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Jun Aruga - One of the best experts on this subject based on the ideXlab platform.
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Auditory function abnormalities in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A) Representative waves of auditory brainstem response (ABR) from WT (left, n = 7) and Slitrk6-KO (right, n = 9) mice. ABR were recorded upon 0- to 80-dB sound pressure level (SPL) stimuli of 2, 4, 8, 16, and 24 kHz. The dash lines indicate the time of click presentation. The scale bars are shown at bottom right. (B) ABR thresholds in WT and Slitrk6-KO mice. Slitrk6-KO mice showed significantly higher thresholds to the 8- and 16-kHz stimuli than those of WT mice. (C) Top: Each peak number in a representative ABR wave. Middle: Comparison of the values of peaks I, II, and III between WT and Slitrk6-KO mice. Peak I of Slitrk6-KO mice was significantly reduced in the range of 8 to 16 kHz, and peak III was also significantly reduced at 24 kHz. Bottom: The latency to peaks I, II, and III. The latency did not show clear differences between WT and Slitrk6-KO mice. (D) Auditory startle response of WT (n = 10) and Slitrk6-KO mice (n = 10). Slitrk6-KO mice showed significantly lower startle responses to 95- to 120-dB sounds. *P
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Altered adaptive responses to a novel environment in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A, B) Open field test. (A) The total distance moved was less in Slitrk6-KO than in WT mice (left). The distance moved in the first 5 min of the test was significantly lower in Slitrk6-KO mice (right). (B) In Slitrk6-KO mice, the total time spent in the center area was greater than that of the WT (left) and was significantly increased in the first 5 min of the test (right). (C–G) Hole-board test. There were no significant differences in distance moved (C), number of rearing episodes (D), and number of head dips (E) between Slitrk6-KO and WT mice. Duration per head dip was significantly decreased in Slitrk6-KO mice (F). Latency time to head dip was significantly decreased in KO mice (G). Values are mean ± standard error of the mean. *P
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Vestibular function anomaly in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A) Dynamic characteristics of horizontal optokinetic response (hOKR) of WT (n = 9) and Slitrk6-KO (n = 9) mice. (B) Horizontal vestibulo-ocular reflex (hVOR). There were no differences in gains (left) or phases (right) between WT (n = 9) and KO (n = 9) in hVOR or hOKR. (C) Vertical vestibulo-ocular reflex (vVOR) of WT (n = 8) and Slitrk6-KO mice (n = 6). Gains of vVOR (left) of the Slitrk6-KO mice were significantly smaller than those of WT. (D) Rota- rod test. Rotation indicates the speed of rotation (rpm) at which the mice fell off or revolved around the rod. The values were comparable between WT (n = 12) and Slitrk6-KO (n = 8) mice, suggesting that there were no strong deficits of balancing function in Slitrk6-KO mice. Values are mean ± standard error of the mean.
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Summary of Slitrk6 KO behavioral analyses.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:Summary of Slitrk6 KO behavioral analyses.
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Normal anxiety level of Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:Normal anxiety level of Slitrk6-KO mice.
Kristian Unger - One of the best experts on this subject based on the ideXlab platform.
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Novel candidate genes of thyroid tumourigenesis identified in Trk-T1 transgenic mice
Endocrine-related Cancer, 2012Co-Authors: Katrin Janine Heiliger, Julia Hess, Paolo Salerno, Giuliana Salvatore, Clara Ugolini, Isolde Summerer, Tatjana Bogdanova, Donata Vitagliano, Herbert Braselmann, Kristian UngerAbstract:For an identification of novel candidate genes in thyroid tumourigenesis, we have investigated gene copy number changes in a Trk-T1 transgenic mouse model of thyroid neoplasia. For this aim, 30 thyroid tumours from Trk-T1 transgenics were investigated by comparative genomic hybridisation. Recurrent gene copy number alterations were identified and genes located in the altered chromosomal regions were analysed by Gene Ontology term enrichment analysis in order to reveal gene functions potentially associated with thyroid tumourigenesis. In thyroid neoplasms from Trk-T1 mice, a recurrent gain on chromosomal bands 1C4–E2.3 (10.0% of cases), and losses on 3H1–H3 (13.3%), 4D2.3–E2 (43.3%) and 14E4–E5 (6.7%) were identified. The genes Twist2, Ptma, Pde6d, Bmpr1b, Pdlim5, Unc5c, Srm, Trp73, Ythdf2, Taf12 and Slitrk5 are located in these chromosomal bands. Copy number changes of these genes were studied by fluorescence in situ hybridisation on 30 human papillary thyroid carcinoma (PTC) samples and altered gene expression was studied by qRT-PCR analyses in 67 human PTC. Copy number gains were detected in 83% of cases for TWIST2 and in 100% of cases for PTMA and PDE6D. DNA losses of SLITRK1 and SLITRK5 were observed in 21% of cases and of SLITRK6 in 16% of cases. Gene expression was significantly up-regulated for UNC5C and TP73 and significantly down-regulated for SLITRK5 in tumours compared with normal tissue. In conclusion, a global genomic copy number analysis of thyroid tumours from Trk-T1 transgenic mice revealed a number of novel gene alterations in thyroid tumourigenesis that are also prevalent in human PTCs. Endocrine-Related Cancer (2012) 19 409–421
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Novel candidate genes of thyroid tumourigenesis identified in Trk-T1 transgenic mice.
'Bioscientifica', 2012Co-Authors: Katrin Janine Heiliger, Julia Hess, Paolo Salerno, Giuliana Salvatore, Clara Ugolini, Isolde Summerer, Tatjana Bogdanova, Donata Vitagliano, Herbert Braselmann, Kristian UngerAbstract:For an identification of novel candidate genes in thyroid tumourigenesis, we have investigated gene copy number changes in a Trk-T1 transgenic mouse model of thyroid neoplasia. For this aim, 30 thyroid tumours from Trk-T1 transgenics were investigated by comparative genomic hybridisation. Recurrent gene copy number alterations were identified and genes located in the altered chromosomal regions were analysed by Gene Ontology term enrichment analysis in order to reveal gene functions potentially associated with thyroid tumourigenesis. In thyroid neoplasms from Trk-T1 mice, a recurrent gain on chromosomal bands 1C4-E2.3 (10.0\% of cases), and losses on 3H1-H3 (13.3\%), 4D2.3-E2 (43.3\%) and 14E4-E5 (6.7\%) were identified. The genes Twist2, Ptma, Pde6d, Bmpr1b, Pdlim5, Unc5c, Srm, Trp73, Ythdf2, Taf12 and Slitrk5 are located in these chromosomal bands. Copy number changes of these genes were studied by fluorescence in situ hybridisation on 30 human papillary thyroid carcinoma (PTC) samples and altered gene expression was studied by qRT-PCR analyses in 67 human PTC. Copy number gains were detected in 83\% of cases for TWIST2 and in 100\% of cases for PTMA and PDE6D. DNA losses of SLITRK1 and SLITRK5 were observed in 21\% of cases and of SLITRK6 in 16\% of cases. Gene expression was significantly up-regulated for UNC5C and TP73 and significantly down-regulated for SLITRK5 in tumours compared with normal tissue. In conclusion, a global genomic copy number analysis of thyroid tumours from Trk-T1 transgenic mice revealed a number of novel gene alterations in thyroid tumourigenesis that are also prevalent in human PTCs
Yoshifumi Matsumoto - One of the best experts on this subject based on the ideXlab platform.
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Auditory function abnormalities in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A) Representative waves of auditory brainstem response (ABR) from WT (left, n = 7) and Slitrk6-KO (right, n = 9) mice. ABR were recorded upon 0- to 80-dB sound pressure level (SPL) stimuli of 2, 4, 8, 16, and 24 kHz. The dash lines indicate the time of click presentation. The scale bars are shown at bottom right. (B) ABR thresholds in WT and Slitrk6-KO mice. Slitrk6-KO mice showed significantly higher thresholds to the 8- and 16-kHz stimuli than those of WT mice. (C) Top: Each peak number in a representative ABR wave. Middle: Comparison of the values of peaks I, II, and III between WT and Slitrk6-KO mice. Peak I of Slitrk6-KO mice was significantly reduced in the range of 8 to 16 kHz, and peak III was also significantly reduced at 24 kHz. Bottom: The latency to peaks I, II, and III. The latency did not show clear differences between WT and Slitrk6-KO mice. (D) Auditory startle response of WT (n = 10) and Slitrk6-KO mice (n = 10). Slitrk6-KO mice showed significantly lower startle responses to 95- to 120-dB sounds. *P
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Altered adaptive responses to a novel environment in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A, B) Open field test. (A) The total distance moved was less in Slitrk6-KO than in WT mice (left). The distance moved in the first 5 min of the test was significantly lower in Slitrk6-KO mice (right). (B) In Slitrk6-KO mice, the total time spent in the center area was greater than that of the WT (left) and was significantly increased in the first 5 min of the test (right). (C–G) Hole-board test. There were no significant differences in distance moved (C), number of rearing episodes (D), and number of head dips (E) between Slitrk6-KO and WT mice. Duration per head dip was significantly decreased in Slitrk6-KO mice (F). Latency time to head dip was significantly decreased in KO mice (G). Values are mean ± standard error of the mean. *P
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Vestibular function anomaly in Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:(A) Dynamic characteristics of horizontal optokinetic response (hOKR) of WT (n = 9) and Slitrk6-KO (n = 9) mice. (B) Horizontal vestibulo-ocular reflex (hVOR). There were no differences in gains (left) or phases (right) between WT (n = 9) and KO (n = 9) in hVOR or hOKR. (C) Vertical vestibulo-ocular reflex (vVOR) of WT (n = 8) and Slitrk6-KO mice (n = 6). Gains of vVOR (left) of the Slitrk6-KO mice were significantly smaller than those of WT. (D) Rota- rod test. Rotation indicates the speed of rotation (rpm) at which the mice fell off or revolved around the rod. The values were comparable between WT (n = 12) and Slitrk6-KO (n = 8) mice, suggesting that there were no strong deficits of balancing function in Slitrk6-KO mice. Values are mean ± standard error of the mean.
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Summary of Slitrk6 KO behavioral analyses.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:Summary of Slitrk6 KO behavioral analyses.
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Normal anxiety level of Slitrk6-KO mice.
2013Co-Authors: Yoshifumi Matsumoto, Kei-ichi Katayama, Takehito Okamoto, Kazuyuki Yamada, Noriko Takashima, Soichi Nagao, Jun ArugaAbstract:Normal anxiety level of Slitrk6-KO mice.
Alfredo Berardelli - One of the best experts on this subject based on the ideXlab platform.
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psychopathological features of obsessive compulsive disorder in an italian family with gilles de la tourette syndrome not linked to the SLITRK1 gene
Psychiatry Research-neuroimaging, 2008Co-Authors: Massimo Pasquini, Giovanni Fabbrini, Isabella Berardelli, Vincenzo Bonifati, Massimo Biondi, Alfredo BerardelliAbstract:We report the psychopathological features in a large Italian family with Gilles de la Tourette syndrome not linked to the SLITRK1 gene. Of the 23 living family members, 14 were evaluated using the Structured Clinical Interview for DSM-IV, the Yale-Brown Obsessive-Compulsive Scale, the Clinical Global Impression and the Global Assessment of Functioning scale. Ten patients were found to have obsessive-compulsive disorder in which tic-like compulsions predominated. The distinctive feature of this family is the high frequency of obsessive-compulsive disorder with various clinical phenotypes.
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a large italian family with gilles de la tourette syndrome clinical study and analysis of the SLITRK1 gene
Movement Disorders, 2007Co-Authors: Giovanni Fabbrini, Massimo Pasquini, Cinzia Aurilia, Isabella Berardelli, Guido J Breedveld, Ben A Oostra, Vincenzo Bonifati, Alfredo BerardelliAbstract:Our objective was to report the clinical characteristics and to investigate the role of SLITRK1 gene in a large Italian family with Tourette syndrome (TS). The diagnosis of TS and chronic motor tics (CMT) was made according to "The Tourette Syndrome Classification Study Group" (1993). Psychiatric diagnoses were made by administering the Structured Clinical Interview for DSM and the Yale-Brown Obsessive Compulsive Scale. Genetic study included direct sequencing and copy number analysis of the SLITRK1 gene, and haplotype analysis. We found tics or other behavioral manifestations in 15 subjects. Of these, 5 received a diagnosis of definite TS, 5 were classified as having definite CMT, 2 had definite nonspecific tic disorder, and 3 patients had obsessive-compulsive disorder without motor or phonic tics. Tics mainly involved the cranio-cervical district. Many patients with tics had coexisting psychiatric disorders, especially obsessive-compulsive disorder, performed poorly at school and had social problems. Direct sequencing and copy number analysis of the SLITRK1 gene, and haplotype analysis suggested that the SLITRK1 locus was not involved in this family. In conclusion, the distinctive clinical features in this family are the motor tics mainly involving the face and the neck and the severe coexisting psychiatric disorders. The negative results of the SLITRK1 analysis point to genetic heterogeneity in TS.
Jungyong Nam - One of the best experts on this subject based on the ideXlab platform.
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structural basis for lar rptp slitrk complex mediated synaptic adhesion
Nature Communications, 2014Co-Authors: Kee Hun Kim, Beom Seok Park, Yeonsoo Choi, Doyoun Kim, Cha Yeon Kim, Soo Jin Kim, Seong-gyu Lee, M N Kim, Gayoung Choii, Jungyong NamAbstract:Synaptic adhesion molecules orchestrate synaptogenesis. The presynaptic leukocyte common antigen-related receptor protein tyrosine phosphatases (LAR-RPTPs) regulate synapse development by interacting with postsynaptic Slit- and Trk-like family proteins (Slitrks), which harbour two extracellular leucine-rich repeats (LRR1 and LRR2). Here we identify the minimal regions of the LAR-RPTPs and Slitrks, LAR-RPTPs Ig1-3 and Slitrks LRR1, for their interaction and synaptogenic function. Subsequent crystallographic and structure-guided functional analyses reveal that the splicing inserts in LAR-RPTPs are key molecular determinants for Slitrk binding and synapse formation. Moreover, structural comparison of the two SLITRK1 LRRs reveal that unique properties on the concave surface of SLITRK1 LRR1 render its specific binding to LAR-RPTPs. Finally, we demonstrate that lateral interactions between adjacent trans-synaptic LAR-RPTPs/Slitrks complexes observed in crystal lattices are critical for SLITRK1-induced lateral assembly and synaptogenic activity. Thus, we propose a model in which Slitrks mediate synaptogenic functions through direct binding to LAR-RPTPs and the subsequent lateral assembly of LAR-RPTPs/Slitrks complexes.
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Slitrks control excitatory and inhibitory synapse formation with LAR receptor protein tyrosine phosphatases
Proceedings of the National Academy of Sciences of the United States of America, 2013Co-Authors: Yeong Shin Yim, Jungyong Nam, Eunjoon Kim, Younghee Kwon, Hong In Yoon, Kangduk Lee, Dong Goo Kim, Chul Hoon KimAbstract:The balance between excitatory and inhibitory synaptic inputs, which is governed by multiple synapse organizers, controls neural circuit functions and behaviors. Slit- and Trk-like proteins (Slitrks) are a family of synapse organizers, whose emerging synaptic roles are incompletely understood. Here, we report that Slitrks are enriched in postsynaptic densities in rat brains. Overexpression of Slitrks promoted synapse formation, whereas RNAi-mediated knockdown of Slitrks decreased synapse density. Intriguingly, Slitrks were required for both excitatory and inhibitory synapse formation in an isoform-dependent manner. Moreover, Slitrks required distinct members of the leukocyte antigen-related receptor protein tyrosine phosphatase (LAR-RPTP) family to trigger synapse formation. Protein tyrosine phosphatase σ (PTPσ), in particular, was specifically required for excitatory synaptic differentiation by Slitrks, whereas PTPδ was necessary for inhibitory synapse differentiation. Taken together, these data suggest that combinatorial interactions of Slitrks with LAR-RPTP family members maintain synapse formation to coordinate excitatory–inhibitory balance.