolipin 1) regulates lysosomal-plasma membrane fusion and its overexpression increased, while inhibition blocked FA efflux.	Calcium	14-18	mucolipin 1	Mus musculus	50-61
32070194-9	2021	Moreover, the efflux of FAs and their reuptake or subsequent extracellular trafficking to adjacent cells may play an important role in cell-to-cell lipid exchange and signaling.Abbreviations: ACTB: beta actin; ADRA1A: adrenergic receptor alpha, 1a; ALB: albumin; ATG5: autophagy related 5; ATG7: autophagy related 7; BafA1: bafilomycin A1; BECN1: beclin 1; BHBA: beta-hydroxybutyrate; BSA: bovine serum albumin; CDH1: e-cadherin; CQ: chloroquine; CTSB: cathepsin B; DGAT: diacylglycerol O-acyltransferase; FA: fatty acid; HFD: high-fat diet; LAMP1: lysosomal-associated membrane protein 1; LD: lipid droplet; LIPA/LAL: lysosomal acid lipase A; LLME: Leu-Leu methyl ester hydrobromide; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; MCOLN1/TRPML1: mucolipin 1; MEF: mouse embryo fibroblast; PBS: phosphate-buffered saline; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PLIN: perilipin; PNPLA2/ATGL patatin-like phospholipase domain containing 2; RUBCN (rubicon autophagy regulator); SM: sphingomyelin; TAG: triacylglycerol; TMEM192: transmembrane protein 192; VLDL: very low density lipoprotein.	Fatty Acids	24-27	mucolipin 1	Mus musculus	752-758
32070194-9	2021	Moreover, the efflux of FAs and their reuptake or subsequent extracellular trafficking to adjacent cells may play an important role in cell-to-cell lipid exchange and signaling.Abbreviations: ACTB: beta actin; ADRA1A: adrenergic receptor alpha, 1a; ALB: albumin; ATG5: autophagy related 5; ATG7: autophagy related 7; BafA1: bafilomycin A1; BECN1: beclin 1; BHBA: beta-hydroxybutyrate; BSA: bovine serum albumin; CDH1: e-cadherin; CQ: chloroquine; CTSB: cathepsin B; DGAT: diacylglycerol O-acyltransferase; FA: fatty acid; HFD: high-fat diet; LAMP1: lysosomal-associated membrane protein 1; LD: lipid droplet; LIPA/LAL: lysosomal acid lipase A; LLME: Leu-Leu methyl ester hydrobromide; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; MCOLN1/TRPML1: mucolipin 1; MEF: mouse embryo fibroblast; PBS: phosphate-buffered saline; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PLIN: perilipin; PNPLA2/ATGL patatin-like phospholipase domain containing 2; RUBCN (rubicon autophagy regulator); SM: sphingomyelin; TAG: triacylglycerol; TMEM192: transmembrane protein 192; VLDL: very low density lipoprotein.	Fatty Acids	24-27	mucolipin 1	Mus musculus	759-765
32070194-9	2021	Moreover, the efflux of FAs and their reuptake or subsequent extracellular trafficking to adjacent cells may play an important role in cell-to-cell lipid exchange and signaling.Abbreviations: ACTB: beta actin; ADRA1A: adrenergic receptor alpha, 1a; ALB: albumin; ATG5: autophagy related 5; ATG7: autophagy related 7; BafA1: bafilomycin A1; BECN1: beclin 1; BHBA: beta-hydroxybutyrate; BSA: bovine serum albumin; CDH1: e-cadherin; CQ: chloroquine; CTSB: cathepsin B; DGAT: diacylglycerol O-acyltransferase; FA: fatty acid; HFD: high-fat diet; LAMP1: lysosomal-associated membrane protein 1; LD: lipid droplet; LIPA/LAL: lysosomal acid lipase A; LLME: Leu-Leu methyl ester hydrobromide; MAP1LC3B/LC3: microtubule associated protein 1 light chain 3 beta; MCOLN1/TRPML1: mucolipin 1; MEF: mouse embryo fibroblast; PBS: phosphate-buffered saline; PIK3C3/VPS34: phosphatidylinositol 3-kinase catalytic subunit type 3; PLIN: perilipin; PNPLA2/ATGL patatin-like phospholipase domain containing 2; RUBCN (rubicon autophagy regulator); SM: sphingomyelin; TAG: triacylglycerol; TMEM192: transmembrane protein 192; VLDL: very low density lipoprotein.	Fatty Acids	24-27	mucolipin 1	Mus musculus	767-778
34026326-0	2021	miR-204 silencing reduces mitochondrial autophagy and ROS production in a murine AD model via the TRPML1-activated STAT3 pathway.	Reactive Oxygen Species	54-57	mucolipin 1	Mus musculus	98-104
34026326-9	2021	TRPML1 overexpression, downregulation of miR-204, or STAT3 pathway activation reduced the Abeta1-42-induced mitochondrial damage, along with ROS production and mitochondrial autophagy in vivo and in vitro.	Reactive Oxygen Species	141-144	mucolipin 1	Mus musculus	0-6
34026326-10	2021	Silencing of miR-204 could upregulate TRPML1 expression, thus suppressing ROS production and mitochondrial autophagy in AD through STAT3 pathway.	Reactive Oxygen Species	74-77	mucolipin 1	Mus musculus	38-44
33221496-9	2021	As an Ac product, sphingosine was found to rescue TRPML1 channel activity and thereby recover lysosome-MVB interaction and reduce exosome release of podocytes from Asah1fl/fl/PodoCre mice.	Sphingosine	18-29	mucolipin 1	Mus musculus	50-56