9,744 research outputs found
sj-docx-1-otj-10.1177_15394492221144433 – Supplemental material for Identification of Subgroups of Activity Participation in Group of Community-Dwelling Older Adults
No full textSupplemental material, sj-docx-1-otj-10.1177_15394492221144433 for Identification of Subgroups of Activity Participation in Group of Community-Dwelling Older Adults by Jun-ichi Uemura, Kohei Uno, Aiko Hoshino, Miki Tanikaga, Masahiro Tanaka and Makoto Chishima in OTJR: Occupation, Participation and Health</p
Proline-rich tyrosine kinase 2 mediates gonadotropin-releasing hormone signaling to a specific extracellularly regulated kinase-sensitive transcriptional locus in the luteinizing hormone beta-subunit gene
No full textG protein-coupled receptor regulation of gene transcription primarily occurs through the phosphorylation of transcription factors by MAPKs. This requires transduction of an activating signal via scaffold proteins that can ultimately determine the outcome by binding signaling kinases and adapter proteins with effects on the target transcription factor and locus of activation. By investigating these mechanisms, we have elucidated how pituitary gonadotrope cells decode an input GnRH signal into coherent transcriptional output from the LH beta-subunit gene promoter. We show that GnRH activates c-Src and multiple members of the MAPK family, c-Jun NH2-terminal kinase 1/2, p38MAPK, and ERK1/2. Using dominant-negative point mutations and chemical inhibitors, we identified that calcium-dependent proline-rich tyrosine kinase 2 specifically acts as a scaffold for a focal adhesion/cytoskeleton-dependent complex comprised of c-Src, Grb2, and mSos that translocates an ERK-activating signal to the nucleus. The locus of action of ERK was specifically mapped to early growth response-1 (Egr-1) DNA binding sites within the LH beta-subunit gene proximal promoter, which was also activated by p38MAPK, but not c-Jun NH2-terminal kinase 1/2. Egr-1 was confirmed as the transcription factor target of ERK and p38MAPK by blockade of protein expression, transcriptional activity, and DNA binding. We have identified a novel GnRH-activated proline-rich tyrosine kinase 2-dependent ERK-mediated signal transduction pathway that specifically regulates Egr-1 activation of the LH beta-subunit proximal gene promoter, and thus provide insight into the molecular mechanisms required for differential regulation of gonadotropin gene expression
sj-docx-1-otj-10.1177_15394492231215515 – Supplemental material for Pandemic-Induced Occupational Disruption and Association With Health in Japanese Community-Dwelling Older Adults
No full textSupplemental material, sj-docx-1-otj-10.1177_15394492231215515 for Pandemic-Induced Occupational Disruption and Association With Health in Japanese Community-Dwelling Older Adults by Jun-ichi Uemura, Kohei Uno, Aiko Hoshino, Tatsuhiko Sano, Miki Tanikaga, Masahiro Tanaka and Junpei Mizuno in OTJR: Occupational Therapy Journal of Research</p
ATF3 upregulation in glia during Wallerian degeneration: differential expression in peripheral nerves and CNS white matter
No full textBackground: Many changes in gene expression occur in distal stumps of injured nerves but the transcriptional control of these events is poorly understood. We have examined the expression of the transcription factors ATF3 and c-Jun by non-neuronal cells during Wallerian degeneration following injury to sciatic nerves, dorsal roots and optic nerves of rats and mice, using immunohistochemistry and in situ hybridization.Results: Following sciatic nerve injury-transection or transection and reanastomosis-ATF3 was strongly upregulated by endoneurial, but not perineurial cells, of the distal stumps of the nerves by 1 day post operation (dpo) and remained strongly expressed in the endoneurium at 30 dpo when axonal regeneration was prevented. Most ATF3+ cells were immunoreactive for the Schwann cell marker, S100. When the nerve was transected and reanastomosed, allowing regeneration of axons, most ATF3 expression had been downregulated by 30 dpo. ATF3 expression was weaker in the proximal stumps of the injured nerves than in the distal stumps and present in fewer cells at all times after injury. ATF3 was upregulated by endoneurial cells in the distal stumps of injured neonatal rat sciatic nerves, but more weakly than in adult animals. ATF3 expression in transected sciatic nerves of mice was similar to that in rats. Following dorsal root injury in adult rats, ATF3 was upregulated in the part of the root between the lesion and the spinal cord (containing Schwann cells), beginning at 1 dpo, but not in the dorsal root entry zone or in the degenerating dorsal column of the spinal cord. Following optic nerve crush in adult rats, ATF3 was found in some cells at the injury site and small numbers of cells within the optic nerve displayed weak immunoreactivity. The pattern of expression of c-Jun in all types of nerve injury was similar to that of ATF3.Conclusion: These findings raise the possibility that ATF3/c-Jun heterodimers may play a role in regulating changes in gene expression necessary for preparing the distal segments of injured peripheral nerves for axonal regeneration. The absence of the ATF3 and c-Jun from CNS glia during Wallerian degeneration may limit their ability to support regeneration
The role of growth associated transcription factors c-Jun and ATMIN in neuronal regeneration and repair
No full textSubsequent to neuronal injury, increased levels of protein synthesis accompany associated rises in transcription factor expression. Two transcription factors involved in the cellular stress response are c-Jun and ATMIN.
Neuron-specific deletion of c-Jun resulted in defects in perineuronal sprouting, lymphocyte recruitment and microglial activation. Motoneurons also exhibited an atrophic phenotype, reduced target reinnervation and resistance to cell death. Additionally, mutants lacking Jun expression in peripheral Schwann Cells exhibited decreased regeneration and target muscle reinnervation, with accompanying deficits in cell survival, which highlights the dual role of c-Jun in response to stress. Homozygous deletion of JNK1, JNK2 or JNK3, or substitution of the c-Jun N-terminal serine phosphoacceptor sites (ser63&73), with alanines (JunAA), did not produce a difference in response to injury. This evidence indicates that N-terminal phosphorylation of ser63&73 does not play an essential function for axonal regeneration in vivo, while the whole c-Jun is clearly needed to successfully mount a regenerative response.
ATMINΔN mutants, which have CNS-specific Nestin::Cre-mediated ATMIN deletion, exhibited higher transcription factor expression (c-Jun, Activating Transcription Factor-3/ATF3) in facial motoneurons – both baseline and following peripheral facial axotomy - and increased central post-traumatic sprouting of CGRP-and galanin-immunoreactive motoneurites. Although there was no effect on gross functional recovery or neuronal cell death, retrograde transport of florescent markers (Fluoro-Gold, MiniRuby) revealed augmented branching under normal conditions and during the reinnervation of peripheral motor targets. In the spinal cord injury model, ATMINΔn animals showed increased numbers of corticospinal tract (CST) axons projecting to both dorsal horns and contralateral CST, as well as bilateral impairment in precise co-ordinated motor behaviour following dorsolateral hemisection. This highlights the role of ATMIN as an important regulator of axonal guidance and pruning in neuronal development and regeneration.
Altogether, these findings demonstrate the essential roles of c-Jun and ATMIN in the neuronal stress response following nerve transection
author
No full textauthorIn other places [Old Joe, the trapper] pointed out otter (or, as he pronounced it, "author") slidesPRINTED ITEM G.M.Story April 1959Not UsedNot UsedWithdrawn[see 'otter']Checked by Jordyn Hughes on Thu 09 Jun 201
JNK and ERK8 as downstream effectors of receptor tyrosine kinases
No full textMAP kinases are a super-family of serine-threonine protein kinases expressed in all eukaryotic cells. In mammals, there are many MAP kinases with different biological functions, grouped in distinctly regulated groups, ERK1/2 (extracellular signal related kinase, ERK), JNKs (jun amino terminal kinase, JNK), p38 and “atypical” MAP kinases. The MAP kinase transduction system is particularly important in growth factors signaling, which in turn control cell growth, proliferation, differentiation, survival and migration by activating receptor tyrosine kinase (RTK) family members, as platelet-derived growth factor (PDGF) and RET.
In the first report, we show that JNK is required for PDGF induction of c-myc expression. Furthermore, we identify a phylogenetically conserved AP-1 responsive element in the human, mouse and even drosophila c-myc promoter. Such element binds, in vivo, to members of the Jun family of transcription factors, c-Jun and JunD, as indicated by chromatin immunoprecipitation analysis. Finally, we show that, through this element, PDGF is able to control the activity of the c-myc transcription factor promoter in an AP-1 dependent fashion, implying the existence of a novel signaling pathway linking the PDGF receptor, through JNK and Jun proteins, to nuclear events culminating in the expression of the c-myc proto-oncogene.
In the second report, we show that RET/PTC3 activates Erk8, a new member of “atypical” MAP kinases group, by an Abl-dependent but Src-independent mechanism and demonstrate a key role for Tyr981 of RET/PTC3 in the initiation of such signaling pathway. Also, by using an alternative Erk8 splice variant, Erk8, lacking the C-terminal domain, we establish a role for this region in the activation of this MAP kinase by RET/PTC3. Finally, the use of a dominant interfering molecule for Erk8 revealed that RET/PTC3 requires this MAP kinase to stimulate the c-jun transcription factor promoter
Patient Preferences for Post‐Radical Cystectomy Treatment in Muscle‐Invasive Bladder Cancer: A Discrete Choice Experiment in Japan
No full textCitation: Shugo Yajima, Shinro Hata, Naoya Masumori, Yoh Matsuoka, Atsuro Sawada, Jun Miki, Mitsuhiro Tambo, Yasuyuki Kobayashi, Ayumu Matsuda, Keita Nakane, Takashi Kobayashi, Hajime Tanaka, Noriya Yamaguchi, Go Kaneko, Russell Miller, Takehiro Seto, Hiroaki Ito, Eiji Kikuchi, Patient Preferences for Post‐Radical Cystectomy Treatment in Muscle‐Invasive Bladder Cancer: A Discrete Choice Experiment in Japan, International Journal of Urology, 2025-03-10, https://doi.org/10.1111/iju.7003
Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang
No full textWong, Chai Kwok = 加入聚合物對均勻湍流及均勻湍流對流的影響 / 黃濟國.Thesis M.Phil. Chinese University of Hong Kong 2013.Includes bibliographical references (leaves 89-91).Abstracts also in Chinese.Title from PDF title page (viewed on 01, November, 2016).Wong, Chai Kwok = Jia ru ju he wu dui jun yun tuan liu ji jun yun tuan liu dui liu de ying xiang / Huang Jiguo
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