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| There are 27 papers published in subject: > since this site started. | |||
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| 1. Tyrosine hydroxylase (TH) upstream-inhibited UPF3 regulator of nonsense transcripts homolog A (UPF3A) subnetwork for learning in human left hemisphere|Prostate via nucleus to mitochondrion to cytosol RNA binding | |||
| Xi Ruipeng,HUANG Juxiang,WANG Lin | |||
Biology 14 September 2020
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| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:High tyrosine hydroxylase (TH) upstream-inhibited UPF3 regulator of nonsense transcripts homolog A (yeast) (UPF3A) molecular subnetwork was constructed, including upstream hypothetical LOC400642 (LOC400642), retinoblastoma binding protein 6 (RBBP6), ubiquitin protein ligase E3 component n-recognin 5 (UBR5); downstream chromosome 10 open reading frame 10 (C10orf10), sulfotransferase family 1A member 2 (SULT1A2) reported relation with learning in human left hemisphere. The common biology process of TH upstream-inhibited UPF3A subnetwork was identified by DAVID, containing upstream RBBP6, upstream UBR5, downstream SULT1A2, second-core UPF3A, first-core TH as protein binding; upstream RBBP6, upstream UBR5 as ubiquitin protein transferase activity, zinc ion binding, ligase activity, cellular response to DNA damage stimulus, protein ubiquitination involved in ubiquitin dependent protein catabolic process; upstream UBR5, second-core UPF3A as RNA binding; downstream SULT1A2, first-core TH as small molecule metabolic process; The common cellular component of upstream RBBP6, upstream UBR5, second-core UPF3A, first-core TH as cytoplasm; upstream RBBP6, upstream UBR5, second-core UPF3A as nucleoplasm; upstream UBR5, second-core UPF3A, first-core TH as nucleus; downstream SULT1A2, second-core UPF3A, first-core TH as cytosol; downstream C10orf10, first-core TH as mitochondrion; The common tissue distributions as Prostate_3rd maybe exist the same pattern with human left hemisphere. We propose and mutual positively verify tyrosine hydroxylase (TH) upstream-inhibited UPF3 regulator of nonsense transcripts homolog A (yeast) (UPF3A) subnetwork for learning in human left hemisphere|Prostate via nucleus to mitochondrion to cytosol RNA binding. | |||
| TO cite this article:Xi Ruipeng,HUANG Juxiang,WANG Lin. Tyrosine hydroxylase (TH) upstream-inhibited UPF3 regulator of nonsense transcripts homolog A (UPF3A) subnetwork for learning in human left hemisphere|Prostate via nucleus to mitochondrion to cytosol RNA binding[OL].[14 September 2020] http://en.paper.edu.cn/en_releasepaper/content/4752808 | |||
| 2. TH upstream-inhibited ARHGAP12 subnetwork for learning in human left hemisphere|CD8+T cells|PLACENTA via cytosol positive regulation of transcription | |||
| CUI Xuelei,WANG Lin,HUANG Juxiang | |||
| Biology 21 December 2019 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:High tyrosine hydroxylase (TH) upstream-inhibited Rho GTPase activating protein 12 (ARHGAP12) molecular subnetwork was constructed, including upstream cytoplasmic FMR1 interacting protein 2 (CYFIP2), NCK adaptor protein 2 (NCK2), retinoblastoma binding protein 6 (RBBP6); downstream forkhead box N3 (FOXN3_2), SMAD family member 1 (SMAD1_2), sulfotransferase family 1A member 2 (SULT1A2) reported relation with learning in human left hemisphere. The common biology process of TH upstream-inhibited ARHGAP12 subnetwork was identified by DAVID, containing upstream CYFIP2, upstream NCK2, upstream RBBP6, downstream FOXN3_2, downstream SMAD1_2, downstream SULT1A2, first-core TH as protein binding; upstream CYFIP2, second-core ARHGAP12 as small GTPase mediated signal transduction; upstream CYFIP2, upstream NCK2 as vascular endothelial growth factor receptor signaling pathway; upstream NCK2, downstream SMAD1_2 as signal transduction, negative regulation of cell proliferation, positive regulation of transcription from RNA polymerase II promoter; upstream NCK2, second-core ARHGAP12 as positive regulation of GTPase activity; downstream FOXN3_2, downstream SMAD1_2 as transcription factor activity sequence specific DNA binding; downstream SULT1A2, first-core TH as small molecule metabolic process; The corresponding common cellular component of upstream CYFIP2, upstream NCK2, downstream SMAD1_2, downstream SULT1A2, second-core ARHGAP12, first-core TH as cytosol; upstream CYFIP2, upstream NCK2, upstream RBBP6, downstream SMAD1_2, first-core TH as cytoplasm. The corresponding common tissue distributions as CD8+T cells_3rd, PLACENTA_3rd maybe exist the same pattern with human left hemisphere. We propose and mutual positively verify tyrosine hydroxylase (TH) upstream-inhibited Rho GTPase activating protein 12 (ARHGAP12) subnetwork for learning in human left hemisphere|CD8+T cells|PLACENTA via cytosol positive regulation of transcription. | |||
| TO cite this article:CUI Xuelei,WANG Lin,HUANG Juxiang. TH upstream-inhibited ARHGAP12 subnetwork for learning in human left hemisphere|CD8+T cells|PLACENTA via cytosol positive regulation of transcription[OL].[21 December 2019] http://en.paper.edu.cn/en_releasepaper/content/4750284 | |||
| 3. Anatomic construction and physiological functions of medial cerebellar nucleus | |||
| Xiao-Yang Zhang,Wing-Ho Yung,Jian-Jun Wang,Jing-Ning Zhu | |||
Biology 24 April 2017
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| Abstract:Medial cerebellar nucleus (MN) is the phylogenetically oldest nucleus in the cerebellum, a classical subcortical motor coordinator. As one of the ultimate integration stations and outputs of the spinocerebellum, the MN holds a key position in the axial, proximal and ocular motor control by projecting to the medial descending systems and eye movement related nuclei. Furthermore, through topographic connections with extensive nonmotor systems, including visceral related nuclei in the brain stem, hypothalamus as well as the limbic system, MN has also been implicated in regulation of various nonsomatic functions, such as feeding, cardiovascular and respiratory, defecation and micturition, immune, as well as emotional activities. In clinic, MN lesion or dysfunction results in motor deficits including spinocerebellar ataxias, and nonmotor symptoms. In this review, we summarize the cytoarchitecture, anatomic afferent and efferent connections, as well as the motor and nonmotor functions of the MN and the related diseases and disorders. We suggest that by bridging the motor and nonmotor systems, the cerebellar MN may help to integrate somatic motor and nonsomatic functions and consequently contribute to generate a coordinated response to internal and external environments. | |||
| TO cite this article:Xiao-Yang Zhang,Wing-Ho Yung,Jian-Jun Wang, et al. Anatomic construction and physiological functions of medial cerebellar nucleus[OL].[24 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4728741 | |||
| 4. A new transgenic mouse model of spinal cord injury | |||
| LI Cheng,LIU Yaobo | |||
Biology 04 April 2017
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| Abstract:Objective: To explore a new model for the study of spinal cord injury, and to prove the possibility of this model. Methods: The Thy1( thymus cell antigen 1, theta)-YFPH transgenic mice and DiI tracing were employed to observe the distribution of corticospinal tract (CST). And lateral spinal cord hemisection injury model was made using the Thy1-YFPH mice. Results: Pyramidal neurons in cerebral cortex layer Ⅴ was specifically labeled and projected to pyramidal decussation in the medulla. In the spinal cord, the YFP labeled projections were distributed at the same locations as dorsal CST (dCST), dorsolateral CST (dlCST) and ventral CST (vCST). YFP positive axons were mostly colocalized with DiI traced dCST both in the spinal cord of uninjured Thy1-YFPH mice. Conclusion: The Thy1-YFPH mice could label the CST in the mouse spinal cord, and could be used as an easy and convenient model to monitor the degeneration, regeneration and remodeling of CST axons after spinal cord injury. | |||
| TO cite this article:LI Cheng,LIU Yaobo. A new transgenic mouse model of spinal cord injury[OL].[ 4 April 2017] http://en.paper.edu.cn/en_releasepaper/content/4724205 | |||
| 5. Blocking Beta2-adrenergic Receptor Reduced Ischemia-induced Blood Brain Barrier Bamage by Regulating Hypoxia-inducible factor-1 alpha Expression during Acute Cerebral Ischemia | |||
| Sun Yanyun,Zhang Xinyu,Shen Xianzhi,Jin Xinchun | |||
| Biology 30 November 2016 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Disruption of the blood brain barrier (BBB) within the thrombolytic time window is an antecedent event to intracerebral hemorrhage in ischemic stroke. Since hypoxia-inducible factor-1 alpha (HIF-1α) was discovered as a mater regulator in hypoxia, we sought to investigate the roles of HIF-1α in BBB damage as well as factors regulating HIF-1α expression after acute ischemia stroke. Our previous research results have showed that pretreatment with HIF-1α inhibitor YC-1 significantly inhibited 2-h MCAO-induced BBB damage by inhibition of occludin degradation and vascular endothelial growth factor (VEGF) mRNA upregulation. Interestingly, blocking beta2-adrenergic receptor (β2-AR) reduced ischemia-induced BBB damage by regulating HIF-1α expression in this research. More important, blocking β2-AR inhibited 2-h OGD-induced HIF-1α upregualtion and reduced occludin degradation induced by OGD-neuron media. Taken together, acute cerebral ischemia disrupts BBB by upregulating HIF-1α and activating the neurons to secret VEGF and MMP-2, while blocking β2-AR inhibited such change. These findings may provide new ideas and strategies to extend the time window of thrombolysis and reduce cerebral hemorrhage. | |||
| TO cite this article:Sun Yanyun,Zhang Xinyu,Shen Xianzhi, et al. Blocking Beta2-adrenergic Receptor Reduced Ischemia-induced Blood Brain Barrier Bamage by Regulating Hypoxia-inducible factor-1 alpha Expression during Acute Cerebral Ischemia[OL].[30 November 2016] http://en.paper.edu.cn/en_releasepaper/content/4712245 | |||
| 6. HIF-1α upregulation-mediated VEGF secretion in contribute to blood brain barrier damage during acute cerebral ischemia | |||
| Sun Yanyun,Wang Xiaona,Wang Mengwei,Jin Xinchun | |||
| Biology 29 November 2016 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Although disruption of the blood brain barrier (BBB) is an antecedent event to intracerebral hemorrhage (ICH) in ischemic stroke, the mechanism of acute BBB disruption within the thrombolytic time window remains less well known. Since hypoxia-inducible factor-1 alpha (HIF-1α) was discovered as a mater regulator in hypoxia, we sought to test our hypothesis that HIF-1α and its downstream vascular endothelial growth factor (VEGF) triggered BBB damage. Using in vivo rat middle cerebral artery occlusion (MCAO) and in vitro oxygen glucose deprivation (OGD) models, our results showed that pretreatment with HIF-1α inhibitor YC-1 significantly inhibited the upregulation of HIF-1α protein and VEGF mRNA as well as occludin degradation and BBB damage in ventral striatum and preoptic area induced by 2-h MCAO. Increased HIF-1α was shown to colocalize with neurons but not astrocytes. Of note, cell study showed that HIF-1α inhibition with YC-1 or siRNA significantly prevented VEGF secretion of neuron promoted by 2-h OGD. Taken together, acute cerebral ischemia led to HIF-1α upregualtion and activated the neurons to secret VEGF, which eventually induced occludin degradation and BBB disruption. These findings may provide new ideas and strategies to extend the time window of thrombolysis and reduce cerebral hemorrhage. | |||
| TO cite this article:Sun Yanyun,Wang Xiaona,Wang Mengwei, et al. HIF-1α upregulation-mediated VEGF secretion in contribute to blood brain barrier damage during acute cerebral ischemia[OL].[29 November 2016] http://en.paper.edu.cn/en_releasepaper/content/4712149 | |||
| 7. Hyperpolarization of outer hair cells: the mechanism underlying urethane-induced cochlear depression | |||
| FU Mingyu,CHEN Mengzi,YAN Xiao,YANG Xueying,XIAO Jinfang,TANG Jie | |||
| Biology 08 May 2016 | |||
| Show/Hide Abstract | Cite this paper︱Full-text: PDF (0 B) | |||
| Abstract:Urethane, a widely used anesthetic in animal research, has been shown to reduce the neural responses to auditory stimuli and to decrease hearing sensitivity. Addition to its direct effects on auditory neurons, urethane may also influence cochlear function. However, the effects of urethane on cochlear function, remain largely unknown. The cochlea not only converts sound vibration into electrical impulses but also amplifies the signal of low-level sound, resulting in the incredible sensitivity and exquisite frequency selectivity of our hearing. In the present study, we compared the cochlear microphonic responses between awake and urethane-anesthetized rats. The results revealed that the amplitude of the cochlear microphonic was decreased by approximately 38% by urethane, resulting in a 5 dB increase in the cochlear microphonic threshold at all of the sound frequencies examined. In mammals, cochlear amplification is attributed to the electromotility of outer hair cells. The motility of outer hair cells is modulated by efferent fibers, which use acetylcholine as the primary neurotransmitter. To deduce the possible mechanism underlying the urethane-induced decrease in cochlear sensitivity, we examined the electrical response properties of isolated outer hair cells using whole-cell patch-clamp recording. We found that urethane hyperpolarizes the outer hair cell membrane potential by as much as 30 mV in a dose-dependent manner. At membrane potentials > -50 mV, urethane increased the membrane conductance and elicited larger outward currents. This urethane-induced outward current in outer hair cells was blocked by strychnine, an antagonist of the α9 subunit of the nicotinic acetylcholine receptor. The function of the outer hair cell motor protein, prestin, was not affected by urethane. These results suggest that under urethane anesthesia, cochlear amplification is reduced due to the hyperpolarization of outer hair cells, whereas the frequency selectivity of cochlea remains unchanged. | |||
| TO cite this article:FU Mingyu,CHEN Mengzi,YAN Xiao, et al. Hyperpolarization of outer hair cells: the mechanism underlying urethane-induced cochlear depression[OL].[ 8 May 2016] http://en.paper.edu.cn/en_releasepaper/content/4687830 | |||
| 8. Ryk is involved in Wnt5a repulsive axon guidance of mouse rubrospinal tract | |||
| Duan Xin,Liu Yaobo | |||
Biology 28 April 2016
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| Abstract:Objective: Red nucleus (RN) is a predominant neuronal population for forelimb skilled motor control and function, rubrospinal tract (RST) projects from RN and delivers signals to spinal cord targets. However little is known about the molecular mechanism underlying RST axon pathfinding in the developing spinal cord. Lots of studies have identified Wnt family proteins as axon guidance cues that control axon pathfinding along the anterior-posterior (A-P) axis. The aim of this study is to investigate whether Wnt signaling pathway plays a role in RST axon pathfinding in the spinal cord. Methods: Whole mount in situ hybridization was used to detect the expression pattern of Wnt5a during the RST axon descending. Immunohistochemistry was performed to detect whether Ryk was expressed in RN neurons. shRNA lentivirus was used to knock down Ryk expression level in RN neurons. Turning assay and Dunn chamber assay were performed to investigate the repulsive guidance of RST axons under Wnt5a gradient. Results: Wnt5a established a decreasing gradient along the A-P axis of the brainstem and spinal cord. Ryk, as the receptor of Wnt5a, was specific expressed in RN neurons during the RST axon descending. Wnt5a protein repelled RST axons and Ryk was involved in Wnt5a repulsion of RST axons. Conclusions: These findings indicate that Wnt5a/Ryk signaling pathway plays a role in the RST axon pathfinding along the spinal cord. | |||
| TO cite this article:Duan Xin,Liu Yaobo. Ryk is involved in Wnt5a repulsive axon guidance of mouse rubrospinal tract[OL].[28 April 2016] http://en.paper.edu.cn/en_releasepaper/content/4685772 | |||
| 9. Ghrelin and neurodegenerative disorders- A review | |||
| SHI Limin,DU Xixun,JIANG Hong,XIE Junxia | |||
| Biology 25 January 2016 | |||
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| Abstract:Ghrelin, the endogenous ligand of the growth hormone secretagogue receptor 1a (GHS-R1a), is a gut-derived, orexigenic peptide hormone that primarily regulates growth hormone secretion, food intake and energy homeostasis. With the wide expression of GHS-R1a in extra-hypothalamic regions, the physiological role of ghrelin is more extensive than solely its involvement in metabolic function. Ghrelin has been shown to be involved in numerous higher brain functions, such as memory, reward, mood, and sleep. Some of these functions are disrupted in neurodegenerative disorders, including Parkinson's disease (PD), Alzheimer's disease (AD) and Huntington's disease (HD). This link between ghrelin and these neurodegenerative diseases is supported by numerous studies. This review aims to provide a comprehensive overview of the most recent evidence of the novel neuromodulatory role of ghrelin in PD, AD and HD. Moreover, the changes in circulating and/or central ghrelin levels that are associated with disease progression are also postulated to be a biomarker for clinical diagnosis and therapy. | |||
| TO cite this article:SHI Limin,DU Xixun,JIANG Hong, et al. Ghrelin and neurodegenerative disorders- A review[OL].[25 January 2016] http://en.paper.edu.cn/en_releasepaper/content/4677259 | |||
| 10. An Improved Protocol for Fluoro-Jade C Staining Method | |||
| GUAN Xin,CHEN Xi,YAO Hui,LI Ge,GUAN Zhenlong,WANG Yanqin | |||
| Biology 13 January 2016 | |||
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| Abstract:Fluoro-Jade C stain is a frequently-used method for labeling degenerating neurons in tissue. In the experimental process, we found that the tissue sections were easily broken and dropped from slide glass in frozen section stained with traditional Fluoro-Jade C method. In order to solve this problem, we modified the protocol of Fluoro-Jade C stain, and have achieved satisfactory results. Twelve adult C57BL/6 male mice were randomly divided into control and PD model groups. The PD model was duplicated with intraperitoneal injection of MPTP (30 mg/kg/d) for 5 days. On the eighth day, the mice were perfused and the midbrain were removed and sectioned with freezing microtome. The sections in same position of each sample were stained by Flurometric TUNEL method; traditional Fluoro-Jade C histofluorescence staining and the improved method of Fluoro-Jade C staining to detect the degenerative dopaminergic neurons. The results showed that there was no degenerative positive neurons in SNc in the control group, while there were some positive neurons FJC and TUNEL-labeled neurons in MPTP-treated mouse, and the traditional and improved FJC staining were both labeled the degenerative neurons. Although the improved FJC staining had the higher background, it can clearly show the degenerative neurons. There were no significant difference among the three methods. The modified FJC histofluorescence staining reduced the damage to the slides, and easier combined with other immunofluorescence. So, the modified FJC staining method can be very simple and rapidly detect the degenerative neurons which made the slides without damage. | |||
| TO cite this article:GUAN Xin,CHEN Xi,YAO Hui, et al. An Improved Protocol for Fluoro-Jade C Staining Method[OL].[13 January 2016] http://en.paper.edu.cn/en_releasepaper/content/4676152 | |||
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