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Author: Grafiati

Published: 10 March 2023

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1

Cho, Steve K., and Sandra L. Hofmann. "pdf1, a Palmitoyl Protein Thioesterase 1 Ortholog in Schizosaccharomyces pombe: a Yeast Model of Infantile Batten Disease." Eukaryotic Cell 3, no. 2 (April 2004): 302–10. http://dx.doi.org/10.1128/ec.3.2.302-310.2004.

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ABSTRACT Infantile Batten disease is a severe neurodegenerative storage disorder caused by mutations in the human PPT1 (palmitoyl protein thioesterase 1) gene, which encodes a lysosomal hydrolase that removes fatty acids from lipid-modified proteins. PPT1 has orthologs in many species, including lower organisms and plants, but not in Saccharomyces cerevisiae. The fission yeast Schizosaccharomyces pombe contains a previously uncharacterized open reading frame (SPBC530.12c) that encodes the S. pombe Ppt1p ortholog fused in frame to a second enzyme that is highly similar to a previously cloned mouse dolichol pyrophosphatase (Dolpp1p). In the present study, we characterized this interesting gene (designated here as pdf1, for palmitoyl protein thioesterase-dolichol pyrophosphate phosphatase fusion 1) through deletion of the open reading frame and complementation by plasmids bearing mutations in various regions of the pdf1 sequence. Strains bearing a deletion of the entire pdf1 open reading frame are nonviable and are rescued by a pdf1 expression plasmid. Inactivating mutations in the Dolpp1p domain do not rescue the lethality, whereas mutations in the Ppt1p domain result in cells that are viable but abnormally sensitive to sodium orthovanadate and elevated extracellular pH. The latter phenotypes have been previously associated with class C and class D vacuolar protein sorting (vps) mutants and vacuolar membrane H+-ATPase (vma) mutants in S. cerevisiae. Importantly, the Ppt1p-deficient phenotype is complemented by the human PPT1 gene. These results indicate that the function of PPT1 has been widely conserved throughout evolution and that S. pombe may serve as a genetically tractable model for the study of human infantile Batten disease.

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2

Ou, Pengju, Lifen Wen, Xiaoli Liu, Jiancheng Huang, Xiaoling Huang, Chaofei Su, Ling Wang, Hai Ni, Boris Reizis, and Cliff Y. Yang. "Thioesterase PPT1 balances viral resistance and efficient T cell crosspriming in dendritic cells." Journal of Experimental Medicine 216, no. 9 (July 1, 2019): 2091–112. http://dx.doi.org/10.1084/jem.20190041.

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Conventional type 1 dendritic cells (cDC1s) are inherently resistant to many viruses but, paradoxically, possess fewer acidic phagosomes that enable antigen retention and cross-presentation. We report that palmitoyl-protein thioesterase 1 (PPT1), which catabolizes lipid-modified proteins in neurons, is highly expressed in cDC1s. PPT1-deficient DCs are more susceptible to vesicular stomatitis virus (VSV) infection, and mice with PPT1 deficiency in cDC1s show impaired response to VSV. Conversely, PPT1-deficient cDC1s enhance the priming of naive CD8+ T cells into tissue-resident KLRG1+ effectors and memory T cells, resulting in rapid clearance of tumors and Listeria monocytogenes. Mechanistically, PPT1 protects steady state DCs from viruses by promoting antigen degradation and endosomal acidification via V-ATPase recruitment. After DC activation, immediate down-regulation of PPT1 is likely to facilitate efficient cross-presentation, production of costimulatory molecules and inflammatory cytokines. Thus, PPT1 acts as a molecular rheostat that allows cDC1s to crossprime efficiently without compromising viral resistance. These results suggest potential therapeutics to enhance cDC1-dependent crosspriming.

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3

Gorenberg, Erica L., Sofia Massaro Tieze, Betül Yücel, Helen R. Zhao, Vicky Chou, Gregory S. Wirak, Susumu Tomita, TuKiet T. Lam, and Sreeganga S. Chandra. "Identification of substrates of palmitoyl protein thioesterase 1 highlights roles of depalmitoylation in disulfide bond formation and synaptic function." PLOS Biology 20, no. 3 (March 31, 2022): e3001590. http://dx.doi.org/10.1371/journal.pbio.3001590.

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Loss-of-function mutations in the depalmitoylating enzyme palmitoyl protein thioesterase 1 (PPT1) cause neuronal ceroid lipofuscinosis (NCL), a devastating neurodegenerative disease. The substrates of PPT1 are largely undescribed, posing a limitation on molecular dissection of disease mechanisms and therapeutic development. Here, we provide a resource identifying >100 novel PPT1 substrates. We utilized Acyl Resin-Assisted Capture (Acyl RAC) and mass spectrometry to identify proteins with increased in vivo palmitoylation in PPT1 knockout (KO) mouse brains. We then validated putative substrates through direct depalmitoylation with recombinant PPT1. This stringent screen elucidated diverse PPT1 substrates at the synapse, including channels and transporters, G-protein–associated molecules, endo/exocytic components, synaptic adhesion molecules, and mitochondrial proteins. Cysteine depalmitoylation sites in transmembrane PPT1 substrates frequently participate in disulfide bonds in the mature protein. We confirmed that depalmitoylation plays a role in disulfide bond formation in a tertiary screen analyzing posttranslational modifications (PTMs). Collectively, these data highlight the role of PPT1 in mediating synapse functions, implicate molecular pathways in the etiology of NCL and other neurodegenerative diseases, and advance our basic understanding of the purpose of depalmitoylation.

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4

Uzbekova, Svetlana, Ana-Paula Teixeira-Gomes, Aurélie Marestaing, Peggy Jarrier-Gaillard, Pascal Papillier, Ekaterina N. Shedova, Galina N. Singina, Rustem Uzbekov, and Valerie Labas. "Protein Palmitoylation in Bovine Ovarian Follicle." International Journal of Molecular Sciences 22, no. 21 (October 29, 2021): 11757. http://dx.doi.org/10.3390/ijms222111757.

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Protein palmitoylation is a reversible post-translational modification by fatty acids (FA), mainly a palmitate (C16:0). Palmitoylation allows protein shuttling between the plasma membrane and cytosol to regulate protein stability, sorting and signaling activity and its deficiency leads to diseases. We aimed to characterize the palmitoyl-proteome of ovarian follicular cells and molecular machinery regulating protein palmitoylation within the follicle. For the first time, 84 palmitoylated proteins were identified from bovine granulosa cells (GC), cumulus cells (CC) and oocytes by acyl-biotin exchange proteomics. Of these, 32 were transmembrane proteins and 27 proteins were detected in bovine follicular fluid extracellular vesicles (ffEVs). Expression of palmitoylation and depalmitoylation enzymes as palmitoyltransferases (ZDHHCs), acylthioesterases (LYPLA1 and LYPLA2) and palmitoylthioesterases (PPT1 and PPT2) were analysed using transcriptome and proteome data in oocytes, CC and GC. By immunofluorescence, ZDHHC16, PPT1, PPT2 and LYPLA2 proteins were localized in GC, CC and oocyte. In oocyte and CC, abundance of palmitoylation-related enzymes significantly varied during oocyte maturation. These variations and the involvement of identified palmitoyl-proteins in oxidation-reduction processes, energy metabolism, protein localization, vesicle-mediated transport, response to stress, G-protein mediated and other signaling pathways suggests that protein palmitoylation may play important roles in oocyte maturation and ffEV-mediated communications within the follicle.

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5

Zhang, Xusheng, Mengting Wang, Bingyan Feng, Qiuyu Zhang, Jia Tong, Mingyong Wang, Chengbiao Lu, and Shiyong Peng. "Seizures in PPT1 Knock-In Mice Are Associated with Inflammatory Activation of Microglia." International Journal of Molecular Sciences 23, no. 10 (May 17, 2022): 5586. http://dx.doi.org/10.3390/ijms23105586.

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Infantile neuronal ceroid lipofuscinosis (INCL), the most severe form of neuronal ceroid lipofuscinoses, is caused by mutations in the lysosomal enzyme palmitoyl protein thioesterase 1 (PPT1). Typical symptoms of this disease include progressive psychomotor developmental retardation, visual failure, seizures, and premature death. Here, we investigated seizure activity and relevant pathological changes in PPT1 knock-in mice (PPT1 KI). The behavior studies in this study demonstrated that PPT1 KI mice had no significant seizure activity until 7 months of age, and local field potentials also displayed epileptiform activity at the same age. The expression levels of Iba-1 and CD68 demonstrated, by Western blot analysis, the inflammatory cytokine TNF-α content measured with enzyme-linked immunosorbent assay, and the number of microglia demonstrated by immunohistochemistry (IHC) were significantly increased at age of 7 months, all of which indicate microglia activation at an age of seizure onset. The increased expression of GFAP were seen at an earlier age of 4 months, and such an increase reached its peak at age of 6 months, indicating that astrocyte activation precedes microglia. The purinergic P2X7 receptor (P2X7R) is an ATP-sensitive ionic channel that is highly expressed in microglia and is fundamental to microglial activation, proliferation, cytokines release and epilepsy. We show that the ATP concentration in hippocampal tissue in PPT1 KI mice was increased using an enhanced ATP assay kit and demonstrated that the antagonist of P2X7R, A-438079, significantly reduced seizures in PPT1 KI mice. In contrast to glial cell activation and proliferation, a significant reduction in synaptic proteins GABAAR was seen in PPT1 KI mice. These results indicate that seizure in PPT1 KI mice may be associated with microglial activation involved in ATP-sensitive P2X7R signaling and impaired inhibitory neurotransmission.

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6

Gupta, P., A. A. Soyombo, A. Atashband, K. E. Wisniewski, J. M. Shelton, J. A. Richardson, R. E. Hammer, and S. L. Hofmann. "Disruption of PPT1 or PPT2 causes neuronal ceroid lipofuscinosis in knockout mice." Proceedings of the National Academy of Sciences 98, no. 24 (November 20, 2001): 13566–71. http://dx.doi.org/10.1073/pnas.251485198.

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7

Shyng, Charles, Hemanth R. Nelvagal, Joshua T. Dearborn, Jaana Tyynelä, Robert E. Schmidt, Mark S. Sands, and Jonathan D. Cooper. "Synergistic effects of treating the spinal cord and brain in CLN1 disease." Proceedings of the National Academy of Sciences 114, no. 29 (July 3, 2017): E5920—E5929. http://dx.doi.org/10.1073/pnas.1701832114.

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Infantile neuronal ceroid lipofuscinosis (INCL, or CLN1 disease) is an inherited neurodegenerative storage disorder caused by a deficiency of the lysosomal enzyme palmitoyl protein thioesterase 1 (PPT1). It was widely believed that the pathology associated with INCL was limited to the brain, but we have now found unexpectedly profound pathology in the human INCL spinal cord. Similar pathological changes also occur at every level of the spinal cord of PPT1-deficient (Ppt1−/−) mice before the onset of neuropathology in the brain. Various forebrain-directed gene therapy approaches have only had limited success in Ppt1−/− mice. Targeting the spinal cord via intrathecal administration of an adeno-associated virus (AAV) gene transfer vector significantly prevented pathology and produced significant improvements in life span and motor function in Ppt1−/− mice. Surprisingly, forebrain-directed gene therapy resulted in essentially no PPT1 activity in the spinal cord, and vice versa. This leads to a reciprocal pattern of histological correction in the respective tissues when comparing intracranial with intrathecal injections. However, the characteristic pathological features of INCL were almost completely absent in both the brain and spinal cord when intracranial and intrathecal injections of the same AAV vector were combined. Targeting both the brain and spinal cord also produced dramatic and synergistic improvements in motor function with an unprecedented increase in life span. These data show that spinal cord pathology significantly contributes to the clinical progression of INCL and can be effectively targeted therapeutically. This has important implications for the delivery of therapies in INCL, and potentially in other similar disorders.

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8

Zainudin, Nur Ain Izzati Mohd, Bradford Condon, Lieselotte De Bruyne, Christof Van Poucke, Qing Bi, Wei Li, Monica Höfte, and B. Gillian Turgeon. "Virulence, Host-Selective Toxin Production, and Development of Three Cochliobolus Phytopathogens Lacking the Sfp-Type 4′-Phosphopantetheinyl Transferase Ppt1." Molecular Plant-Microbe Interactions® 28, no. 10 (October 2015): 1130–41. http://dx.doi.org/10.1094/mpmi-03-15-0068-r.

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The Sfp-type 4′-phosphopantetheinyl transferase Ppt1 is required for activation of nonribosomal peptide synthetases, including α-aminoadipate reductase (AAR) for lysine biosynthesis and polyketide synthases, enzymes that biosynthesize peptide and polyketide secondary metabolites, respectively. Deletion of the PPT1 gene, from the maize pathogen Cochliobolus heterostrophus and the rice pathogen Cochliobolus miyabeanus, yielded strains that were significantly reduced in virulence to their hosts. In addition, ppt1 mutants of C. heterostrophus race T and Cochliobolus victoriae were unable to biosynthesize the host-selective toxins (HST) T-toxin and victorin, respectively, as judged by bioassays. Interestingly, ppt1 mutants of C. miyabeanus were shown to produce tenfold higher levels of the sesterterpene-type non-HST ophiobolin A, as compared with the wild-type strain. The ppt1 strains of all species were also reduced in tolerance to oxidative stress and iron depletion; both phenotypes are associated with inability to produce extracellular siderophores biosynthesized by the nonribosomal peptide synthetase Nps6. Colony surfaces were hydrophilic, a trait previously associated with absence of C. heterostrophus Nps4. Mutants were decreased in asexual sporulation and C. heterostrophus strains were female-sterile in sexual crosses; the latter phenotype was observed previously with mutants lacking Nps2, which produces an intracellular siderophore. As expected, mutants were albino, since they cannot produce the polyketide melanin and were auxotrophic for lysine because they lack an AAR.

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9

Duarte, Diana, and Nuno Vale. "How Antimalarials and Antineoplastic Drugs can Interact in Combination Therapies: A Perspective on the Role of PPT1 Enzyme." Current Drug Metabolism 22, no. 13 (November 2021): 1009–16. http://dx.doi.org/10.2174/1389200222666211118114057.

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: Antimalarial drugs from different classes have demonstrated anticancer effects in different types of cancer cells, but their complete mode of action in cancer remains unknown. Recently, several studies reported the important role of palmitoyl-protein thioesterase 1 (PPT1), a lysosomal enzyme, as the molecular target of chloroquine and its derivates in cancer. It was also found that PPT1 is overexpressed in different types of cancer, such as breast, colon, etc. Our group has found a synergistic interaction between antimalarial drugs, such as mefloquine, artesunate and chloroquine and antineoplastic drugs in breast cancer cells, but the mechanism of action was not determined. Here, we describe the importance of autophagy and lysosomal inhibitors in tumorigenesis and hypothesize that other antimalarial agents besides chloroquine could also interact with PPT1 and inhibit the mechanistic target of rapamycin (mTOR) signalling, an important pathway in cancer progression. We believe that PPT1 inhibition results in changes in the lysosomal metabolism that result in less accumulation of antineoplastic drugs in lysosomes, which increases the bioavailability of the antineoplastic agents. Taken together, these mechanisms help to explain the synergism of antimalarial and antineoplastic agents in cancer cells.

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10

Yuan, Wei, Liaoxun Lu, Muding Rao, Yang Huang, Chun-e. Liu, Shuang Liu, Yue Zhao, et al. "GFAP hyperpalmitoylation exacerbates astrogliosis and neurodegenerative pathology in PPT1-deficient mice." Proceedings of the National Academy of Sciences 118, no. 13 (March 22, 2021): e2022261118. http://dx.doi.org/10.1073/pnas.2022261118.

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The homeostasis of protein palmitoylation and depalmitoylation is essential for proper physiological functions in various tissues, in particular the central nervous system (CNS). The dysfunction of PPT1 (PPT1-KI, infantile neuronal ceroid lipofuscinosis [INCL] mouse model), which catalyze the depalmitoylation process, results in serious neurodegeneration accompanied by severe astrogliosis in the brain. Endeavoring to determine critical factors that might account for the pathogenesis in CNS by palm-proteomics, glial fibrillary acidic protein (GFAP) was spotted, indicating that GFAP is probably palmitoylated. Questions concerning if GFAP is indeed palmitoylated in vivo and how palmitoylation of GFAP might participate in neural pathology remain unexplored and are waiting to be investigated. Here we show that GFAP is readily palmitoylated in vitro and in vivo; specifically, cysteine-291 is the unique palmitoylated residue in GFAP. Interestingly, it was found that palmitoylated GFAP promotes astrocyte proliferation in vitro. Furthermore, we showed that PPT1 depalmitoylates GFAP, and the level of palmitoylated GFAP is overwhelmingly up-regulated in PPT1-knockin mice, which lead us to speculate that the elevated level of palmitoylated GFAP might accelerate astrocyte proliferation in vivo and ultimately led to astrogliosis in INCL. Indeed, blocking palmitoylation by mutating cysteine-291 into alanine in GFAP attenuate astrogliosis, and remarkably, the concurrent neurodegenerative pathology in PPT1-knockin mice. Together, these findings demonstrate that hyperpalmitoylated GFAP plays critical roles in regulating the pathogenesis of astrogliosis and neurodegeneration in the CNS, and most importantly, pinpointing that cysteine-291 in GFAP might be a valuable pharmaceutical target for treating INCL and other potential neurodegenerative diseases.

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11

Uchida, Naonori, Kengo Suzuki, Ryoichi Saiki, Tomohiro Kainou, Katsunori Tanaka, Hideyuki Matsuda, and Makoto Kawamukai. "Phenotypes of Fission Yeast Defective in Ubiquinone Production Due to Disruption of the Gene for p-Hydroxybenzoate Polyprenyl Diphosphate Transferase." Journal of Bacteriology 182, no. 24 (December 15, 2000): 6933–39. http://dx.doi.org/10.1128/jb.182.24.6933-6939.2000.

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ABSTRACT Ubiquinone is an essential component of the electron transfer system in both prokaryotes and eukaryotes and is synthesized from chorismate and polyprenyl diphosphate by eight steps.p-Hydroxybenzoate (PHB) polyprenyl diphosphate transferase catalyzes the condensation of PHB and polyprenyl diphosphate in ubiquinone biosynthesis. We isolated the gene (designated ppt1) encoding PHB polyprenyl diphosphate transferase from Schizosaccharomyces pombe and constructed a strain with a disrupted ppt1 gene. This strain could not grow on minimal medium supplemented with glucose. Expression ofCOQ2 from Saccharomyces cerevisiae in the defective S. pombe strain restored growth and enabled the cells to produce ubiquinone-10, indicating that COQ2 andppt1 are functional homologs. Theppt1-deficient strain required supplementation with antioxidants, such as cysteine, glutathione, and α-tocopherol, to grow on minimal medium. This suggests that ubiquinone can act as an antioxidant, a premise supported by our observation that theppt1-deficient strain is sensitive to H2O2 and Cu2+. Interestingly, we also found that the ppt1-deficient strain produced a significant amount of H2S, which suggests that oxidation of sulfide by ubiquinone may be an important pathway for sulfur metabolism in S. pombe. Ppt1-green fluorescent protein fusion proteins localized to the mitochondria, indicating that ubiquinone biosynthesis occurs in the mitochondria in S. pombe. Thus, analysis of the phenotypes of S. pombe strains deficient in ubiquinone production clearly demonstrates that ubiquinone has multiple functions in the cell apart from being an integral component of the electron transfer system.

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12

Shyng, Charles, and Mark S. Sands. "Astrocytosis in infantile neuronal ceroid lipofuscinosis: friend or foe?" Biochemical Society Transactions 42, no. 5 (September 18, 2014): 1282–85. http://dx.doi.org/10.1042/bst20140188.

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Infantile neuronal ceroid lipofuscinosis (INCL; infantile Batten disease) is an inherited paediatric neurodegenerative disease. INCL is caused by a deficiency in the lysosomal enzyme palmitoyl-protein thioesterase-1 (PPT1) and is thus classified as a lysosomal storage disease. Pathological examination of both human and murine INCL brains reveals progressive, widespread neuroinflammation. In fact, astrocyte activation appears to be the first histological sign of disease. However, the role of astrocytosis in INCL was poorly understood. The hallmark of astrocyte activation is the up-regulation of intermediate filaments, such as glial fibrillary acidic protein (GFAP) and vimentin. The role of astrocytosis in INCL was studied in a murine model lacking PPT1 and the intermediate filaments GFAP and vimentin (triple-knockout). This murine model of INCL with attenuated astrocytosis had an exacerbated pathological and clinical phenotype. The triple-knockout mouse had a significantly shortened lifespan, and accelerated cellular and humoural neuroinflammatory response compared with the parental PPT1−/− mouse. The data obtained from the triple-knockout mouse strongly suggest that astrocyte activation plays a beneficial role in early INCL disease progression. A more thorough understanding of the glial responses to lysosomal enzyme deficiencies and the accumulation of undergraded substrates will be crucial to developing effective therapeutics.

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13

Heyman, T., B. Agoutin, S. Friant, F. X. Wilhelm, and M. L. Wilhelm. "Plus-strand DNA Synthesis of the Yeast Retrotransposon Ty1 is Initiated at Two Sites, PPT1 Next to the 3′ LTR and PPT2 Within thepolGene. PPT1 is Sufficient for Ty1 Transposition." Journal of Molecular Biology 253, no. 2 (October 1995): 291–303. http://dx.doi.org/10.1006/jmbi.1995.0553.

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14

Cho, Seongeun, Philip E. Dawson, and Glyn Dawson. "Antisense palmitoyl protein thioesterase 1 (PPT1) treatment inhibits PPT1 activity and increases cell death in LA-N-5 neuroblastoma cells." Journal of Neuroscience Research 62, no. 2 (2000): 234–40. http://dx.doi.org/10.1002/1097-4547(20001015)62:2<234::aid-jnr8>3.0.co;2-8.

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15

Scifo, Enzo, Agnieszka Szwajda, Rabah Soliymani, Francesco Pezzini, Marzia Bianchi, Arvydas Dapkunas, Janusz Dębski, et al. "Quantitative analysis of PPT1 interactome in human neuroblastoma cells." Data in Brief 4 (September 2015): 207–16. http://dx.doi.org/10.1016/j.dib.2015.05.016.

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16

Calero, Guillermo, Praveena Gupta, M. Cristina Nonato, Sagun Tandel, Edward R. Biehl, Sandra L. Hofmann, and Jon Clardy. "The Crystal Structure of Palmitoyl Protein Thioesterase-2 (PPT2) Reveals the Basis for Divergent Substrate Specificities of the Two Lysosomal Thioesterases, PPT1 and PPT2." Journal of Biological Chemistry 278, no. 39 (July 10, 2003): 37957–64. http://dx.doi.org/10.1074/jbc.m301225200.

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17

Balouch, Bailey, Halle Nagorsky, Truc Pham, James Thai LaGraff, and Quynh Chu-LaGraff. "Human INCL fibroblasts display abnormal mitochondrial and lysosomal networks and heightened susceptibility to ROS-induced cell death." PLOS ONE 16, no. 2 (February 9, 2021): e0239689. http://dx.doi.org/10.1371/journal.pone.0239689.

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Infantile Neuronal Ceroid Lipofuscinosis (INCL) is a pediatric neurodegenerative disorder characterized by progressive retinal and central nervous system deterioration during infancy. This lysosomal storage disorder results from a deficiency in the Palmitoyl Protein Thioesterase 1 (PPT1) enzyme—a lysosomal hydrolase which cleaves fatty acid chains such as palmitate from lipid-modified proteins. In the absence of PPT1 activity, these proteins fail to be degraded, leading to the accumulation of autofluorescence storage material in the lysosome. The underlying molecular mechanisms leading to INCL pathology remain poorly understood. A role for oxidative stress has been postulated, yet little evidence has been reported to support this possibility. Here we present a comprehensive cellular characterization of human PPT1-deficient fibroblast cells harboring Met1Ile and Tyr247His compound heterozygous mutations. We detected autofluorescence storage material and observed distinct organellar abnormalities of the lysosomal and mitochondrial structures, which supported previous postulations about the role of ER, mitochondria and oxidative stress in INCL. An increase in the number of lysosomal structures was found in INCL patient fibroblasts, which suggested an upregulation of lysosomal biogenesis, and an association with endoplasmic reticulum stress response. The mitochondrial network also displayed abnormal spherical punctate morphology instead of normal elongated tubules with extensive branching, supporting the involvement of mitochondrial and oxidative stress in INCL cell death. Autofluorescence accumulation and lysosomal pathologies can be mitigated in the presence of conditioned wild type media suggesting that a partial restoration via passive introduction of the enzyme into the cellular environment may be possible. We also demonstrated, for the first time, that human INCL fibroblasts have a heightened susceptibility to exogenous reactive oxygen species (ROS)-induced cell death, which suggested an elevated basal level of endogenous ROS in the mutant cell. Collectively, these findings support the role of intracellular organellar networks in INCL pathology, possibly due to oxidative stress.

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18

Duarte, Diana, Mariana Nunes, Sara Ricardo, and Nuno Vale. "Combination of Antimalarial and CNS Drugs with Antineoplastic Agents in MCF-7 Breast and HT-29 Colon Cancer Cells: Biosafety Evaluation and Mechanism of Action." Biomolecules 12, no. 10 (October 16, 2022): 1490. http://dx.doi.org/10.3390/biom12101490.

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Drug combination and drug repurposing are two strategies that allow to find novel oncological therapies, in a faster and more economical process. In our previous studies, we developed a novel model of drug combination using antineoplastic and different repurposed drugs. We demonstrated the combinations of doxorubicin (DOX) + artesunate, DOX + chloroquine, paclitaxel (PTX) + fluoxetine, PTX + fluphenazine, and PTX + benztropine induce significant cytotoxicity in Michigan Cancer Foundation-7 (MCF-7) breast cancer cells. Furthermore, it was found that 5-FU + thioridazine and 5-fluorouracil (5-FU) + sertraline can synergistically induce a reduction in the viability of human colorectal adenocarcinoma cell line (HT-29). In this study, we aim to (1) evaluate the biosafety profile of these drug combinations for non-tumoral cells and (2) determine their mechanism of action in cancer cells. To do so, human fetal lung fibroblast cells (MRC-5) fibroblast cells were incubated for 48 h with all drugs, alone and in combination in concentrations of 0.25, 0.5, 1, 2, and 4 times their half-maximal inhibitory concentration (IC50). Cell morphology and viability were evaluated. Next, we designed and constructed a cell microarray to perform immunohistochemistry studies for the evaluation of palmitoyl-protein thioesterase 1 (PPT1), Ki67, cleaved-poly (ADP-ribose) polymerase (cleaved-PARP), multidrug resistance-associated protein 2 (MRP2), P-glycoprotein (P-gp), and nuclear factor-kappa-B (NF-kB) p65 expression. We demonstrate that these combinations are cytotoxic for cancer cells and safe for non-tumoral cells at lower concentrations. Furthermore, it is also demonstrated that PPT1 may have an important role in the mechanism of action of these combinations, as demonstrated by their ability to decrease PPT1 expression. These results support the use of antimalarial and central nervous system (CNS) drugs in combination regimens with chemotherapeutic agents; nevertheless, additional studies are recommended to further explore their complete mechanisms of action.

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19

Didoni, G., E. Ghigo, and F. Minuto. "PPT1 COST-OF-ILLNESS STUDY IN ACROMEGALIC PATIENTS IN ITALY." Value in Health 7, no. 6 (November 2004): 797. http://dx.doi.org/10.1016/s1098-3015(10)66137-2.

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20

Hu, Kangdi, Wanjie Li, Jiaxin Gao, Qizheng Liu, Haitao Wang, Yue Wang, and Jianli Sang. "Role of Ppt1 in multiple stress responses in Candida albicans." Chinese Science Bulletin 59, no. 31 (July 22, 2014): 4060–68. http://dx.doi.org/10.1007/s11434-014-0552-7.

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21

Appu, Abhilash P., Maria B. Bagh, Tamal Sadhukhan, Avisek Mondal, Sydney Casey, and Anil B. Mukherjee. "Cln3 ‐mutations underlying juvenile neuronal ceroid lipofuscinosis cause significantly reduced levels of Palmitoyl‐protein thioesterases‐1 (Ppt1)‐protein and Ppt1‐enzyme activity in the lysosome." Journal of Inherited Metabolic Disease 42, no. 5 (May 14, 2019): 944–54. http://dx.doi.org/10.1002/jimd.12106.

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22

Velázquez-Robledo, R., H. A. Contreras-Cornejo, L. Macías-Rodríguez, A. Hernández-Morales, J. Aguirre, S. Casas-Flores, J. López-Bucio, and A. Herrera-Estrella. "Role of the 4-Phosphopantetheinyl Transferase of Trichoderma virens in Secondary Metabolism and Induction of Plant Defense Responses." Molecular Plant-Microbe Interactions® 24, no. 12 (December 2011): 1459–71. http://dx.doi.org/10.1094/mpmi-02-11-0045.

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Trichoderma virens is a ubiquitous soil fungus successfully used in biological control due to its efficient colonization of plant roots. In fungi, 4-phosphopantetheinyl transferases (PPTases) activate enzymes involved in primary and secondary metabolism. Therefore, we cloned the PPTase gene ppt1 from T. virens and generated PPTase-deficient (Δppt1) and overexpressing strains to investigate the role of this enzyme in biocontrol and induction of plant defense responses. The Δppt1 mutants were auxotrophic for lysine, produced nonpigmented conidia, and were unable to synthesize nonribosomal peptides. Although spore germination was severely compromised under both low and high iron availability, mycelial growth occurred faster than the wild type, and the mutants were able to efficiently colonize plant roots. The Δppt1 mutants were unable of inhibiting growth of phytopathogenic fungi in vitro. Arabidopsis thaliana seedlings co-cultivated with wild-type T. virens showed increased expression of pPr1a:uidA and pLox2:uidA markers, which correlated with enhanced accumulation of salicylic acid (SA), jasmonic acid, camalexin, and resistance to Botrytis cinerea. Co-cultivation of A. thaliana seedlings with Δppt1 mutants compromised the SA and camalexin responses, resulting in decreased protection against the pathogen. Our data reveal an important role of T. virens PPT1 in antibiosis and induction of SA and camalexin-dependent plant defense responses.

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Nishida, Ikuhisa, Ryota Yanai, Yasuhiro Matsuo, Tomohiro Kaino, and Makoto Kawamukai. "Benzoic acid inhibits Coenzyme Q biosynthesis in Schizosaccharomyces pombe." PLOS ONE 15, no. 11 (November 24, 2020): e0242616. http://dx.doi.org/10.1371/journal.pone.0242616.

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Coenzyme Q (CoQ, ubiquinone) is an essential component of the electron transport system in aerobic organisms. Human type CoQ10, which has 10 units of isoprene in its quinone structure, is especially valuable as a food supplement. Therefore, studying the biosynthesis of CoQ10 is important not only for increasing metabolic knowledge, but also for improving biotechnological production. Herein, we show that Schizosaccharomyces pombe utilizes p-aminobenzoate (PABA) in addition to p-hydroxybenzoate (PHB) as a precursor for CoQ10 synthesis. We explored compounds that affect the synthesis of CoQ10 and found benzoic acid (Bz) at >5 μg/mL inhibited CoQ biosynthesis without accumulation of apparent CoQ intermediates. This inhibition was counteracted by incubation with a 10-fold lower amount of PABA or PHB. Overexpression of PHB-polyprenyl transferase encoded by ppt1 (coq2) also overcame the inhibition of CoQ biosynthesis by Bz. Inhibition by Bz was efficient in S. pombe and Schizosaccharomyces japonicus, but less so in Saccharomyces cerevisiae, Aureobasidium pullulans, and Escherichia coli. Bz also inhibited a S. pombe ppt1 (coq2) deletion strain expressing human COQ2, and this strain also utilized PABA as a precursor of CoQ10. Thus, Bz is likely to inhibit prenylation reactions involving PHB or PABA catalyzed by Coq2.

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24

Metelitsina, Tatyana I., Darrel J. Waggoner, and Michael A. Grassi. "BATTEN DISEASE CAUSED BY A NOVEL MUTATION IN THE PPT1 GENE." Retinal Cases & Brief Reports 10, no. 3 (2016): 211–13. http://dx.doi.org/10.1097/icb.0000000000000227.

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Appu, Abhilash Puthuvelvippel, Maria Bagh, Tamal Sadhukhan, Avisek Mondal, and Anil B. Mukherjee. "Lysosomal PPT1‐insufficiency is a common pathogenic link between INCL and JNCL." FASEB Journal 34, S1 (April 2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.08988.

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26

Wandinger, Sebastian K., Michael H. Suhre, Harald Wegele, and Johannes Buchner. "The phosphatase Ppt1 is a dedicated regulator of the molecular chaperone Hsp90." EMBO Journal 25, no. 2 (January 12, 2006): 367–76. http://dx.doi.org/10.1038/sj.emboj.7600930.

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27

Pouwels, Simon D., Alen Faiz, Lisette E. den Boef, Reneé Gras, Maarten van den Berge, H. Marike Boezen, Ron Korstanje, et al. "Genetic variance is associated with susceptibility for cigarette smoke-induced DAMP release in mice." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 3 (September 1, 2017): L559—L580. http://dx.doi.org/10.1152/ajplung.00466.2016.

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Chronic obstructive pulmonary disease (COPD) is characterized by unresolved neutrophilic airway inflammation and is caused by chronic exposure to toxic gases, such as cigarette smoke (CS), in genetically susceptible individuals. Recent data indicate a role for damage-associated molecular patterns (DAMPs) in COPD. Here, we investigated the genetics of CS-induced DAMP release in 28 inbred mouse strains. Subsequently, in lung tissue from a subset of strains, the expression of the identified candidate genes was analyzed. We tested whether small interfering RNA-dependent knockdown of candidate genes altered the susceptibility of the human A549 cell line to CS-induced cell death and DAMP release. Furthermore, we tested whether these genes were differentially regulated by CS exposure in bronchial brushings obtained from individuals with a family history indicative of either the presence or absence of susceptibility for COPD. We observed that, of the four DAMPs tested, double-stranded DNA (dsDNA) showed the highest correlation with neutrophilic airway inflammation. Genetic analyses identified 11 candidate genes governing either CS-induced or basal dsDNA release in mice. Two candidate genes ( Elac2 and Ppt1) showed differential expression in lung tissue on CS exposure between susceptible and nonsusceptible mouse strains. Knockdown of ELAC2 and PPT1 in A549 cells altered susceptibility to CS extract-induced cell death and DAMP release. In bronchial brushings, CS-induced expression of ENOX1 and ARGHGEF11 was significantly different between individuals susceptible or nonsusceptible for COPD. Our study shows that genetic variance in a mouse model is associated with CS-induced DAMP release, and that this might contribute to susceptibility for COPD.

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Schreiber, Thiemo B., Nina Mäusbacher, Joanna Soroka, Sebastian K. Wandinger, Johannes Buchner, and Henrik Daub. "Global Analysis of Phosphoproteome Regulation by the Ser/Thr Phosphatase Ppt1 inSaccharomyces cerevisiae." Journal of Proteome Research 11, no. 4 (March 14, 2012): 2397–408. http://dx.doi.org/10.1021/pr201134p.

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29

Sarkar, Chinmoy, Goutam Chandra, Shiyong Peng, Zhongjian Zhang, Aiyi Liu, and Anil B. Mukherjee. "Neuroprotection and lifespan extension in Ppt1−/− mice by NtBuHA: therapeutic implications for INCL." Nature Neuroscience 16, no. 11 (September 22, 2013): 1608–17. http://dx.doi.org/10.1038/nn.3526.

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30

Segal-Salto, Michal, Tamar Sapir, and Orly Reiner. "Reversible Cysteine Acylation Regulates the Activity of Human Palmitoyl-Protein Thioesterase 1 (PPT1)." PLOS ONE 11, no. 1 (January 5, 2016): e0146466. http://dx.doi.org/10.1371/journal.pone.0146466.

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31

Zhang, Dawei, Binaya Shrestha, Weining Niu, Pingfang Tian, and Tianwei Tan. "Phenotypes and fed-batch fermentation of ubiquinone-overproducing fission yeast using ppt1 gene." Journal of Biotechnology 128, no. 1 (January 2007): 120–31. http://dx.doi.org/10.1016/j.jbiotec.2006.09.012.

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32

Dawson, Glyn, Christina Schroeder, and Philip E. Dawson. "Palmitoyl:protein thioesterase (PPT1) inhibitors can act as pharmacological chaperones in infantile Batten disease." Biochemical and Biophysical Research Communications 395, no. 1 (April 2010): 66–69. http://dx.doi.org/10.1016/j.bbrc.2010.03.137.

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33

AGUADO, Begoña, and R. Duncan CAMPBELL. "Characterization of a human MHC class III region gene product with S-thioesterase activity." Biochemical Journal 341, no. 3 (July 26, 1999): 679–89. http://dx.doi.org/10.1042/bj3410679.

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Palmitoylated proteins contain a 16-carbon saturated fatty acyl group that is post-translationally attached by a labile thioester bond. These modified proteins are mainly membrane-bound; the lability of the thioester bond allows the process to be reversible, a unique property of this modification. We report here that the gene for G14, located in the class III region of the human MHC, encodes a polypeptide with significant sequence similarity to mammalian palmitoyl protein thioesterase (PPT1), an enzyme that removes palmitate from palmitoylated proteins. The gene for G14, also known as PPT2, is transcribed as at least five different transcripts, which are expressed in different cell lines of the immune system. Immunoprecipitation of these mammalian cells, with an anti-G14 antiserum, showed a specific band of approx. 42 kDa in cell extracts and supernatants. Expression of the G14 cDNA in the baculovirus system revealed that it encoded a secreted glycosylated polypeptide with S-thioesterase activity. The enzymic activity of the recombinant G14 protein was further characterized in quantitative spectrophotometric assays, which revealed that it had the highest S-thioesterase activity for the acyl groups palmitic and myristic acid followed by other long-chain acyl substrates. The S-thioesterase activity of the G14 protein was found to be considerably higher in supernatants than in cell extracts, which was consistent with the protein's being secreted. The G14 polypeptide contains, in addition to an N-terminal lipase domain, a C-terminal domain common to the cytokine receptor superfamily, which might determine the substrate specificity and/or the protein target of the G14 protein.

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34

Ma, Jin-Fang, Jin-Kui Guo, Lian-Wei Peng, Cui-Yun Chen, and Li-Xin Zhang. "Decrease of Photosystem II Photochemistry in Arabidopsis ppt1 Mutant Is Dependent on Leaf Age." Journal of Integrative Plant Biology 48, no. 12 (December 2006): 1409–14. http://dx.doi.org/10.1111/j.1744-7909.2006.00386.x.

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35

Ahtiainen, Laura, Kaisu Luiro, Maria Kauppi, Jaana Tyynelä, Outi Kopra, and Anu Jalanko. "Palmitoyl protein thioesterase 1 (PPT1) deficiency causes endocytic defects connected to abnormal saposin processing." Experimental Cell Research 312, no. 9 (May 2006): 1540–53. http://dx.doi.org/10.1016/j.yexcr.2006.01.034.

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36

Shyng, Charles, Hemanth R. Nelvagal, Josh T. Dearborn, Jonathan D. Cooper, and Mark S. Sands. "27. Therapeutic Efficacy of Intracranial and Intrathecal AAV2/9-PPT1 in Infantile Batten Disease." Molecular Therapy 24 (May 2016): S12—S13. http://dx.doi.org/10.1016/s1525-0016(16)32836-2.

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37

Sullivan, PW, and R. MacLaren. "PPT1: COST-EFFECTIVENESS OF RECOMBINANT HUMAN ERYTHROPOIETIN FOR PREVENTING TRANSFUSIONS IN CRITICALLY ILL PATIENTS." Value in Health 6, no. 3 (May 2003): 338. http://dx.doi.org/10.1016/s1098-3015(10)64194-0.

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38

Sanders, Douglas N., Fabiana H. Farias, Gary S. Johnson, Vivian Chiang, James R. Cook, Dennis P. O’Brien, Sandra L. Hofmann, Jui-Yun Lu, and Martin L. Katz. "A mutation in canine PPT1 causes early onset neuronal ceroid lipofuscinosis in a Dachshund." Molecular Genetics and Metabolism 100, no. 4 (August 2010): 349–56. http://dx.doi.org/10.1016/j.ymgme.2010.04.009.

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39

Rebecca, Vito W., Michael C. Nicastri, Colin Fennelly, Cynthia I. Chude, Julie S. Barber-Rotenberg, Amruta Ronghe, Quentin McAfee, et al. "PPT1 Promotes Tumor Growth and Is the Molecular Target of Chloroquine Derivatives in Cancer." Cancer Discovery 9, no. 2 (November 15, 2018): 220–29. http://dx.doi.org/10.1158/2159-8290.cd-18-0706.

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40

Liu, Yue, Wenzhen Zhao, Guobao Gu, Liming Lu, Jingsheng Feng, Qiangsu Guo, and Zhide Ding. "Palmitoyl-protein thioesterase 1 (PPT1): An obesity-induced rat testicular marker of reduced fertility." Molecular Reproduction and Development 81, no. 1 (December 3, 2013): 55–65. http://dx.doi.org/10.1002/mrd.22281.

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41

Lyly, Annina, Carina von Schantz, Tarja Salonen, Outi Kopra, Jani Saarela, Matti Jauhiainen, Aija Kyttälä, and Anu Jalanko. "Glycosylation, transport, and complex formation of palmitoyl protein thioesterase 1 (PPT1) – distinct characteristics in neurons." BMC Cell Biology 8, no. 1 (2007): 22. http://dx.doi.org/10.1186/1471-2121-8-22.

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42

Henderson, Michael X., Gregory S. Wirak, Yong-quan Zhang, Feng Dai, Stephen D. Ginsberg, Natalia Dolzhanskaya, John F. Staropoli, et al. "Neuronal ceroid lipofuscinosis with DNAJC5/CSPα mutation has PPT1 pathology and exhibit aberrant protein palmitoylation." Acta Neuropathologica 131, no. 4 (December 10, 2015): 621–37. http://dx.doi.org/10.1007/s00401-015-1512-2.

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43

MAYORDOMO, Isabel, and Pascual SANZ. "The Saccharomyces cerevisiae 14-3-3 protein Bmh2 is required for regulation of the phosphorylation status of Fin1, a novel intermediate filament protein." Biochemical Journal 365, no. 1 (July 1, 2002): 51–56. http://dx.doi.org/10.1042/bj20020053.

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In order to identify proteins that interact with Bmh2, a yeast member of the 14-3-3 protein family, we performed a two-hybrid screening using LexA-Bmh2 as bait. We identified Fin1, a novel intermediate filament protein, as the protein that showed the highest degree of interaction. We also identified components of the vesicular transport machinery such as Gic2 and Msb3, proteins involved in transcriptional regulation such as Mbf1, Gcr2 and Reg2, and a variety of other different proteins (Ppt1, Lre1, Rps0A and Ylr177w). We studied the interaction between Bmh2 and Fin1 in more detail and found that Bmh2 only interacted with phosphorylated forms of Fin1. In addition, we showed that Glc7, the catalytic subunit of the protein phosphatase 1 complex, was also able to interact with Fin1.

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44

Ghosh, Moumita, Jasodhara Chowdhury, Shubhadeep Das, Mukut Banerjee, and Swapna Chakraborty. "A Rare Case Report of Siblings with Infantile and Late Infantile Forms of Neuronal Ceroid Lipofuscinoses." Journal of Nepal Paediatric Society 33, no. 3 (December 16, 2013): 220–22. http://dx.doi.org/10.3126/jnps.v33i3.7924.

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Neuronal Ceroid Lipofuscinoses is a neurodegenerative disorder predominantly involving grey matter. The 4 classic forms are Infantile type, Late Infantile type, Juvenile type and Adult type. We present a case of 3 siblings of unrelated parents where the eldest had Infantile form of NCL, the second child had Late Infantile Form, and the third child is normal. Both children having different phenotypic presentations have curvilinear inclusion bodies on EM of axillary skin biopsy, low levels of tripeptidyl amino peptidase 1(TPP1) and normal levels of palmitoyl protein thioesterase 1(PPT1), a finding classically present in the Late Infantile variety involving CLN2 mutation. After extensive search we failed to find a case report describing a similar finding. DOI: http://dx.doi.org/10.3126/jnps.v33i3.7924 J. Nepal Paediatr. Soc. 2013;33(3):220-222

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45

Nelvagal, Hemanth R., Samantha L. Eaton, Sophie H. Wang, Elizabeth M. Eultgen, Keigo Takahashi, Steven Q. Le, LaRachel Nesbitt, et al. "Efficacy of recombinant human PPT1 enzyme replacement therapy in mouse and sheep models of CLN1 disease." Molecular Genetics and Metabolism 135, no. 2 (February 2022): S88. http://dx.doi.org/10.1016/j.ymgme.2021.11.227.

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46

Wiemann, Philipp, Sabine Albermann, Eva-Maria Niehaus, Lena Studt, Katharina W. von Bargen, Nelson L. Brock, Hans-Ulrich Humpf, Jeroen S. Dickschat, and Bettina Tudzynski. "The Sfp-Type 4′-Phosphopantetheinyl Transferase Ppt1 of Fusarium fujikuroi Controls Development, Secondary Metabolism and Pathogenicity." PLoS ONE 7, no. 5 (May 25, 2012): e37519. http://dx.doi.org/10.1371/journal.pone.0037519.

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47

Nicastri, Michael C., Vito W. Rebecca, Ravi K. Amaravadi, and Jeffrey D. Winkler. "Dimeric quinacrines as chemical tools to identify PPT1, a new regulator of autophagy in cancer cells." Molecular & Cellular Oncology 5, no. 1 (November 30, 2017): e1395504. http://dx.doi.org/10.1080/23723556.2017.1395504.

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48

Cooper, J. D., P. Gupta, E. Bible, S. Hofmann, and P. Lantos). "Profound loss of GABAergic interneurons in the PPT1 knockout mouse model of infantile neuronal ceroid lipofuscinosis." Neuropathology and Applied Neurobiology 28, no. 2 (March 2002): 158–59. http://dx.doi.org/10.1046/j.1365-2990.2002.39286_29.x.

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49

Suhre, Michael H., Harald Wegele, and Sebastian K. Wandinger. "Expression, purification and refolding of the phosphatase domain of protein phosphatase 1 (Ppt1) from Saccharomyces cerevisiae." International Journal of Biological Macromolecules 39, no. 1-3 (August 2006): 23–28. http://dx.doi.org/10.1016/j.ijbiomac.2005.12.019.

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50

Ozono, Tatsuhiko, Makoto Kinoshita, Aya Narita, Asami Hirakiyama, Motomichi Kosuga, Torayuki Okuyama, and Kei Fukada. "Juvenile-onset neuronal ceroid lipofuscinosis (CLN1) disease with a novel deletion and duplication in the PPT1 gene." Journal of the Neurological Sciences 388 (May 2018): 4–6. http://dx.doi.org/10.1016/j.jns.2018.02.030.

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