| Glycolysis-Mediated Activation of v-ATPase by Nicotinamide Mononucleotide Ameliorates Lipid-Induced Cardiomyopathy by Repressing the CD36-TLR4 Axis. | Glycolysis-Mediated Activation of v-ATPase by Nicotinamide Mononucleotide Ameliorates Lipid-Induced Cardiomyopathy by Repressing the CD36-TLR4 Axis.
Wang S, Han Y, Liu R, Hou M, Neumann D, Zhang J, Wang F, Li Y, Zhao X, Schianchi F, Dai C, Liu L, Nabben M, Glatz JFC, Wu X, Lu X, Li X, Luiken JJFP., Free PMC Article | 03/5/2024 |
| Upregulation of ATP6V0D2 benefits intracellular survival of Leishmania donovani in erythrocytes-engulfing macrophages. | Upregulation of ATP6V0D2 benefits intracellular survival of Leishmania donovani in erythrocytes-engulfing macrophages.
Hong J, Mukherjee B, Sanjoba C, Yamagishi J, Goto Y., Free PMC Article | 02/21/2024 |
| Loss of the Golgi-localized v-ATPase subunit does not alter insulin granule formation or pancreatic islet beta-cell function. | Loss of the Golgi-localized v-ATPase subunit does not alter insulin granule formation or pancreatic islet β-cell function.
Boyer CK, Blom SE, Machado AE, Rohli KE, Maxson ME, Stephens SB. | 02/21/2024 |
| Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by Tyr[682]-phosphorylated APP betaCTF. | Lysosomal dysfunction in Down syndrome and Alzheimer mouse models is caused by v-ATPase inhibition by Tyr(682)-phosphorylated APP βCTF.
Im E, Jiang Y, Stavrides PH, Darji S, Erdjument-Bromage H, Neubert TA, Choi JY, Wegiel J, Lee JH, Nixon RA., Free PMC Article | 09/8/2023 |
| Leishmania infection-induced multinucleated giant cell formation via upregulation of ATP6V0D2 expression. | Leishmania infection-induced multinucleated giant cell formation via upregulation of ATP6V0D2 expression.
Hong J, Sanjoba C, Fujii W, Yamagishi J, Goto Y., Free PMC Article | 10/15/2022 |
| Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1. | Inhibiting ATP6V0D2 Aggravates Liver Ischemia-Reperfusion Injury by Promoting NLRP3 Activation via Impairing Autophagic Flux Independent of Notch1/Hes1.
Wang Z, Wang H, Chen X, Han S, Zhu Y, Wang H, Cheng F, Pu L., Free PMC Article | 11/13/2021 |
| Role of V-ATPase a3-Subunit in Mouse CTL Function. | Role of V-ATPase a3-Subunit in Mouse CTL Function.
Chitirala P, Ravichandran K, Schirra C, Chang HF, Krause E, Kazmaier U, Lauterbach MA, Rettig J. | 02/20/2021 |
| Innate immune responses through Toll-like receptor 3 require human-antigen-R-mediated Atp6v0d2 mRNA stabilization. | Innate immune responses through Toll-like receptor 3 require human-antigen-R-mediated Atp6v0d2 mRNA stabilization.
Zainol MIB, Kawasaki T, Monwan W, Murase M, Sueyoshi T, Kawai T., Free PMC Article | 11/21/2020 |
| Atp6v0d2-deficient macrophages have augmented mitochondrial damage, enhanced inflammasome activation and reduced clearance of Salmonella typhimurium. The susceptibility of atp6v0d2 knockout mice to DSS-induced colitis and Salmonella typhimurium-induced death, highlights the in vivo significance of ATP6V0D2-mediated autophagosome-lysosome fusion. | The macrophage-specific V-ATPase subunit ATP6V0D2 restricts inflammasome activation and bacterial infection by facilitating autophagosome-lysosome fusion.
Xia Y, Liu N, Xie X, Bi G, Ba H, Li L, Zhang J, Deng X, Yao Y, Tang Z, Yin B, Wang J, Jiang K, Li Z, Choi Y, Gong F, Cheng X, O'Shea JJ, Chae JJ, Laurence A, Yang XP., Free PMC Article | 06/20/2020 |
| The authors identified that ATP6V0d2 mediates leucine-induced mTORC1 activation in macrophages, which further regulates macrophage differentiation. | ATP6V0d2 mediates leucine-induced mTORC1 activation and polarization of macrophages.
Li P, Deng X, Luo J, Chen Y, Bi G, Gong F, Wei Z, Liu N, Li H, Laurence A, Yang XP., Free PMC Article | 05/16/2020 |
| Lactate inhibits ATP6V0d2 expression in tumor-associated macrophages to promote HIF-2alpha-mediated tumor progression. | Lactate inhibits ATP6V0d2 expression in tumor-associated macrophages to promote HIF-2α-mediated tumor progression.
Liu N, Luo J, Kuang D, Xu S, Duan Y, Xia Y, Wei Z, Xie X, Yin B, Chen F, Luo S, Liu H, Wang J, Jiang K, Gong F, Tang ZH, Cheng X, Li H, Li Z, Laurence A, Wang G, Yang XP., Free PMC Article | 12/21/2019 |
| ATP6V0d2 controls Leishmania parasitophorous vacuole biogenesis via cholesterol homeostasis. | ATP6V0d2 controls Leishmania parasitophorous vacuole biogenesis via cholesterol homeostasis.
Pessoa CC, Reis LC, Ramos-Sanchez EM, Orikaza CM, Cortez C, de Castro Levatti EV, Badaró ACB, Yamamoto JUDS, D'Almeida V, Goto H, Mortara RA, Real F., Free PMC Article | 12/7/2019 |
| High V-ATPase expression is associated with Bone Pain Induced by Multiple Myeloma. | Bone Pain Induced by Multiple Myeloma Is Reduced by Targeting V-ATPase and ASIC3.
Hiasa M, Okui T, Allette YM, Ripsch MS, Sun-Wada GH, Wakabayashi H, Roodman GD, White FA, Yoneda T., Free PMC Article | 09/9/2017 |
| we propose that PTH has a direct effect on osteoblasts and osteoclasts, and that this effect is mediated through PTH1R, thus contributing to bone remodeling | Bovine parathyroid hormone enhances osteoclast bone resorption by modulating V-ATPase through PTH1R.
Liu S, Zhu W, Li S, Ma J, Zhang H, Li Z, Zhang L, Zhang B, Li Z, Liang X, Shi W., Free PMC Article | 10/29/2016 |
| Insulin significantly activated ERK1/2 MAP kinase as well as markedly induced the expression of NFATc1, an osteoclast marker gene, and Atp6v0d2, an osteoclast fusion-related gene. | Insulin enhances RANKL-induced osteoclastogenesis via ERK1/2 activation and induction of NFATc1 and Atp6v0d2.
Oh JH, Lee JY, Joung SH, Oh YT, Kim HS, Lee NK. | 09/24/2016 |
| V-ATPase has a role in modulating a macrophage phenotype towards tumor-associated macrophages through the action of the a2 isoform of V-ATPase | Tumor-associated vacuolar ATPase subunit promotes tumorigenic characteristics in macrophages.
Katara GK, Jaiswal MK, Kulshrestha A, Kolli B, Gilman-Sachs A, Beaman KD. | 02/7/2015 |
| Luteolin can be effective in reducing bone resorption and that this effect of luteolin may be through disruption of osteoclast V-ATPase a3-d2 interaction. | Luteolin inhibition of V-ATPase a3-d2 interaction decreases osteoclast resorptive activity.
Crasto GJ, Kartner N, Yao Y, Li K, Bullock L, Datti A, Manolson MF. | 09/28/2013 |
| PKCdelta deficiency does not perturb formation of the ruffled border or trafficking of lysosomal vesicles containing the vacuolar-ATPase (v-ATPase). | Protein kinase C-delta deficiency perturbs bone homeostasis by selective uncoupling of cathepsin K secretion and ruffled border formation in osteoclasts.
Cremasco V, Decker CE, Stumpo D, Blackshear PJ, Nakayama KI, Nakayama K, Lupu TS, Graham DB, Novack DV, Faccio R., Free PMC Article | 02/9/2013 |
| these findings suggest that the critical role of ATP6v0d2 may be limited to the control of bone homeostasis under normal development. | ATP6v0d2 deficiency increases bone mass, but does not influence ovariectomy-induced bone loss.
Kim T, Ha H, Kim N, Park ES, Rho J, Kim EC, Lorenzo J, Choi Y, Lee SH., Free PMC Article | 01/15/2011 |
| The data indicate that integrity of lipid rafts regulates the activity of V-ATPase in osteoclasts, suggesting that cholesterol-lowering agents might be useful for inhibiting osteoclast-dependent bone resorption. | Proteomic analysis of osteoclast lipid rafts: the role of the integrity of lipid rafts on V-ATPase activity in osteoclasts.
Ryu J, Kim H, Chang EJ, Kim HJ, Lee Y, Kim HH. | 09/27/2010 |
| Atp6v0d2 (d2), an isoform of the d subunit in the V-ATPase, showed 5-fold higher expression than that of Atp6v0d1 (d1) in mature osteoclasts, indicating a potential function in osteoclastic bone resorption. | Atp6v0d2 is an essential component of the osteoclast-specific proton pump that mediates extracellular acidification in bone resorption.
Wu H, Xu G, Li YP., Free PMC Article | 01/21/2010 |
| MEF2 and MITF function cooperatively with NFATc1 to transactivate the V-ATPase d2 promoter during RANKL-induced osteoclastogenesis. | Myocyte enhancer factor 2 and microphthalmia-associated transcription factor cooperate with NFATc1 to transactivate the V-ATPase d2 promoter during RANKL-induced osteoclastogenesis.
Feng H, Cheng T, Steer JH, Joyce DA, Pavlos NJ, Leong C, Kular J, Liu J, Feng X, Zheng MH, Xu J., Free PMC Article | 01/21/2010 |
| Data indicate for the first time that the NFATc1/Atp6v0d2 and DC-STAMP signaling axis plays a key role in the osteoclast multinucleation process, which is essential for efficient bone resorption. | NFATc1 induces osteoclast fusion via up-regulation of Atp6v0d2 and the dendritic cell-specific transmembrane protein (DC-STAMP).
Kim K, Lee SH, Ha Kim J, Choi Y, Kim N., Free PMC Article | 01/21/2010 |
| d2 is expressed mainly in kidney and at lower levels in heart, spleen, skeletal muscle, and testis. The d2 isoform can complement the yeast vma6Delta phenotype when cells are grown at 25, but not 30, degrees C. | Expression and function of the mouse V-ATPase d subunit isoforms.
Nishi T, Kawasaki-Nishi S, Forgac M. | 01/21/2010 |
| d2 protein displayed association with membranes and the localization in lysosomes and antigen-containing endosomes. | Selective expression of vacuolar H+-ATPase subunit d2 by particular subsets of dendritic cells among leukocytes.
Sato K, Shikano S, Xia G, Takao J, Chung JS, Cruz PD Jr, Xie XS, Ariizumi K. | 01/21/2010 |