Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Hiroki Kato Last modified date:2024.06.27

Assistant Professor / Department of Dental Science, Faculty of Dental Science / Department of Dental Science / Faculty of Dental Science

1. Zakaria, F., Sonoda, S., Kato, H., Ma, L., Uehara, N., Kyumoto-Nakamura, Y., Sharifa, M., Yu, L., Dai, L., Yamauchi-Tomoda, E., Aijima, R., Yamaza, H., Nishimura, F., Yamaza, T., Erythropoietin receptor signal is crucial for periodontal ligament stem cell-based tissue reconstruction in periodontal disease., Sci Rep., 14:6719, 2024.03.
2. Uehara, N., Shibusawa, N., Mikami, Y., Kyumoto-Nakamura, Y., Sonoda, S., Kato, H., Yamaza, T., Kukita, T. , Bone metastatic mammary tumor cell-derived extracellular vesicles inhibit osteoblast maturation via JNK signaling., Arch Biochem Biophys., 750:109821, 2023.11.
3. Sun, X., Kong, J., Dong, S., Kato, H., Sato, H., Hirofuji, Y., Ito, Y., Wang, L., Kato, T.A., Torio, M., Sakai, Y., Ohga, S., Fukumoto, S., Masuda, K. , TRPV4-mediated Ca2+ deregulation causes mitochondrial dysfunction via the AKT/α-synuclein pathway in dopaminergic neurons., FASEB Bioadv., 5: 507-520, 2023.10.
4. Dong, S., Kifune, T., Kato, H., Wang, L., Kong, J., Hirofuji, Y., Sun, X., Sato, H., Ito, Y., Kato, T.A., Sakai, Y., Ohga, S., Fukumoto, S., Masuda, K., Effects of melatonin on dopaminergic neuron development via IP3-mediated mitochondrial Ca2+ regulation in autism spectrum disorder., Biochem Biophys Res Commun., 681: 7-12, 2023.09.
5. Sun, Xiao; Dong, Shuangshan; Kato, Hiroki; Kong, Jun; Ito, Yosuke; Hirofuji, Yuta; Sato, Hiroshi; Kato, Takahiro A.; Sakai, Yasunari; Ohga, Shouichi; Fukumoto, Satoshi; Masuda, Keiji, Mitochondrial Calcium-Triggered Oxidative Stress and Developmental Defects in Dopaminergic Neurons Differentiated from Deciduous Teeth-Derived Dental Pulp Stem Cells with MFF Insufficiency, ANTIOXIDANTS, 10.3390/antiox11071361, 11, 7, 2022.07.
6. Hayashi, Yoshinori; Kato, Hiroki; Nonaka, Kazuaki; Nakanishi, Hiroshi, Stem cells from human exfoliated deciduous teeth attenuate mechanical allodynia in mice through distinct from the siglec-9/MCP-1-mediated tissue-repairing mechanism, SCIENTIFIC REPORTS, 10.1038/s41598-021-99585-2, 11, 1, 2021.10.
7. Xiao Sun, Hiroki Kato, Hiroshi Sato, Michiko Torio, Xu Han, Yu Zhang, Yuta Hirofuji, Takahiro A Kato, Yasunari Sakai, Shouichi Ohga, Satoshi Fukumoto, Keiji Masuda, Impaired neurite development and mitochondrial dysfunction associated with calcium accumulation in dopaminergic neurons differentiated from the dental pulp stem cells of a patient with metatropic dysplasia, Biochemistry and Biophysics Reports, 10.1016/j.bbrep.2021.100968., 26, 100968, 2021.07, Transient receptor potential vanilloid member 4 (TRPV4) is a Ca2+ permeable nonselective cation channel, and mutations in the TRPV4 gene cause congenital skeletal dysplasias and peripheral neuropathies. Although TRPV4 is widely expressed in the brain, few studies have assessed the pathogenesis of TRPV4 mutations in the brain. We aimed to elucidate the pathological associations between a specific TRPV4 mutation and neurodevelopmental defects using dopaminergic neurons (DNs) differentiated from dental pulp stem cells (DPSCs). DPSCs were isolated from a patient with metatropic dysplasia and multiple neuropsychiatric symptoms caused by a gain-of-function TRPV4 mutation, c.1855C>T (p.L619F). The mutation was corrected by CRISPR/Cas9 to obtain isogenic control DPSCs. Mutant DPSCs differentiated into DNs without undergoing apoptosis; however, neurite development was significantly impaired in mutant vs. control DNs. Mutant DNs also showed accumulation of mitochondrial Ca2+ and reactive oxygen species, low adenosine triphosphate levels despite a high mitochondrial membrane potential, and lower peroxisome proliferator-activated receptor gamma coactivator 1-alpha expression and mitochondrial content. These results suggested that the persistent Ca2+ entry through the constitutively activated TRPV4 might perturb the adaptive coordination of multiple mitochondrial functions, including oxidative phosphorylation, redox control, and biogenesis, required for dopaminergic circuit development in the brain. Thus, certain mutations in TRPV4 that are associated with skeletal dysplasia might have pathogenic effects on brain development, and mitochondria might be a potential therapeutic target to alleviate the neuropsychiatric symptoms of TRPV4-related diseases..
8. Masuda, Keiji; Han, Xu; Kato, Hiroki; Sato, Hiroshi; Zhang, Yu; Sun, Xiao; Hirofuji, Yuta; Yamaza, Haruyoshi; Yamada, Aya; Fukumoto, Satoshi, Dental Pulp-Derived Mesenchymal Stem Cells for Modeling Genetic Disorders, INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 10.3390/ijms22052269, 22, 5, 2021.03, A subpopulation of mesenchymal stem cells, developmentally derived from multipotent neural crest cells that form multiple facial tissues, resides within the dental pulp of human teeth. These stem cells show high proliferative capacity in vitro and are multipotent, including adipogenic, myogenic, osteogenic, chondrogenic, and neurogenic potential. Teeth containing viable cells are harvested via minimally invasive procedures, based on various clinical diagnoses, but then usually discarded as medical waste, indicating the relatively low ethical considerations to reuse these cells for medical applications. Previous studies have demonstrated that stem cells derived from healthy subjects are an excellent source for cell-based medicine, tissue regeneration, and bioengineering. Furthermore, stem cells donated by patients affected by genetic disorders can serve as in vitro models of disease-specific genetic variants, indicating additional applications of these stem cells with high plasticity. This review discusses the benefits, limitations, and perspectives of patient-derived dental pulp stem cells as alternatives that may complement other excellent, yet incomplete stem cell models, such as induced pluripotent stem cells, together with our recent data..
9. Akamine, Satoshi; Okuzono, Sayaka; Yamamoto, Hiroyuki; Setoyama, Daiki; Sagata, Noriaki; Ohgidani, Masahiro; Kato, Takahiro A.; Ishitani, Tohru; Kato, Hiroki; Masuda, Keiji; Matsushita, Yuki; Ono, Hiroaki; Ishizaki, Yoshito; Sanefuji, Masafumi; Saitsu, Hirotomo; Matsumoto, Naomichi; Kang, Dongchon; Kanba, Shigenobu; Nakabeppu, Yusaku; Sakai, Yasunari; Ohga, Shouichi, GNAO1 organizes the cytoskeletal remodeling and firing of developing neurons, FASEB JOURNAL, 10.1096/fj.202001113R, 34, 12, 16601-16621, 2020.12, Developmental and epileptic encephalopathy (DEE) represents a group of neurodevelopmental disorders characterized by infantile-onset intractable seizures and unfavorable prognosis of psychomotor development. To date, hundreds of genes have been linked to the onset of DEE. GNAO1 is a DEE-associated gene encoding the alpha-O1 subunit of guanine nucleotide-binding protein (GαO ). Despite the increasing number of reported children with GNAO1 encephalopathy, the molecular mechanisms underlying their neurodevelopmental phenotypes remain elusive. We herein present that co-immunoprecipitation and mass spectrometry analyses identified another DEE-associated protein, SPTAN1, as an interacting partner of GαO . Silencing of endogenous Gnao1 attenuated the neurite outgrowth and calcium-dependent signaling. Inactivation of GNAO1 in human-induced pluripotent stem cells gave rise to anomalous brain organoids that only weakly expressed SPTAN1 and Ankyrin-G. Furthermore, GNAO1-deficient organoids failed to conduct synchronized firing to adjacent neurons. These data indicate that GαO and other DEE-associated proteins organize the cytoskeletal remodeling and functional polarity of neurons in the developing brain..
10. Noriaki Sagata, Shin‐ichi Kano, Masahiro Ohgidani, Shogo Inamine, Yasunari Sakai, Hiroki Kato, Keiji Masuda, Takeshi Nakahara, Makiko Nakahara‐Kido, Shouichi Ohga, Masutaka Furue, Akira Sawa, Shigenobu Kanba, Takahiro A. Kato, Forskolin rapidly enhances neuron-like morphological change of directly induced-neuronal cells from neurofibromatosis type 1 patients, Neuropsychopharmacol Rep., 2020.10, Aim: Neurofibromatosis type 1 (NF1) is a multifaceted disease, and frequently comorbid with neurodevelopmental disorders such as autism spectrum disorder (ASD) and learning disorder. Dysfunction of adenylyl cyclase (AC) is one of the candidate pathways in abnormal development of neuronal cells in the brain of NF1 patients, while its dynamic abnormalities have not been observed. Direct conversion technology can generate induced-neuronal (iN) cells directly from human fibroblasts within 2 weeks. Just recently, we have revealed that forskolin, an AC activator, rescues the gene expression pattern of iN cells derived from NF1 patients (NF1-iN cells). In this microreport, we show the dynamic effect of forskolin on NF1-iN cells.

Methods: iN cells derived from healthy control (HC-iN cells) and NF1-iN cells were treated with forskolin (final concentration 10 μM), respectively. Morphological changes of iN cells were captured by inverted microscope with CCD camera every 2 minutes for 90 minutes.

Results: Prior to forskolin treatment, neuron-like spherical-form cells were observed in HC-iN cells, but most NF1-iN cells were not spherical-form but flatform. Only 20 minutes after forskolin treatment, the morphology of the iN cells were dramatically changed from flatform to spherical form, especially in NF1-iN cells.

Conclusion: The present pilot data indicate that forskolin or AC activators may have therapeutic effects on the growth of neuronal cells in NF1 patients. Further translational research should be conducted to validate our pilot findings for future drug development of ASD.
11. Soichiro Sonoda, Sara Murata, Kento Nishida, Hiroki Kato, Norihisa Uehara, Yukari N. Kyumoto, Haruyoshi Yamaza, Ichiro Takahashi, Toshio Kukita, Takayoshi Yamaza, Extracellular vesicles from deciduous pulp stem cells recover bone loss by regulating telomerase activity in an osteoporosis mouse model, Stem Cell Research and Therapy, 10.1186/s13287-020-01818-0, 11, 1, 2020.07, Background: Systemic transplantation of stem cells from human exfoliated deciduous teeth (SHED) recovers bone loss in animal models of osteoporosis; however, the mechanisms underlying this remain unclear. Here, we hypothesized that trophic factors within SHED-releasing extracellular vesicles (SHED-EVs) rescue osteoporotic phenotype. Methods: EVs were isolated from culture supernatant of SHED. SHED-EVs were treated with or without ribonuclease and systemically administrated into ovariectomized mice, followed by the function of recipient bone marrow mesenchymal stem cells (BMMSCs) including telomerase activity, osteoblast differentiation, and sepmaphorine-3A (SEMA3A) secretion. Subsequently, human BMMSCs were stimulated by SHED-EVs with or without ribonuclease treatment, and then human BMMSCs were examined regarding the function of telomerase activity, osteoblast differentiation, and SEMA3A secretion. Furthermore, SHED-EV-treated human BMMSCs were subcutaneously transplanted into the dorsal skin of immunocompromised mice with hydroxyapatite tricalcium phosphate (HA/TCP) careers and analyzed the de novo bone-forming ability. Results: We revealed that systemic SHED-EV-infusion recovered bone volume in ovariectomized mice and improved the function of recipient BMMSCs by rescuing the mRNA levels of Tert and telomerase activity, osteoblast differentiation, and SEMA3A secretion. Ribonuclease treatment depleted RNAs, including microRNAs, within SHED-EVs, and these RNA-depleted SHED-EVs attenuated SHED-EV-rescued function of recipient BMMSCs in the ovariectomized mice. These findings were supported by in vitro assays using human BMMSCs incubated with SHED-EVs. Conclusion: Collectively, our findings suggest that SHED-secreted RNAs, such as microRNAs, play a crucial role in treating postmenopausal osteoporosis by targeting the telomerase activity of recipient BMMSCs..
12. Kentaro Nonaka, Xu Han, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yuta Hirofuji, Keiji Masuda, Novel gain-of-function mutation of TRPV4 associated with accelerated chondrogenic differentiation of dental pulp stem cells derived from a patient with metatropic dysplasia, Biochemistry and Biophysics Reports, 10.1016/j.bbrep.2019.100648, 19, 2019.09, Metatropic dysplasia is a congenital skeletal dysplasia characterized by severe platyspondyly, dumbbell-like deformity of long tubular bones, and progressive kyphoscoliosis with growth. It is caused by mutations in the gene TRPV4, encoding the transient receptor potential vanilloid 4, which acts as a calcium channel. Many heterozygous single base mutations of this gene have been associated with the disorder, showing autosomal dominant inheritance. Although abnormal endochondral ossification has been observed by histological examination of bone in a patient with lethal metatropic dysplasia, the etiology of the disorder remains largely unresolved. As dental pulp stem cells (DPSCs) are mesenchymal stem cells that differentiate into bone lineage cells, DPSCs derived from patients with congenital skeletal dysplasia might be useful as a disease-specific cellular model for etiological investigation. The purpose of this study was to clarify the pathological association between TRPV4 mutation and chondrocyte differentiation by analyzing DPSCs from a patient with non-lethal metatropic dysplasia. We identified a novel heterozygous single base mutation, c.1855C>T in TRPV4. This was predicted to be a missense mutation, p.L619F, in putative transmembrane segment 5. The mutation was repaired by CRISPR/Cas9 system to obtain isogenic control DPSCs for further analysis. The expression of stem cell markers and fibroblast-like morphology were comparable between patient-derived mutant and control DPSCs, although expression of TRPV4 was lower in mutant DPSCs than control DPSCs. Despite the lower TRPV4 expression in mutant DPSCs, the intracellular Ca2+ level was comparable at the basal level between mutant and control DPSCs, while its level was markedly higher following stimulation with 4α-phorbol 12,13-didecanoate (4αPDD), a specific agonist for TRPV4, in mutant DPSCs than in control DPSCs. In the presence of 4αPDD, we observed accelerated early chondrocyte differentiation and upregulated mRNA expression of SRY-box 9 (SOX9) in mutant DPSCs. Our findings suggested that the novel missense mutation c.1855C>T of TRPV4 was a gain-of-function mutation leading to enhanced intracellular Ca2+ level, which was associated with accelerated chondrocyte differentiation and SOX9 upregulation. Our results also suggest that patient-derived DPSCs can be a useful disease-specific cellular model for elucidating the pathological mechanism of metatropic dysplasia..
13. Xu Han, Hiroki Kato, Hiroshi Sato, Yuta Hirofuji, Satoshi Fukumoto, Keiji Masuda, Accelerated osteoblastic differentiation in patient-derived dental pulp stem cells carrying a gain-of-function mutation of TRPV4 associated with metatropic dysplasia, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2019.12.123, 523, 4, 841-846, 2020.03, Metatropic dysplasia (MD) is a congenital skeletal dysplasia characterized by severe platyspondyly and dumbbell-like long-bone deformities. These skeletal phenotypes are predominantly caused by autosomal dominant gain-of-function (GOF) mutations in transient receptor potential vanilloid 4 (TRPV4), which encodes a nonselective Ca2+-permeable cation channel. Previous studies have shown that constitutive TRPV4 channel activation leads to irregular chondrogenic proliferation and differentiation, and thus to the disorganized endochondral ossification seen in MD. Therefore, the present study investigated the role of TRPV4 in osteoblast differentiation and MD pathogenesis. Specifically, the behavior of osteoblasts differentiated from patient-derived dental pulp stem cells carrying a heterozygous single base TRPV4 mutation, c.1855C > T (p.L619F) was compared to that of osteoblasts differentiated from isogenic control cells (in which the mutation was corrected using the CRISPR/Cas9 system). The mutant osteoblasts exhibited enhanced calcification (indicated by intense Alizarin Red S staining), increased intracellular Ca2+ levels, strongly upregulated runt-related transcription factor 2 and osteocalcin expression, and increased expression and nuclear translocation of nuclear factor-activated T cell c1 (NFATc1) compared to control cells. These results suggest that the analyzed TRPV4 GOF mutation disrupts osteoblastic differentiation and induces MD-associated disorganized endochondral ossification by increasing Ca2+/NFATc1 pathway activity. Thus, inhibiting the NFATc1 pathway may be a promising potential therapeutic strategy to attenuate skeletal deformities in MD..
14. Huong Thi Nguyen Nguyen, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yasunari Sakai, Shoichi Ohga, Kazuaki Nonaka, Keiji Masuda, Positive effect of exogenous brain-derived neurotrophic factor on impaired neurite development and mitochondrial function in dopaminergic neurons derived from dental pulp stem cells from children with attention deficit hyperactivity disorder, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2019.04.084, 2019.01, Attention deficit hyperactivity disorder (ADHD) is one of the most common neurodevelopmental disorders and is characterized by impaired attention, hyperactivity, and impulsivity. While multiple etiologies are implicated in ADHD, its underlying mechanism(s) remain unclear. Although previous studies have suggested dysregulation of dopaminergic signals, mitochondria, and brain-derived neurotrophic factor (BDNF) in ADHD, few studies have reported these associations directly. Stem cells from human exfoliated deciduous teeth (SHED) can efficiently differentiate into dopaminergic neurons (DNs) and are thus a useful disease-specific cellular model for the study of neurodevelopmental disorders associated with DN dysfunction. This study aimed to elucidate the relationships between DNs, mitochondria, and BDNF in ADHD by analyzing DNs differentiated from SHED obtained from three boys with ADHD and comparing them to those from three typically developing boys. In the absence of exogenous BDNF in the cell culture media, DNs derived from boys with ADHD (ADHD-DNs) exhibited impaired neurite outgrowth and branching, decreased mitochondrial mass in neurites, and abnormal intracellular ATP levels. In addition, BDNF mRNA was significantly decreased in ADHD-DNs. Supplementation with BDNF, however, significantly improved neurite development and mitochondrial function in ADHD-DNs. These results suggest that ADHD-DNs may have impaired neurite development and mitochondrial function associated with insufficient production of BDNF, which may be improved by exogenous BDNF supplementation. Findings such as these, from patient-derived SHED, may contribute to the future development of treatment strategies for aberrant dopaminergic signaling, mitochondrial functioning, and BDNF levels implicated in ADHD pathogenesis..
15. Yu Zhang, Hiroki Kato, Hiroshi Sato, Haruyoshi Yamaza, Yuta Hirofuji, Xu Han, Keiji Masuda, Kazuaki Nonaka, Folic acid-mediated mitochondrial activation for protection against oxidative stress in human dental pulp stem cells derived from deciduous teeth, Biochemical and biophysical research communications, 10.1016/j.bbrc.2018.11.169, 2019.01.
16. Xu Han, Kentaro Nonaka, Hiroki Kato, Haruyoshi Yamaza, Hiroshi Sato, Takashi Kifune, Yuta Hirofuji, Keiji Masuda, Osteoblastic differentiation improved by bezafibrate-induced mitochondrial biogenesis in deciduous tooth-derived pulp stem cells from a child with Leigh syndrome, Biochemistry and Biophysics Reports, 10.1016/j.bbrep.2018.11.003, 17, 32-37, 2019.03.
17. Huong Thi Nguyen Nguyen, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Yuta Hirofuji, Hiroshi Sato, Thanh Thi Mai Pham, Fumiko Takayama, Yasunari Sakai, Shoichi Ohga, Tomoaki Taguchi, Kazuaki Nonaka, Impaired neurite development associated with mitochondrial dysfunction in dopaminergic neurons differentiated from exfoliated deciduous tooth-derived pulp stem cells of children with autism spectrum disorder, Biochemistry and Biophysics Reports, 10.1016/j.bbrep.2018.09.004, 16, 24-31, 2018.12.
18. Thanh Thi Mai Pham, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Hiroshi Sato, Huong Thi Nguyen Nguyen, Xu Han, Yu Zhang, Tomoaki Taguchi, Kazuaki Nonaka, Altered development of dopaminergic neurons differentiated from stem cells from human exfoliated deciduous teeth of a patient with Down syndrome, BMC Neurology, 10.1186/s12883-018-1140-2, 18, 1, 2018.08.
19. Saki Hirofuji, Yuta Hirofuji, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Hiroshi Sato, Fumiko Takayama, Michiko Torio, Yasunari Sakai, Shoichi Ohga, Tomoaki Taguchi, Kazuaki Nonaka, Mitochondrial dysfunction in dopaminergic neurons differentiated from exfoliated deciduous tooth-derived pulp stem cells of a child with Rett syndrome, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2018.03.077, 498, 4, 898-904, 2018.04.
20. Yumiko I. Matsuishi, Hiroki Kato, Keiji Masuda, Haruyoshi Yamaza, Yuta Hirofuji, Hiroshi Sato, Hiroko Wada, Tamotsu Kiyoshima, Kazuaki Nonaka, Accelerated dentinogenesis by inhibiting the mitochondrial fission factor, dynamin related protein 1, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2017.12.026, 495, 2, 1655-1660, 2018.01.
21. Hiroki Kato, Xu Han, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Hiroshi Sato, Thanh Thi Mai Pham, Tomoaki Taguchi, Kazuaki Nonaka, Direct effects of mitochondrial dysfunction on poor bone health in Leigh syndrome, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2017.09.045, 493, 1, 207-212, 2017.11.
22. Hiroshi Sato, Hiroki Kato, Haruyoshi Yamaza, Keiji Masuda, Huong Thi Nguyen Nguyen, Thanh Thi Mai Pham, Xu Han, Yuta Hirofuji, Kazuaki Nonaka, Engineering of Systematic Elimination of a Targeted Chromosome in Human Cells, BioMed Research International, 10.1155/2017/6037159, 2017, 2017.01.
23. Hiroki Kato, Thanh Thi Mai Pham, Haruyoshi Yamaza, Keiji Masuda, Yuta Hirofuji, Xu Han, Hiroshi Sato, Tomoaki Taguchi, Kazuaki Nonaka, Mitochondria regulate the differentiation of stem cells from human exfoliated deciduous teeth, Cell Structure and Function, 10.1247/csf.17012, 42, 2, 105-116, 2017.05.
24. Shiori Akabane, Midori Uno, Naoki Tani, Shunta Shimazaki, Natsumi Ebara, Hiroki Kato, Hidetaka Kosako, Toshihiko Oka, PKA Regulates PINK1 Stability and Parkin Recruitment to Damaged Mitochondria through Phosphorylation of MIC60, Molecular Cell, 10.1016/j.molcel.2016.03.037, 62, 3, 371-384, 2016.05.
25. Morika Suzuki, Hiroki Kato, Naomi Hachiya, Mitochondrial physiology and cerebrospinal protection, Neuroanesthesia and Cerebrospinal Protection, 10.1007/978-4-431-54490-6_6, 63-70, 2015.08.
26. Morika Suzuki, Hiroyuki Uchino, Hiroki Kato, Propofol prevents mitochondrial fragmentation, Journal of Tokyo Medical University, 73, 3, 268-275, 2015.01.
27. L. F. Burbulla, J. C. Fitzgerald, K. Stegen, J. Westermeier, A. K. Thost, Hiroki Kato, D. Mokranjac, J. Sauerwald, L. M. Martins, D. Woitalla, D. Rapaport, O. Riess, T. Proikas-Cezanne, T. M. Rasse, R. Krüger, Mitochondrial proteolytic stress induced by loss of mortalin function is rescued by Parkin and PINK1, Cell Death and Disease, 10.1038/cddis.2014.103, 5, 4, 2014.01.
28. Tohru Ichimura, Masato Taoka, Ikuo Shoji, Hiroki Kato, Tomonobu Sato, Shigetsugu Hatakeyama, Toshiaki Isobe, Naomi Hachiya, 14-3-3 proteins sequester a pool of soluble TRIM32 ubiquitin ligase to repress autoubiquitylation and cytoplasmic body formation, Journal of Cell Science, 10.1242/jcs.122069, 126, 9, 2014-2026, 2013.05.
29. Hiroki Kato, Qiping Lu, Doron Rapaport, Vera Kozjak-Pavlovic, Tom70 Is Essential for PINK1 Import into Mitochondria, PLoS One, 10.1371/journal.pone.0058435, 8, 3, 2013.03.
30. Lena F. Burbulla, Carina Schelling, Hiroki Kato, Doron Rapaport, Dirk Woitalla, Carola Schiesling, Claudia Schulte, Manu Sharma, Thomas Illig, Peter Bauer, Stephan Jung, Alfred Nordheim, Ludger Schöls, Olaf Riess, Rejko Krüger, Dissecting the role of the mitochondrial chaperone mortalin in Parkinson's disease
Functional impact of disease-related variants on mitochondrial homeostasis, Human Molecular Genetics, 10.1093/hmg/ddq370, 19, 22, 4437-4452, 2010.11.
31. York Kamenisch, Maria Fousteri, Jennifer Knoch, Anna Katharina Von Thaler, Birgit Fehrenbacher, Hiroki Kato, Thomas Becker, Martijn E T Dollé, Raoul Kuiper, Marc Majora, Martin Schaller, Gijsbertus T J Van Der Horst, Harry Van Steeg, Martin Röcken, Doron Rapaport, Jean Krutmann, Leon H. Mullenders, Mark Berneburg, Proteins of nucleotide and base excision repair pathways interact in mitochondria to protect from loss of subcutaneous fat, a hallmark of aging, Journal of Experimental Medicine, 10.1084/jem.20091834, 207, 2, 379-390, 2010.02.
32. Naotada Ishihara, Masatoshi Nomura, Akihiro Jofuku, Hiroki Kato, Satoshi Suzuki, Keiji Masuda, Hidenori Otera, Yae Nakanishi, Ikuya Nonaka, Yu Ichi Goto, Naoko Taguchi, Hidetaka Morinaga, Maki Maeda, Ryoichi Takayanagi, Sadaki Yokota, Katsuyoshi Mihara, Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice, Nature Cell Biology, 10.1038/ncb1907, 11, 8, 958-966, 2009.07.
33. Toshihiko Oka, Tomoko Sayano, Shoko Tamai, Sadaki Yokota, Hiroki Kato, Gen Fujii, Katsuyoshi Mihara, Identification of a novel protein MICS1 that is involved in maintenance of mitochondrial morphology and apoptotic release of cytochrome c, Molecular Biology of the Cell, 10.1091/mbc.E07-12-1205, 19, 6, 2597-2608, 2008.06.
34. Hiroki Kato, Katsuyoshi Mihara, Identification of Tom5 and Tom6 in the preprotein translocase complex of human mitochondrial outer membrane, Biochemical and Biophysical Research Communications, 10.1016/j.bbrc.2008.02.150, 369, 3, 958-963, 2008.05.
35. Hidenori Otera, Yohsuke Taira, Chika Horie, Yurina Suzuki, Hiroyuki Suzuki, Kiyoko Setoguchi, Hiroki Kato, Toshihiko Oka, Katsuyoshi Mihara, A novel insertion pathway of mitochondrial outer membrane proteins with multiple transmembrane segments, Journal of Cell Biology, 10.1083/jcb.200702143, 179, 7, 1355-1363, 2007.12.
36. Hiroki Kato, Kenjiro Sakaki, Katsuyoshi Mihara, Ubiquitin-proteasome-dependent degradation of mammalian ER stearoyl-CoA desaturase, Journal of Cell Science, 10.1242/jcs.02951, 119, 11, 2342-2353, 2006.06.