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655 results on '"Aleksic, Branko"'

1. De novo MCM6 variants in neurodevelopmental disorders: a recognizable phenotype related to zinc binding residues

Author

Smits, Daphne J., Schot, Rachel, Popescu, Cristiana A., Dias, Kerith-Rae, Ades, Lesley, Briere, Lauren C., Sweetser, David A., Kushima, Itaru, Aleksic, Branko, Khan, Suliman, Karageorgou, Vasiliki, Ordonez, Natalia, Sleutels, Frank J. G. T., van der Kaay, Daniëlle C. M., Van Mol, Christine, Van Esch, Hilde, Bertoli-Avella, Aida M., Roscioli, Tony, and Mancini, Grazia M. S.

Published
2023
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4. Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice

Author

Mori, Daisuke, Ikeda, Ryosuke, Sawahata, Masahito, Yamaguchi, Sho, Kodama, Akiko, Hirao, Takashi, Arioka, Yuko, Okumura, Hiroki, Inami, Chihiro, Suzuki, Toshiaki, Hayashi, Yu, Kato, Hidekazu, Nawa, Yoshihiro, Miyata, Seiko, Kimura, Hiroki, Kushima, Itaru, Aleksic, Branko, Mizoguchi, Hiroyuki, Nagai, Taku, Nakazawa, Takanobu, Hashimoto, Ryota, Kaibuchi, Kozo, Kume, Kazuhiko, Yamada, Kiyofumi, and Ozaki, Norio

Published
2024
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5. Publisher Correction: Rates, distribution and implications of postzygotic mosaic mutations in autism spectrum disorder

Author

Lim, Elaine T, Uddin, Mohammed, De Rubeis, Silvia, Chan, Yingleong, Kamumbu, Anne S, Zhang, Xiaochang, D’Gama, Alissa M, Kim, Sonia N, Hill, Robert Sean, Goldberg, Arthur P, Poultney, Christopher, Minshew, Nancy J, Kushima, Itaru, Aleksic, Branko, Ozaki, Norio, Parellada, Mara, Arango, Celso, Penzol, Maria J, Carracedo, Angel, Kolevzon, Alexander, Hultman, Christina M, Weiss, Lauren A, Fromer, Menachem, Chiocchetti, Andreas G, Freitag, Christine M, Church, George M, Scherer, Stephen W, Buxbaum, Joseph D, and Walsh, Christopher A

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Autism Sequencing Consortium, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

Published
2020

6. Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism

Author

Satterstrom, F Kyle, Kosmicki, Jack A, Wang, Jiebiao, Breen, Michael S, De Rubeis, Silvia, An, Joon-Yong, Peng, Minshi, Collins, Ryan, Grove, Jakob, Klei, Lambertus, Stevens, Christine, Reichert, Jennifer, Mulhern, Maureen S, Artomov, Mykyta, Gerges, Sherif, Sheppard, Brooke, Xu, Xinyi, Bhaduri, Aparna, Norman, Utku, Brand, Harrison, Schwartz, Grace, Nguyen, Rachel, Guerrero, Elizabeth E, Dias, Caroline, Consortium, Autism Sequencing, Aleksic, Branko, Anney, Richard, Barbosa, Mafalda, Bishop, Somer, Brusco, Alfredo, Bybjerg-Grauholm, Jonas, Carracedo, Angel, Chan, Marcus CY, Chiocchetti, Andreas G, Chung, Brian HY, Coon, Hilary, Cuccaro, Michael L, Curró, Aurora, Bernardina, Bernardo Dalla, Doan, Ryan, Domenici, Enrico, Dong, Shan, Fallerini, Chiara, Fernández-Prieto, Montserrat, Ferrero, Giovanni Battista, Freitag, Christine M, Fromer, Menachem, Gargus, J Jay, Geschwind, Daniel, Giorgio, Elisa, González-Peñas, Javier, Guter, Stephen, Halpern, Danielle, Hansen-Kiss, Emily, He, Xin, Herman, Gail E, Hertz-Picciotto, Irva, Hougaard, David M, Hultman, Christina M, Ionita-Laza, Iuliana, Jacob, Suma, Jamison, Jesslyn, Jugessur, Astanand, Kaartinen, Miia, Knudsen, Gun Peggy, Kolevzon, Alexander, Kushima, Itaru, Lee, So Lun, Lehtimäki, Terho, Lim, Elaine T, Lintas, Carla, Lipkin, W Ian, Lopergolo, Diego, Lopes, Fátima, Ludena, Yunin, Maciel, Patricia, Magnus, Per, Mahjani, Behrang, Maltman, Nell, Manoach, Dara S, Meiri, Gal, Menashe, Idan, Miller, Judith, Minshew, Nancy, Montenegro, Eduarda MS, Moreira, Danielle, Morrow, Eric M, Mors, Ole, Mortensen, Preben Bo, Mosconi, Matthew, Muglia, Pierandrea, Neale, Benjamin M, Nordentoft, Merete, Ozaki, Norio, Palotie, Aarno, Parellada, Mara, Passos-Bueno, Maria Rita, Pericak-Vance, Margaret, Persico, Antonio M, and Pessah, Isaac

Subjects
Biological Sciences, Bioinformatics and Computational Biology, Biomedical and Clinical Sciences, Genetics, Brain Disorders, Mental Health, Pediatric, Human Genome, Clinical Research, Autism, Intellectual and Developmental Disabilities (IDD), Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Mental health, Neurological, Autistic Disorder, Case-Control Studies, Cell Lineage, Cerebral Cortex, Cohort Studies, Exome, Female, Gene Expression Regulation, Developmental, Gene Frequency, Genetic Predisposition to Disease, Humans, Male, Mutation, Missense, Neurobiology, Neurons, Phenotype, Sex Factors, Single-Cell Analysis, Exome Sequencing, Autism Sequencing Consortium, iPSYCH-Broad Consortium, autism spectrum disorder, cell type, cytoskeleton, excitatory neurons, excitatory-inhibitory balance, exome sequencing, genetics, inhibitory neurons, liability, neurodevelopment, Medical and Health Sciences, Developmental Biology, Biological sciences, Biomedical and clinical sciences
Abstract

We present the largest exome sequencing study of autism spectrum disorder (ASD) to date (n = 35,584 total samples, 11,986 with ASD). Using an enhanced analytical framework to integrate de novo and case-control rare variation, we identify 102 risk genes at a false discovery rate of 0.1 or less. Of these genes, 49 show higher frequencies of disruptive de novo variants in individuals ascertained to have severe neurodevelopmental delay, whereas 53 show higher frequencies in individuals ascertained to have ASD; comparing ASD cases with mutations in these groups reveals phenotypic differences. Expressed early in brain development, most risk genes have roles in regulation of gene expression or neuronal communication (i.e., mutations effect neurodevelopmental and neurophysiological changes), and 13 fall within loci recurrently hit by copy number variants. In cells from the human cortex, expression of risk genes is enriched in excitatory and inhibitory neuronal lineages, consistent with multiple paths to an excitatory-inhibitory imbalance underlying ASD.

Published
2020

7. Exome sequencing analysis of Japanese autism spectrum disorder case-control sample supports an increased burden of synaptic function-related genes

Author

Kimura, Hiroki, Nakatochi, Masahiro, Aleksic, Branko, Guevara, James, Toyama, Miho, Hayashi, Yu, Kato, Hidekazu, Kushima, Itaru, Morikawa, Mako, Ishizuka, Kanako, Okada, Takashi, Tsurusaki, Yoshinori, Fujita, Atsushi, Miyake, Noriko, Ogi, Tomoo, Takata, Atsushi, Matsumoto, Naomichi, Buxbaum, Joseph, Ozaki, Norio, and Sebat, Jonathan

Published
2022
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8. Identification of ultra-rare disruptive variants in voltage-gated calcium channel-encoding genes in Japanese samples of schizophrenia and autism spectrum disorder

Author

Wang, Chenyao, Horigane, Shin-ichiro, Wakamori, Minoru, Ueda, Shuhei, Kawabata, Takeshi, Fujii, Hajime, Kushima, Itaru, Kimura, Hiroki, Ishizuka, Kanako, Nakamura, Yukako, Iwayama, Yoshimi, Ikeda, Masashi, Iwata, Nakao, Okada, Takashi, Aleksic, Branko, Mori, Daisuke, Yoshida, Takashi, Bito, Haruhiko, Yoshikawa, Takeo, Takemoto-Kimura, Sayaka, and Ozaki, Norio

Published
2022
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10. Rates, distribution and implications of postzygotic mosaic mutations in autism spectrum disorder

Author

Lim, Elaine T, Uddin, Mohammed, De Rubeis, Silvia, Chan, Yingleong, Kamumbu, Anne S, Zhang, Xiaochang, D'Gama, Alissa M, Kim, Sonia N, Hill, Robert Sean, Goldberg, Arthur P, Poultney, Christopher, Minshew, Nancy J, Kushima, Itaru, Aleksic, Branko, Ozaki, Norio, Parellada, Mara, Arango, Celso, Penzol, Maria J, Carracedo, Angel, Kolevzon, Alexander, Hultman, Christina M, Weiss, Lauren A, Fromer, Menachem, Chiocchetti, Andreas G, Freitag, Christine M, Church, George M, Scherer, Stephen W, Buxbaum, Joseph D, and Walsh, Christopher A

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Brain Disorders, Autism, Genetics, Pediatric, Mental Health, Intellectual and Developmental Disabilities (IDD), 2.1 Biological and endogenous factors, Aetiology, Mental health, Autism Spectrum Disorder, Databases, Genetic, Genetic Predisposition to Disease, Genetic Variation, Humans, Mosaicism, Mutation, Missense, Zygote, Autism Sequencing Consortium, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

We systematically analyzed postzygotic mutations (PZMs) in whole-exome sequences from the largest collection of trios (5,947) with autism spectrum disorder (ASD) available, including 282 unpublished trios, and performed resequencing using multiple independent technologies. We identified 7.5% of de novo mutations as PZMs, 83.3% of which were not described in previous studies. Damaging, nonsynonymous PZMs within critical exons of prenatally expressed genes were more common in ASD probands than controls (P < 1 × 10-6), and genes carrying these PZMs were enriched for expression in the amygdala (P = 5.4 × 10-3). Two genes (KLF16 and MSANTD2) were significantly enriched for PZMs genome-wide, and other PZMs involved genes (SCN2A, HNRNPU and SMARCA4) whose mutation is known to cause ASD or other neurodevelopmental disorders. PZMs constitute a significant proportion of de novo mutations and contribute importantly to ASD risk.

Published
2017

12. Study of the genetic association between selected 3q29 region genes and schizophrenia and autism spectrum disorder in the Japanese population.

Author

Otgonbayar, Gantsooj, Tzuyao Lo, Yu Hayashi, Sho Furuta, Aleksic, Branko, Yoshihiro Nawa, Itaru Kushima, Hidekazu Kato, Hiroki Kimura, and Norio Ozaki

Subjects
AUTISM spectrum disorders, JAPANESE people, SCHIZOPHRENIA, MISSENSE mutation, GENETIC disorders, GAIN-of-function mutations
Abstract

Psychiatric disorders are highly inheritable, and most psychiatric disorders exhibit genetic overlap. Recent studies associated the 3q29 recurrent deletion with schizophrenia (SCZ) and autism spectrum disorder (ASD). In this study, we investigated the association of genes in the 3q29 region with SCZ and ASD. TM4SF19 and PAK2 were chosen as candidate genes for this study based on evidence from previous research. We sequenced TM4SF19 and PAK2 in 437 SCZ cases, 187 ASD cases and 524 controls in the Japanese population. Through targeted sequencing, we identified 6 missense variants among the cases (ASD & SCZ), 3 missense variants among controls, and 1 variant common to both cases and controls; however, no loss-of-function variants were identified. Fisher's exact test showed a significant association of variants in TM4SF19 among cases (p=0.0160). These results suggest TM4SF19 variants affect the etiology of SCZ and ASD in the Japanese population. Further research examining 3q29 region genes and their association with SCZ and ASD is thus needed. [ABSTRACT FROM AUTHOR]

Published
2024
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13. Association between copy number variations in parkin (PRKN) and schizophrenia and autism spectrum disorder: A case–control study.

Author

Lo, Tzuyao, Kushima, Itaru, Kimura, Hiroki, Aleksic, Branko, Okada, Takashi, Kato, Hidekazu, Inada, Toshiya, Nawa, Yoshihiro, Torii, Youta, Yamamoto, Maeri, Kimura, Ryo, Funabiki, Yasuko, Kosaka, Hirotaka, Numata, Shusuke, Kasai, Kiyoto, Sasaki, Tsukasa, Yokoyama, Shigeru, Munesue, Toshio, Hashimoto, Ryota, and Yasuda, Yuka

Subjects
AUTISM spectrum disorders, SCHIZOPHRENIA, PARKIN (Protein), COMPARATIVE genomic hybridization, PARKINSON'S disease, OLANZAPINE
Abstract

Aim: The present study aimed to examine the association between copy number variations (CNVs) in parkin (PRKN) and schizophrenia (SCZ) and autism spectrum disorder (ASD) in a large case–control sample. Method: Array comparative genomic hybridization was performed on 3111 cases with SCZ, 1236 cases with ASD, and 2713 controls. We systematically prioritized likely pathogenic CNVs (LP‐CNVs) in PRKN and examined their association with SCZ and ASD. Results: In total, 3014 SCZ cases (96.9%), 1205 ASD cases (97.5%), and 2671 controls (98.5%) passed quality control. We found that monoallelic carriers of LP‐CNVs in PRKN were common (70/6890, 1.02%) and were not at higher risk of SCZ (p = 0.29) or ASD (p = 0.72). We observed that the distribution pattern of LP‐CNVs in the Japanese population was consistent with those in other populations. We also identified a patient diagnosed with SCZ and early‐onset Parkinson's disease carrying biallelic pathogenic CNVs in PRKN. The absence of Parkinson's symptoms in 10 other monoallelic carriers of the same pathogenic CNV further reflects the lack of effect of monoallelic pathogenic variants in PRKN in the absence of a second hit. Conclusion: The present findings suggest that monoallelic CNVs in PRKN do not confer a significant risk for SCZ or ASD. However, further studies to investigate the association between biallelic CNVs in PRKN and SCZ and ASD are warranted. [ABSTRACT FROM AUTHOR]

Published
2024
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14. Functional characterization of rare NRXN1 variants identified in autism spectrum disorders and schizophrenia

Author

Kanako Ishizuka, Tomoyuki Yoshida, Takeshi Kawabata, Ayako Imai, Hisashi Mori, Hiroki Kimura, Toshiya Inada, Yuko Okahisa, Jun Egawa, Masahide Usami, Itaru Kushima, Mako Morikawa, Takashi Okada, Masashi Ikeda, Aleksic Branko, Daisuke Mori, Toshiyuki Someya, Nakao Iwata, and Norio Ozaki

Subjects
NRXN1, Neurodevelopmental disorder, Autism spectrum disorders, Schizophrenia, Targeted resequencing, Ultra-rare variants, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571
Abstract

Abstract Background Rare genetic variants contribute to the etiology of both autism spectrum disorder (ASD) and schizophrenia (SCZ). Most genetic studies limit their focus to likely gene-disrupting mutations because they are relatively easier to interpret their effects on the gene product. Interpretation of missense variants is also informative to some pathophysiological mechanisms of these neurodevelopmental disorders; however, their contribution has not been elucidated because of relatively small effects. Therefore, we characterized missense variants detected in NRXN1, a well-known neurodevelopmental disease-causing gene, from individuals with ASD and SCZ. Methods To discover rare variants with large effect size and to evaluate their role in the shared etiopathophysiology of ASD and SCZ, we sequenced NRXN1 coding exons with a sample comprising 562 Japanese ASD and SCZ patients, followed by a genetic association analysis in 4273 unrelated individuals. Impact of each missense variant detected here on cell surface expression, interaction with NLGN1, and synaptogenic activity was analyzed using an in vitro functional assay and in silico three-dimensional (3D) structural modeling. Results Through mutation screening, we regarded three ultra-rare missense variants (T737M, D772G, and R856W), all of which affected the LNS4 domain of NRXN1α isoform, as disease-associated variants. Diagnosis of individuals with T737M, D772G, and R856W was 1ASD and 1SCZ, 1ASD, and 1SCZ, respectively. We observed the following phenotypic and functional burden caused by each variant. (i) D772G and R856W carriers had more serious social disabilities than T737M carriers. (ii) In vitro assay showed reduced cell surface expression of NRXN1α by D772G and R856W mutations. In vitro functional analysis showed decreased NRXN1α-NLGN1 interaction of T737M and D772G mutants. (iii) In silico 3D structural modeling indicated that T737M and D772G mutations could destabilize the rod-shaped structure of LNS2-LNS5 domains, and D772G and R856W could disturb N-glycan conformations for the transport signal. Conclusions The combined data suggest that missense variants in NRXN1 could be associated with phenotypes of neurodevelopmental disorders beyond the diagnosis of ASD and/or SCZ.

Published
2020
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15. Exome sequencing of Japanese schizophrenia multiplex families supports the involvement of calcium ion channels

Author

Miho Toyama, Yuto Takasaki, Aleksic Branko, Hiroki Kimura, Hidekazu Kato, Yoshihiro Nawa, Itaru Kushima, Kanako Ishizuka, Teppei Shimamura, Tomoo Ogi, and Norio Ozaki

Subjects
Medicine, Science
Abstract

Background Most sequencing studies of schizophrenia (SCZ) have focused on de novo genetic variants due to interpretability. However, investigating shared rare variants among patients in the same multiplex family is also important. Relatively large-scale analyses of SCZ multiplex families have been done in Caucasian populations, but whether detected variants are also pathogenic in the Japanese population is unclear because of ethnic differences in rare variants. Materials and methods We performed whole-exome sequencing (WES) of 14 Japanese SCZ multiplex families. After quality control and filtering, we identified rare variants shared among affected persons within the same family. A gene ontology (GO) analysis was performed to identify gene categories possibly affected by these candidate variants. Results We found 530 variants in 486 genes as potential candidate variants from the 14 SCZ multiplex families examined. The GO analysis demonstrated significant enrichment in calcium channel activity. Conclusion This study provides supporting evidence that calcium ion channel activity is involved in SCZ. WES of multiplex families is a potential means of identifying disease-associated rare variants for SCZ.

Published
2022

21. Rare single-nucleotide DAB1 variants and their contribution to Schizophrenia and autism spectrum disorder susceptibility

Author

Nawa, Yoshihiro, Kimura, Hiroki, Mori, Daisuke, Kato, Hidekazu, Toyama, Miho, Furuta, Sho, Yu, Yanjie, Ishizuka, Kanako, Kushima, Itaru, Aleksic, Branko, Arioka, Yuko, Morikawa, Mako, Okada, Takashi, Inada, Toshiya, Kaibuchi, Kozo, Ikeda, Masashi, Iwata, Nakao, Suzuki, Michio, Okahisa, Yuko, Egawa, Jun, Someya, Toshiyuki, Nishimura, Fumichika, Sasaki, Tsukasa, and Ozaki, Norio

Published
2020
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22. ARHGAP10, which encodes Rho GTPase-activating protein 10, is a novel gene for schizophrenia risk

Author

Sekiguchi, Mariko, Sobue, Akira, Kushima, Itaru, Wang, Chenyao, Arioka, Yuko, Kato, Hidekazu, Kodama, Akiko, Kubo, Hisako, Ito, Norimichi, Sawahata, Masahito, Hada, Kazuhiro, Ikeda, Ryosuke, Shinno, Mio, Mizukoshi, Chikara, Tsujimura, Keita, Yoshimi, Akira, Ishizuka, Kanako, Takasaki, Yuto, Kimura, Hiroki, Xing, Jingrui, Yu, Yanjie, Yamamoto, Maeri, Okada, Takashi, Shishido, Emiko, Inada, Toshiya, Nakatochi, Masahiro, Takano, Tetsuya, Kuroda, Keisuke, Amano, Mutsuki, Aleksic, Branko, Yamomoto, Takashi, Sakuma, Tetsushi, Aida, Tomomi, Tanaka, Kohichi, Hashimoto, Ryota, Arai, Makoto, Ikeda, Masashi, Iwata, Nakao, Shimamura, Teppei, Nagai, Taku, Nabeshima, Toshitaka, Kaibuchi, Kozo, Yamada, Kiyofumi, Mori, Daisuke, and Ozaki, Norio

Published
2020
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23. Rare genetic variants in the gene encoding histone lysine demethylase 4C (KDM4C) and their contributions to susceptibility to schizophrenia and autism spectrum disorder

Author

Kato, Hidekazu, Kushima, Itaru, Mori, Daisuke, Yoshimi, Akira, Aleksic, Branko, Nawa, Yoshihiro, Toyama, Miho, Furuta, Sho, Yu, Yanjie, Ishizuka, Kanako, Kimura, Hiroki, Arioka, Yuko, Tsujimura, Keita, Morikawa, Mako, Okada, Takashi, Inada, Toshiya, Nakatochi, Masahiro, Shinjo, Keiko, Kondo, Yutaka, Kaibuchi, Kozo, Funabiki, Yasuko, Kimura, Ryo, Suzuki, Toshimitsu, Yamakawa, Kazuhiro, Ikeda, Masashi, Iwata, Nakao, Takahashi, Tsutomu, Suzuki, Michio, Okahisa, Yuko, Takaki, Manabu, Egawa, Jun, Someya, Toshiyuki, and Ozaki, Norio

Published
2020
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31. Analysis of human neuronal cells carrying ASTN2 deletion: A cross-disorder risk variant of schizophrenia, autism spectrum disorder, and bipolar disorder

Author

Arioka, Yuko, primary, Hayashi, Yu, additional, Okumura, Hiroki, additional, Kushima, Itaru, additional, Mori, Daisuke, additional, Lo, Tzuyao, additional, Otgonbayar, Gantsooj, additional, Kato, Hidekazu, additional, Nawa, Yoshihiro, additional, Kimura, Hiroki, additional, Aleksic, Branko, additional, and Ozaki, Norio, additional

Published
2023
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33. Proteomic analysis of lymphoblastoid cell lines from schizophrenic patients

Author

Yoshimi, Akira, Yamada, Shinnosuke, Kunimoto, Shohko, Aleksic, Branko, Hirakawa, Akihiro, Ohashi, Mitsuki, Matsumoto, Yurie, Hada, Kazuhiro, Itoh, Norimichi, Arioka, Yuko, Kimura, Hiroki, Kushima, Itaru, Nakamura, Yukako, Shiino, Tomoko, Mori, Daisuke, Tanaka, Satoshi, Hamada, Shuko, Noda, Yukihiro, Nagai, Taku, Yamada, Kiyofumi, and Ozaki, Norio

Published
2019
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40. X chromosome aneuploidies and schizophrenia: association analysis and phenotypic characterization

Author

Kushima, Itaru, primary, Aleksic, Branko, additional, Kimura, Hiroki, additional, Nakatochi, Masahiro, additional, Lo, Tzuyao, additional, Ikeda, Masashi, additional, Arai, Makoto, additional, Hashimoto, Ryota, additional, Numata, Shusuke, additional, Okamura, Yasunobu, additional, Obara, Taku, additional, Inada, Toshiya, additional, and Ozaki, Norio, additional

Published
2022
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41. Cross-Disorder Analysis of Genic and Regulatory Copy Number Variations in Bipolar Disorder, Schizophrenia, and Autism Spectrum Disorder

Author

Kushima, Itaru, primary, Nakatochi, Masahiro, additional, Aleksic, Branko, additional, Okada, Takashi, additional, Kimura, Hiroki, additional, Kato, Hidekazu, additional, Morikawa, Mako, additional, Inada, Toshiya, additional, Ishizuka, Kanako, additional, Torii, Youta, additional, Nakamura, Yukako, additional, Tanaka, Satoshi, additional, Imaeda, Miho, additional, Takahashi, Nagahide, additional, Yamamoto, Maeri, additional, Iwamoto, Kunihiro, additional, Nawa, Yoshihiro, additional, Ogawa, Nanayo, additional, Iritani, Shuji, additional, Hayashi, Yu, additional, Lo, Tzuyao, additional, Otgonbayar, Gantsooj, additional, Furuta, Sho, additional, Iwata, Nakao, additional, Ikeda, Masashi, additional, Saito, Takeo, additional, Ninomiya, Kohei, additional, Okochi, Tomo, additional, Hashimoto, Ryota, additional, Yamamori, Hidenaga, additional, Yasuda, Yuka, additional, Fujimoto, Michiko, additional, Miura, Kenichiro, additional, Itokawa, Masanari, additional, Arai, Makoto, additional, Miyashita, Mitsuhiro, additional, Toriumi, Kazuya, additional, Ohi, Kazutaka, additional, Shioiri, Toshiki, additional, Kitaichi, Kiyoyuki, additional, Someya, Toshiyuki, additional, Watanabe, Yuichiro, additional, Egawa, Jun, additional, Takahashi, Tsutomu, additional, Suzuki, Michio, additional, Sasaki, Tsukasa, additional, Tochigi, Mamoru, additional, Nishimura, Fumichika, additional, Yamasue, Hidenori, additional, Kuwabara, Hitoshi, additional, Wakuda, Tomoyasu, additional, Kato, Takahiro A., additional, Kanba, Shigenobu, additional, Horikawa, Hideki, additional, Usami, Masahide, additional, Kodaira, Masaki, additional, Watanabe, Kyota, additional, Yoshikawa, Takeo, additional, Toyota, Tomoko, additional, Yokoyama, Shigeru, additional, Munesue, Toshio, additional, Kimura, Ryo, additional, Funabiki, Yasuko, additional, Kosaka, Hirotaka, additional, Jung, Minyoung, additional, Kasai, Kiyoto, additional, Ikegame, Tempei, additional, Jinde, Seiichiro, additional, Numata, Shusuke, additional, Kinoshita, Makoto, additional, Kato, Tadafumi, additional, Kakiuchi, Chihiro, additional, Yamakawa, Kazuhiro, additional, Suzuki, Toshimitsu, additional, Hashimoto, Naoki, additional, Ishikawa, Shuhei, additional, Yamagata, Bun, additional, Nio, Shintaro, additional, Murai, Toshiya, additional, Son, Shuraku, additional, Kunii, Yasuto, additional, Yabe, Hirooki, additional, Inagaki, Masumi, additional, Goto, Yu-ichi, additional, Okumura, Yuto, additional, Ito, Tomoya, additional, Arioka, Yuko, additional, Mori, Daisuke, additional, and Ozaki, Norio, additional

Published
2022
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43. Phenotypes for general behavior, activity, and body temperature in 3q29 deletion model mice

Author

Mori, Daisuke, primary, Ikeda, Ryosuke, additional, Sawahata, Masahito, additional, Yamaguchi, Sho, additional, Kodama, Akiko, additional, Hirao, Takashi, additional, Arioka, Yuko, additional, Okumura, Hiroki, additional, Inami, Chihiro, additional, Suzuki, Toshiaki, additional, Hayashi, Yu, additional, Kato, Hidekazu, additional, Nawa, Yoshihiro, additional, Miyata, Seiko, additional, Kimura, Hiroki, additional, Kushima, Itaru, additional, Aleksic, Branko, additional, Mizoguchi, Hiroyuki, additional, Nagai, Taku, additional, Nakazawa, Takanobu, additional, Hashimoto, Ryota, additional, Kaibuchi, Kozo, additional, Kume, Kazuhiko, additional, Yamada, Kiyofumi, additional, and Ozaki, Norio, additional

Published
2022
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48. Novel rare variants in F-box protein 45 (FBXO45) in schizophrenia

Author

Wang, Chenyao, Koide, Takayoshi, Kimura, Hiroki, Kunimoto, Shohko, Yoshimi, Akira, Nakamura, Yukako, Kushima, Itaru, Banno, Masahiro, Kawano, Naoko, Takasaki, Yuto, Xing, Jingrui, Noda, Yukihiro, Mouri, Akihiro, Aleksic, Branko, Ikeda, Masashi, Okada, Takashi, Iidaka, Tetsuya, Inada, Toshiya, Iwata, Nakao, and Ozaki, Norio

Published
2014
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