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162 results on '"Hu, Jia‐Hua"'

4. Influence of the substituents of the thiol ligand on the optical properties of AuCu14.

Author

Zhao, Yu-Jing, Yang, Jin-Sen, Li, Jing, Si, Yu-Bing, Xiao, Lu-Yao, Wang, Zhao-Yang, Hu, Jia-Hua, Dong, Xi-Yan, and Zang, Shuang-Quan

Subjects
LIGANDS (Chemistry), OPTICAL properties, POLAR effects (Chemistry), CRYSTALS
Abstract

Detailed photophysical processes of two AuCu14 clusters with different substituents (–F or –C(CH3)3) of the thiol ligand were studied in this work. The electronic effect of the substituents led to structural shrinkage, thus enhancing the luminous intensity. The internal conversion (IC) and intersystem crossing (ISC) rates in the AuCu14-C(CH3)3 crystal were slower compared with the AuCu14-F crystal, which was caused by the steric effect. [ABSTRACT FROM AUTHOR]

Published
2024
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6. Behavioral and Neurochemical Phenotyping of Mice Incapable of Homer1a Induction

Author

Datko, Michael C, Hu, Jia-Hua, Williams, Melanie, Reyes, Cindy M, Lominac, Kevin D, von Jonquieres, Georg, Klugmann, Matthias, Worley, Paul F, and Szumlinski, Karen K

Subjects
Basic Behavioral and Social Science, Genetics, Brain Disorders, Behavioral and Social Science, Drug Abuse (NIDA only), Substance Misuse, Neurosciences, Aetiology, 2.1 Biological and endogenous factors, Mental health, Good Health and Well Being, Homer1a, cocaine, glutamate, dopamine, nucleus accumbens, anxiety, sensitization, Psychology, Cognitive Sciences
Abstract

Immediate early and constitutively expressed products of the Homer1 gene regulate the functional assembly of post-synaptic density proteins at glutamatergic synapses to influence excitatory neurotransmission and synaptic plasticity. Earlier studies of Homer1 gene knock-out (KO) mice indicated active, but distinct, roles for IEG and constitutively expressed Homer1 gene products in regulating cognitive, emotional, motivational and sensorimotor processing, as well as behavioral and neurochemical sensitivity to cocaine. More recent characterization of transgenic mice engineered to prevent generation of the IEG form (a.k.a Homer1a KO) pose a critical role for Homer1a in cocaine-induced behavioral and neurochemical sensitization of relevance to drug addiction and related neuropsychiatric disorders. Here, we extend our characterization of the Homer1a KO mouse and report a modest pro-depressant phenotype, but no deleterious effects of the KO upon spatial learning/memory, prepulse inhibition, or cocaine-induced place-conditioning. As we reported previously, Homer1a KO mice did not develop cocaine-induced behavioral or neurochemical sensitization within the nucleus accumbens; however, virus-mediated Homer1a over-expression within the nucleus accumbens reversed the sensitization phenotype of KO mice. We also report several neurochemical abnormalities within the nucleus accumbens of Homer1a KO mice that include: elevated basal dopamine and reduced basal glutamate content, Group1 mGluR agonist-induced glutamate release and high K+-stimulated release of dopamine and glutamate within this region. Many of the neurochemical anomalies exhibited by Homer1a KO mice are recapitulated upon deletion of the entire Homer1 gene; however, Homer1 deletion did not affect NAC dopamine or alter K+-stimulated neurotransmitter release within this region. These data show that the selective deletion of Homer1a produces a behavioral and neurochemical phenotype that is distinguishable from that produced by deletion of the entire Homer1 gene. Moreover, the data indicate a specific role for Homer1a in regulating cocaine-induced behavioral and neurochemical sensitization of potential relevance to the psychotogenic properties of this drug.

Published
2017

7. Staggered Assembly of a Dimeric Au13 Cluster: Impacts on Coupling of Geometric Isomerism.

Author

Yang, Jin‐Sen, Zhao, Yu‐Jing, Li, Xin‐Mao, Dong, Xi‐Yan, Si, Yu‐Bing, Xiao, Lu‐Yao, Hu, Jia‐Hua, Yu, Zhihao, and Zang, Shuang‐Quan

Subjects
CONFORMATIONAL isomerism, GOLD clusters, LIGHT absorption, OPTICAL properties, GEOMETRIC connections, ELECTRONIC structure, PHOSPHORESCENCE spectroscopy, PHOTOINDUCED electron transfer
Abstract

The specific states of aggregation of metal atoms in sub‐nanometer‐sized gold clusters are related to the different quantum confinement volumes of electrons, leading to novel optical and electronic properties. These volumes can be tuned by changing the relative positions of the gold atoms to generate isomers. Studying the isomeric gold core and the electron coupling between the basic units is fundamentally important for nanoelectronic devices and luminescence; however, appropriate cases are lacking. In this study, the structure of the first staggered di‐superatomic Au25‐S was solved using single‐crystal X‐ray diffraction. The optical properties of Au25‐S were studied by comparing with eclipsed Au25‐E. From Au25‐E to Au25‐S, changes in the electronic structures occurred, resulting in significantly different optical absorptions originating from the coupling between the two Au13 modules. Au25‐S shows a longer electron decay lifetime of 307.7 ps before populating the lowest triplet emissive state, compared to 1.29 ps for Au25‐E. The experimental and theoretical results show that variations in the geometric isomerism lead to distinct photophysical processes owing to isomerism‐dependent electronic coupling. This study offers new insights into the connection between the geometric isomerism of nanosized building blocks and the optical properties of their assemblies, opening new possibilities for constructing function‐specific nanomaterials. [ABSTRACT FROM AUTHOR]

Published
2024
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8. Protein Kinase C Epsilon Activity in the Nucleus Accumbens and Central Nucleus of the Amygdala Mediates Binge Alcohol Consumption

Author

Cozzoli, Debra K, Courson, Justin, Rostock, Charlotte, Campbell, Rianne R, Wroten, Melissa G, McGregor, Hadley, Caruana, Amanda L, Miller, Bailey W, Hu, Jia-Hua, Zhang, Ping Wu, Xiao, Bo, Worley, Paul F, Crabbe, John C, Finn, Deborah A, and Szumlinski, Karen K

Subjects
Substance Misuse, Alcoholism, Alcohol Use and Health, Pediatric, Underage Drinking, Cardiovascular, Stroke, Oral and gastrointestinal, Cancer, Good Health and Well Being, Animals, Binge Drinking, Central Amygdaloid Nucleus, Ethanol, Mice, Mice, Inbred C57BL, Mice, Transgenic, Nucleus Accumbens, Protein Kinase C-epsilon, Receptors, Metabotropic Glutamate, Signal Transduction, Alcohol use disorders, Drinking in the dark, Glutamate, HDID-1 mice, Homer, Scheduled high alcohol consumption, Biological Sciences, Medical and Health Sciences, Psychology and Cognitive Sciences, Psychiatry
Abstract

BackgroundProtein kinase C epsilon (PKCε) is emerging as a potential target for the development of pharmacotherapies to treat alcohol use disorders, yet little is known regarding how a history of a highly prevalent form of drinking, binge alcohol intake, influences enzyme priming or the functional relevance of kinase activity for excessive alcohol intake.MethodsImmunoblotting was employed on tissue from subregions of the nucleus accumbens (NAc) and the amygdala to examine both idiopathic and binge drinking-induced changes in constitutive PKCε priming. The functional relevance of PKCε translocation for binge drinking and determination of potential upstream signaling pathways involved were investigated using neuropharmacologic approaches within the context of two distinct binge drinking procedures, drinking in the dark and scheduled high alcohol consumption.ResultsBinge alcohol drinking elevated p(Ser729)-PKCε levels in both the NAc and the central nucleus of the amygdala (CeA). Moreover, immunoblotting studies of selectively bred and transgenic mouse lines revealed a positive correlation between the propensity to binge drink alcohol and constitutive p(Ser729)-PKCε levels in the NAc and CeA. Finally, neuropharmacologic inhibition of PKCε translocation within both regions reduced binge alcohol consumption in a manner requiring intact group 1 metabotropic glutamate receptors, Homer2, phospholipase C, and/or phosphotidylinositide-3 kinase function.ConclusionsTaken together, these data indicate that PKCε signaling in both the NAc and CeA is a major contributor to binge alcohol drinking and to the genetic propensity to consume excessive amounts of alcohol.

Published
2016

10. A Prolyl-Isomerase Mediates Dopamine-Dependent Plasticity and Cocaine Motor Sensitization

Author

Park, Joo Min, Hu, Jia-Hua, Milshteyn, Aleksandr, Zhang, Ping-Wu, Moore, Chester G, Park, Sungjin, Datko, Michael C, Domingo, Racquel D, Reyes, Cindy M, Wang, Xiaodong J, Etzkorn, Felicia A, Xiao, Bo, Szumlinski, Karen K, Kern, Dorothee, Linden, David J, and Worley, Paul F

Subjects
Neurosciences, Basic Behavioral and Social Science, Drug Abuse (NIDA only), Substance Misuse, Behavioral and Social Science, Brain Disorders, Neurological, Good Health and Well Being, Amino Acid Sequence, Animals, Brain, Carrier Proteins, Cocaine, Cocaine-Related Disorders, Dopamine, Embryo, Mammalian, Homer Scaffolding Proteins, Long-Term Potentiation, Mice, Molecular Sequence Data, NIMA-Interacting Peptidylprolyl Isomerase, Peptidylprolyl Isomerase, Phosphorylation, Receptors, AMPA, Receptors, Dopamine D1, Receptors, Kainic Acid, Receptors, N-Methyl-D-Aspartate, Synapses, Biological Sciences, Medical and Health Sciences, Developmental Biology
Abstract

Synaptic plasticity induced by cocaine and other drugs underlies addiction. Here we elucidate molecular events at synapses that cause this plasticity and the resulting behavioral response to cocaine in mice. In response to D1-dopamine-receptor signaling that is induced by drug administration, the glutamate-receptor protein metabotropic glutamate receptor 5 (mGluR5) is phosphorylated by microtubule-associated protein kinase (MAPK), which we show potentiates Pin1-mediated prolyl-isomerization of mGluR5 in instances where the product of an activity-dependent gene, Homer1a, is present to enable Pin1-mGluR5 interaction. These biochemical events potentiate N-methyl-D-aspartate receptor (NMDAR)-mediated currents that underlie synaptic plasticity and cocaine-evoked motor sensitization as tested in mice with relevant mutations. The findings elucidate how a coincidence of signals from the nucleus and the synapse can render mGluR5 accessible to activation with consequences for drug-induced dopamine responses and point to depotentiation at corticostriatal synapses as a possible therapeutic target for treating addiction.

Published
2013

20. Silver Cluster‐Porphyrin‐Assembled Materials as Advanced Bioprotective Materials for Combating Superbacteria.

Author

Cao, Man, Wang, Shan, Hu, Jia‐Hua, Lu, Bing‐Huai, Wang, Qian‐You, and Zang, Shuang‐Quan

Subjects
METHICILLIN-resistant staphylococcus aureus, BACTERIAL inactivation, REACTIVE oxygen species, SILVER, PERSONAL protective equipment, METAL clusters, SILVER nanoparticles
Abstract

Superbugs are bacteria that have grown resistant to most antibiotics, seriously threating the health of people. Silver (Ag) nanoparticles are known to exert a wide‐spectrum antimicrobial property, yet remains challenging against superbugs. Here, Ag clusters are assembled using porphyrin‐based linkers and a novel framework structure (Ag9‐AgTPyP) is produced, in which nine‐nuclearity Ag9 clusters are uniformly separated by Ag‐centered porphyrin units (AgTPyP) in two dimensions, demonstrating open permeant porosity. Ag9‐AgTPyP eliminates over 99.99999% and 99.999% methicillin‐resistant Staphylococcus aureus (MRSA) and Pseudomonas aeruginosa (P. aeruginosa) within 2 h upon visible‐light irradiation, which are superior to a majority of bacteria inactivation photocatalysts. The novel‐established long‐term charge‐transfer states from AgTPyP to adjacent Ag9 cluster that has preferential affinity to O2 greatly promote reactive oxygen species (ROS) production efficiency; and its unique framework accelerates the ROS transportation. Personal protective equipment (masks and protective suits) incorporating Ag9‐AgTPyP film also shows excellent performances against superbugs. This superbugs‐killing efficiency is unprecedented among silver complexes and porphyrin derivatives. Utilizing efficient photogenerated electrons and holes between metal cluster and linkers can open up new interests of research in photocatalytic areas. [ABSTRACT FROM AUTHOR]

Published
2022
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22. Identification of circRNA–miRNA networks for exploring an underlying prognosis strategy for breast cancer

Author

Yang, Su-jin, primary, Wang, Dan-dan, additional, Zhou, Si-ying, additional, Zhang, Qian, additional, Wang, Jin-yan, additional, Zhong, Shan-liang, additional, Zhang, He-da, additional, Wang, Xing-yun, additional, Xia, Xing, additional, Chen, Wei, additional, Yang, Su-yu, additional, Hu, Jia-hua, additional, Zhao, Jian-hua, additional, and Tang, Jin-hai, additional

Published
2020
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27. Circular RNA circASS1 is downregulated in breast cancer cells MDA-MB-231 and suppressed invasion and migration

Author

Hou, Jun-chen, primary, Xu, Zhi, additional, Zhong, Shan-liang, additional, Zhang, He-da, additional, Jiang, Lin-hong, additional, Chen, Xiu, additional, Zhu, Ling-ping, additional, Li, Jian, additional, Zhou, Si-ying, additional, Yang, Su-jin, additional, He, Yun-jie, additional, Wang, Dan-dan, additional, Deng, Fei, additional, Zhang, Qian, additional, Wang, Jin-yan, additional, Hu, Jia-hua, additional, Zhang, Wei, additional, Wu, Yang, additional, Ding, Li, additional, Zhao, Jian-hua, additional, and Tang, Jin-hai, additional

Published
2019
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28. MiR-29a: a potential therapeutic target and promising biomarker in tumors

Author

Wang, Jin-yan, primary, Zhang, Qian, additional, Wang, Dan-dan, additional, Yan, Wei, additional, Sha, Huan-huan, additional, Zhao, Jian-hua, additional, Yang, Su-jin, additional, Zhang, He-da, additional, Hou, Jun-chen, additional, Xu, Han-zi, additional, He, Yun-jie, additional, Hu, Jia-hua, additional, Zhong, Shan-liang, additional, and Tang, Jin-hai, additional

Published
2018
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29. FRMPD4 mutations cause X-linked intellectual disability and disrupt dendritic spine morphogenesis

Author

Piard, Juliette, primary, Hu, Jia-Hua, additional, Campeau, Philippe M, additional, Rzońca, Sylwia, additional, Van Esch, Hilde, additional, Vincent, Elizabeth, additional, Han, Mei, additional, Rossignol, Elsa, additional, Castaneda, Jennifer, additional, Chelly, Jamel, additional, Skinner, Cindy, additional, Kalscheuer, Vera M, additional, Wang, Ruihua, additional, Lemyre, Emmanuelle, additional, Kosińska, Joanna, additional, Stawinski, Piotr, additional, Bal, Jerzy, additional, Hoffman, Dax A, additional, Schwartz, Charles E, additional, Van Maldergem, Lionel, additional, Wang, Tao, additional, and Worley, Paul F, additional

Published
2017
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31. The role of circRNAs in cancers

Author

Zhu, Ling-Ping, primary, He, Yun-Jie, additional, Hou, Jun-Chen, additional, Chen, Xiu, additional, Zhou, Si-Ying, additional, Yang, Su-Jin, additional, Li, Jian, additional, Zhang, He-Da, additional, Hu, Jia-Hua, additional, Zhong, Shan-Liang, additional, Zhao, Jian-Hua, additional, and Tang, Jin-Hai, additional

Published
2017
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34. Enhanced polyubiquitination of Shank3 and NMDA receptor in a mouse model of autism

Author

Bangash, M Ali, Park, Joo Min, Melnikova, Tatiana, Wang, Dehua, Jeon, Soo Kyeong, Lee, Deidre, Syeda, Sbaa, Kim, Juno, Kouser, Mehreen, Schwartz, Joshua, Cui, Yiyuan, Zhao, Xia, Speed, Haley E., Kee, Sara E., Tu, Jian Cheng, Hu, Jia-Hua, Petralia, Ronald S., Linden, David J., Powell, Craig M., Savonenko, Alena, Xiao, Bo, and Worley, Paul F.

Subjects
Long-Term Synaptic Depression, Long-Term Potentiation, Microfilament Proteins, Ubiquitination, Nerve Tissue Proteins, Receptors, Metabotropic Glutamate, Hippocampus, Receptors, N-Methyl-D-Aspartate, Article, Disease Models, Animal, Mice, nervous system, Synapses, Animals, Humans, Interpersonal Relations, Autistic Disorder, Carrier Proteins
Abstract

We have created a mouse genetic model that mimics a human mutation of Shank3 that deletes the C terminus and is associated with autism. Expressed as a single copy [Shank3(+/ΔC) mice], Shank3ΔC protein interacts with the wild-type (WT) gene product and results in90% reduction of Shank3 at synapses. This "gain-of-function" phenotype is linked to increased polyubiquitination of WT Shank3 and its redistribution into proteasomes. Similarly, the NR1 subunit of the NMDA receptor is reduced at synapses with increased polyubiquitination. Assays of postsynaptic density proteins, spine morphology, and synapse number are unchanged in Shank3(+/ΔC) mice, but the amplitude of NMDAR responses is reduced together with reduced NMDAR-dependent LTP and LTD. Reciprocally, mGluR-dependent LTD is markedly enhanced. Shank3(+/ΔC) mice show behavioral deficits suggestive of autism and reduced NMDA receptor function. These studies reveal a mechanism distinct from haploinsufficiency by which mutations of Shank3 can evoke an autism-like disorder.

Published
2010

36. Homers at the Interface between Reward and Pain

Author

Obara, Ilona, primary, Goulding, Scott P., additional, Gould, Adam T., additional, Lominac, Kevin D., additional, Hu, Jia-Hua, additional, Zhang, Ping Wu, additional, von Jonquieres, Georg, additional, Dehoff, Marlin, additional, Xiao, Bo, additional, Seeburg, Peter H., additional, Worley, Paul F., additional, Klugmann, Matthias, additional, and Szumlinski, Karen K., additional

Published
2013
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37. Retraction Notice to: Enhanced Polyubiquitination of Shank3 and NMDA Receptor in a Mouse Model of Autism

Author

Bangash, M. Ali, primary, Park, Joo Min, additional, Melnikova, Tatiana, additional, Wang, Dehua, additional, Jeon, Soo Kyeong, additional, Lee, Deidre, additional, Syeda, Sbaa, additional, Kim, Juno, additional, Kouser, Mehreen, additional, Schwartz, Joshua, additional, Cui, Yiyuan, additional, Zhao, Xia, additional, Speed, Haley E., additional, Kee, Sara E., additional, Tu, Jian Cheng, additional, Hu, Jia-Hua, additional, Petralia, Ronald S., additional, Linden, David J., additional, Powell, Craig M., additional, Savonenko, Alena, additional, Xiao, Bo, additional, and Worley, Paul F., additional

Published
2013
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38. Preso1 dynamically regulates group I metabotropic glutamate receptors

Author

Hu, Jia-Hua, primary, Yang, Linlin, additional, Kammermeier, Paul J, additional, Moore, Chester G, additional, Brakeman, Paul R, additional, Tu, Jiancheng, additional, Yu, Shouyang, additional, Petralia, Ronald S, additional, Li, Zhe, additional, Zhang, Ping-Wu, additional, Park, Joo Min, additional, Dong, Xinzhong, additional, Xiao, Bo, additional, and Worley, Paul F, additional

Published
2012
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39. Role of Homer Proteins in the Maintenance of Sleep-Wake States

Author

Naidoo, Nirinjini, primary, Ferber, Megan, additional, Galante, Raymond J., additional, McShane, Blake, additional, Hu, Jia Hua, additional, Zimmerman, John, additional, Maislin, Greg, additional, Cater, Jacqui, additional, Wyner, Abraham, additional, Worley, Paul, additional, and Pack, Allan I., additional

Published
2012
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41. RETRACTED: Enhanced Polyubiquitination of Shank3 and NMDA Receptor in a Mouse Model of Autism

Author

Bangash, M Ali, primary, Park, Joo Min, additional, Melnikova, Tatiana, additional, Wang, Dehua, additional, Jeon, Soo Kyeong, additional, Lee, Deidre, additional, Syeda, Sbaa, additional, Kim, Juno, additional, Kouser, Mehreen, additional, Schwartz, Joshua, additional, Cui, Yiyuan, additional, Zhao, Xia, additional, Speed, Haley E., additional, Kee, Sara E., additional, Tu, Jian Cheng, additional, Hu, Jia-Hua, additional, Petralia, Ronald S., additional, Linden, David J., additional, Powell, Craig M., additional, Savonenko, Alena, additional, Xiao, Bo, additional, and Worley, Paul F., additional

Published
2011
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42. Disrupted mGluR5-Homer scaffolds mediate abnormal mGluR5 signaling, circuit function and behavior in a mouse model of Fragile X Syndrome

Author

Ronesi, Jennifer A., Collins, Katie A., Hays, Seth A., Tsai, Nien-Pei, Guo, Weirui, Birnbaum, Shari G., Hu, Jia-Hua, Worley, Paul F., Gibson, Jay R., and Huber, Kimberly M.

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, Patch-Clamp Techniques, animal diseases, Receptor, Metabotropic Glutamate 5, Long-Term Potentiation, translation, Mice, Transgenic, In Vitro Techniques, Receptors, Metabotropic Glutamate, Hippocampus, Article, Methoxyhydroxyphenylglycol, Fragile X Mental Retardation Protein, Mice, Homer Scaffolding Proteins, mental disorders, Homer1a, neocortex, Serine, Animals, Immunoprecipitation, long-term depression, Rats, Long-Evans, Cycloheximide, group I mGluRs, PI3 Kinase, Protein Synthesis Inhibitors, UP states, Analysis of Variance, Physics, TOR Serine-Threonine Kinases, EF2 Kinase, Electric Stimulation, Rats, Mice, Inbred C57BL, ERK, Disease Models, Animal, nervous system, Gene Expression Regulation, Fragile X Syndrome, Mutation, mTOR, Exploratory Behavior, Nerve Net, Carrier Proteins, Peptides, Signal Transduction
Abstract

Enhanced metabotropic glutamate receptor subunit 5 (mGluR5) function is causally associated with the pathophysiology of fragile X syndrome, a leading inherited cause of intellectual disability and autism. Here we provide evidence that altered mGluR5-Homer scaffolds contribute to mGluR5 dysfunction and phenotypes in the fragile X syndrome mouse model, Fmr1 knockout (Fmr1(-/y)). In Fmr1(-/y) mice, mGluR5 was less associated with long Homer isoforms but more associated with the short Homer1a. Genetic deletion of Homer1a restored mGluR5-long Homer scaffolds and corrected several phenotypes in Fmr1(-/y) mice, including altered mGluR5 signaling, neocortical circuit dysfunction and behavior. Acute, peptide-mediated disruption of mGluR5-Homer scaffolds in wild-type mice mimicked many Fmr1(-/y) phenotypes. In contrast, Homer1a deletion did not rescue altered mGluR-dependent long-term synaptic depression or translational control of target mRNAs of fragile X mental retardation protein, the gene product of Fmr1. Our findings reveal new functions for mGluR5-Homer interactions in the brain and delineate distinct mechanisms of mGluR5 dysfunction in a mouse model of cognitive dysfunction and autism.

Published
2012

43. Homeostatic Scaling Requires Group I mGluR Activation Mediated by Homer1a

Author

Hu, Jia-Hua, primary, Park, Joo Min, additional, Park, Sungjin, additional, Xiao, Bo, additional, Dehoff, Marlin H., additional, Kim, Sangmok, additional, Hayashi, Takashi, additional, Schwarz, Martin K., additional, Huganir, Richard L., additional, Seeburg, Peter H., additional, Linden, David J., additional, and Worley, Paul F., additional

Published
2010
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