Relevant bibliographies by topics / GSK-3β MODULATION

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Academic literature on the topic 'GSK-3β MODULATION'

Author: Grafiati
Published: 11 September 2023

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Journal articles on the topic "GSK-3β MODULATION"

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Vyas, Dharmesh R., Espen E. Spangenburg, Tsghe W. Abraha, Thomas E. Childs, and Frank W. Booth. "GSK-3β negatively regulates skeletal myotube hypertrophy." American Journal of Physiology-Cell Physiology 283, no. 2 (August 1, 2002): C545—C551. http://dx.doi.org/10.1152/ajpcell.00049.2002.

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To determine whether changes in glycogen synthase kinase-3β (GSK-3β) phosphorylation contribute to muscle hypertrophy, we delineated the effects of GSK-3β activity on C2C12 myotube size. We also examined possible insulin-like growth factor I (IGF-I) signaling of NFAT (nuclear factors of activated T cells)-inducible gene activity and possible modulation of NFAT activation by GSK-3β. Application of IGF-I (250 ng/ml) or LiCl (10 mM) alone (i.e., both inhibit GSK-3β activity) increased the area of C2C12 myotubes by 80 and 85%, respectively. The application of IGF-I (250 ng/ml) elevated GSK-3β phosphorylation and reduced GSK-3β kinase activity by ∼800% and ∼25%, respectively. LY-294002 (100 μM) and wortmannin (150 μM), specific inhibitors of phosphatidylinositol 3′-kinase, attenuated IGF-I-induced GSK-3β phosphorylation by 67 and 92%, respectively. IGF-I suppressed the kinase activity of GSK-3β. IGF-I (250 ng/ml), but not LiCl (10 mM), induced an increase in NFAT-activated luciferase reporter activity. Cotransfection of a constitutively active GSK-3β (cGSK-3β) inhibited the induction by IGF-I of NFAT-inducible reporter activity. LiCl, which inhibits GSK-3β, removed the block by cGSK-3β on IGF-I-inducible NFAT-responsive reporter gene activity. These data suggest that the IGF-I-induced increase in skeletal myotube size is signaled, in part, through the inhibition of GSK-3β.
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Li, C., H. Xin, Y. Shi, and J. Mu. "Knockdown of TRIM24 suppresses growth and induces apoptosis in acute myeloid leukemia through downregulation of Wnt/GSK-3β/β-catenin signaling." Human & Experimental Toxicology 39, no. 12 (July 16, 2020): 1725–36. http://dx.doi.org/10.1177/0960327120938845.

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Tripartite motif-containing protein 24 (TRIM24) has currently emerged as a crucial cancer-related gene present in a wide range of human cancer types. However, the involvement of TRIM24 in acute myeloid leukemia (AML) has not been well investigated. The present study aims to investigate the significance, cellular function, and potential regulatory mechanism of TRIM24 in AML. We found that TRIM24 expression was significantly upregulated in AML compared with normal tissues. AML patients with low expression of TRIM24 had higher survival rates than those expressing TRIM24 at higher levels. High expression of TRIM24 was also detected in AML cells and its knockdown markedly restricted proliferation and promoted apoptosis in AML cells. Further investigation revealed that TRIM24 contributed to the regulation of Wnt/β-catenin signaling, which was associated with modulating the phosphorylation status of glycogen synthase kinase-3β (GSK-3β). Inactivation of GSK-3β partially reversed the TRIM24 knockdown-mediated antitumor effects observed in AML cells. Furthermore, knockdown of TRIM24 retarded the growth of AML-derived xenograft tumors in nude mice in vivo. Overall, these findings demonstrate that knockdown of TRIM24 impedes the AML tumor growth through the modulation of Wnt/GSK-3β/β-catenin signaling. These findings highlight the potential TRIM24 as an attractive anticancer target to treat AML.
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Bai, J., P. Jia, Y. Zhang, K. Wang, and G. Wu. "Paraoxonase 2 protects against oxygen-glucose deprivation/reoxygenation-induced neuronal injury by enhancing Nrf2 activation via GSK-3β modulation." Human & Experimental Toxicology 40, no. 8 (February 24, 2021): 1342–54. http://dx.doi.org/10.1177/0960327121996032.

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Paraoxonase 2 (PON2) is a powerful antioxidant that mediates cell survival under oxidative stress; however, its protection neurons against cerebral ischemia-reperfusion injury-induced oxidative stress remains unclear. This study aimed to determine the precise regulating role of PON2 in neuronal survival under oxidative stress. An in vitro model of cerebral ischemia-reperfusion injury was used to assess the effect of PON2 on oxidative stress induced by oxygen–glucose deprivation/reoxygenation (OGD/R). Results showed that PON2 expression in neurons was decreased due to OGD/R exposure. A series of functional experiments revealed that upregulated PON2 improved OGD/R-impaired viability and attenuated OGD/R-induced increases in apoptosis and reactive oxygen species in neurons. Decreased PON2 expression enhanced neuronal sensitivity to OGD/R-induced injury. Overexpressed PON2 markedly enhanced the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) in the nucleus and increased the levels of Nrf2-mediated transcriptional activity. Furthermore, PON2 enhanced the Nrf2 activation by modulating glycogen synthase kinase-3β (GSK-3β). Inhibition of GSK-3β substantially abrogated the PON2 knockdown-mediated suppression of Nrf2 activity. Notably, Nrf2 inhibition partially reversed the neuroprotective effects of PON2 overexpression in OGD/R-exposed neurons. These findings indicate that PON2 alleviates OGD/R-induced apoptosis and oxidative stress in neurons by potentiating Nrf2 activation via GSK-3β modulation. This study highlights the potential neuroprotective function of PON2 against cerebral ischemia-reperfusion injury.
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Zhu, Jiang, Mario J. Rebecchi, Peter S. A. Glass, Peter R. Brink, and Lixin Liu. "Cardioprotection of the aged rat heart by GSK-3β inhibitor is attenuated: age-related changes in mitochondrial permeability transition pore modulation." American Journal of Physiology-Heart and Circulatory Physiology 300, no. 3 (March 2011): H922—H930. http://dx.doi.org/10.1152/ajpheart.00860.2010.

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It is well established that inhibition of glycogen synthase kinase (GSK)-3β in the young adult myocardium protects against ischemia-reperfusion (I/R) injury through inhibition of mitochondrial permeability transition pore (mPTP) opening. Here, we investigated age-associated differences in the ability of GSK-3β inhibitor [SB-216763 (SB)] to protect the heart and to modulate mPTP opening during I/R injury. Fischer 344 male rats were assigned from their respective young or old age groups. Animals were subjected to 30 min ischemia following 120 min reperfusion to determine myocardial infarction (MI) size in vivo. Ischemic tissues were collected 10 min after reperfusion for nicotinamide adenine dinucleotide (NAD+) measurements and immunoblotting. In parallel experiments, ventricular myocytes isolated from young or old rats were exposed to oxidative stress through generation of reactive oxygen species (ROS), and mPTP opening times were measured by using confocal microscopy. Our results showed that SB decreased MI in young SB-treated rats compared with young untreated I/R animals, whereas SB failed to significantly affect MI in the old animals. SB also significantly increased GSK-3β phosphorylation in young rats, but phosphorylation levels were already highly elevated in old control groups. There were no significant differences observed between SB-treated and untreated old animals. NAD+levels were better maintained in young SB-treated animals compared with the young untreated group during I/R, but this relative improvement was not observed in old animals. SB also significantly prolonged the time to mPTP opening induced by ROS in young cardiomyocytes, but not in aged cardiomyocytes. These results demonstrate that this GSK-3β inhibitor fails to protect the aged myocardium in response to I/R injury or prevent mPTP opening following a rise in ROS and suggest that healthy aging alters mPTP regulation by GSK-3β.
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Qiu, Qi, Xia Lei, Yueying Wang, Hui Xiong, Yanming Xu, Huifeng Sun, Hongdan Xu, and Ning Zhang. "Naringin Protects against Tau Hyperphosphorylation in Aβ25–35-Injured PC12 Cells through Modulation of ER, PI3K/AKT, and GSK-3β Signaling Pathways." Behavioural Neurology 2023 (February 15, 2023): 1–16. http://dx.doi.org/10.1155/2023/1857330.

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Alzheimer’s disease (AD) is the most common form of dementia and a significant social and economic burden. Estrogens can exert neuroprotective effects and may contribute to the prevention, attenuation, or even delay in the onset of AD; however, long-term estrogen therapy is associated with harmful side effects. Thus, estrogen alternatives are of interest for countering AD. Naringin, a phytoestrogen, is a key active ingredient in the traditional Chinese medicine Drynaria. Naringin is known to protect against nerve injury induced by amyloid beta-protein (Aβ) 25–35, but the underlying mechanisms of this protection are unclear. To investigate the mechanisms of naringin neuroprotection, we observed the protective effect on Aβ25–35-injured C57BL/6J mice’s learning and memory ability and hippocampal neurons. Then, an Aβ25–35 injury model was established with adrenal phaeochromocytoma (PC12) cells. We examined the effect of naringin treatment on Aβ25–35-injured PC12 cells and its relationship with estrogen receptor (ER), phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT), and glycogen synthase kinase (GSK)-3β signaling pathways. Estradiol (E2) was used as a positive control for neuroprotection. Naringin treatment resulted in improved learning and memory ability, the morphology of hippocampal neurons, increased cell viability, and reduced apoptosis. We next examined the expression of ERβ, p-AKT (Ser473, Thr308), AKT, p-GSK-3β (Ser9), GSK-3β, p-Tau (Thr231, Ser396), and Tau in PC12 cells treated with Aβ25–35 and either naringin or E2, with and without inhibitors of the ER, PI3K/AKT, and GSK-3β pathways. Our results demonstrated that naringin inhibits Aβ25–35-induced Tau hyperphosphorylation by modulating the ER, PI3K/AKT, and GSK-3β signaling pathways. Furthermore, the neuroprotective effects of naringin were comparable to those of E2 in all treatment groups. Thus, our results have furthered our understanding of naringin’s neuroprotective mechanisms and indicate that naringin may comprise a viable alternative to estrogen therapy.
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Chen, Rong-Fu, Yun-Nan Lin, Keng-Fan Liu, Chun-Ting Wang, Savitha Ramachandran, Ching-Jen Wang, and Yur-Ren Kuo. "The Acceleration of Diabetic Wound Healing by Low-Intensity Extracorporeal Shockwave Involves in the GSK-3β Pathway." Biomedicines 9, no. 1 (December 30, 2020): 21. http://dx.doi.org/10.3390/biomedicines9010021.

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Previous studies have demonstrated that extracorporeal shock wave therapy (ESWT) could accelerate diabetic wound healing and that the inhibition of glycogen synthase kinase-3β (GSK-3β) is involved in epithelial differentiation during wound healing. This study investigated whether the enhancement of diabetic wound healing by ESWT is associated with the GSK-3β-mediated Wnt/β-catenin signaling pathway. A dorsal skin wounding defect model using streptozotocin-induced diabetic rodents was established. Rats were divided into 4 groups: group 1, normal controls without diabetes; group 2, diabetic controls without treatment; group 3, diabetic rats receiving ESWT; and group 4, rats receiving 6-bromoindirubin-3′oxime (BIO), a GSK-3β inhibitor, to trigger Wnt/β-catenin signaling. Tissue samples were collected and analyzed by immunohistochemical (IHC) staining and quantitative RT-PCR. The ESWT and BIO-treated groups both exhibited significant promotion of wound healing compared to the healing in controls without treatment. RT-PCR analysis of Wnt-1, -3a, -4, -5a, and -10 and β-catenin expression showed significantly increased expression in the ESWT group. The IHC staining showed that Wnt-3a and -5a and β-catenin levels were significantly increased in the ESWT and BIO treatment groups compared to the control groups. ESWT enhancement of diabetic wound healing is associated with modulation of the GSK-3β-mediated Wnt/β-catenin signaling pathway.
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Silva, Guilherme M., Rosivaldo S. Borges, Kelton L. B. Santos, Leonardo B. Federico, Isaque A. G. Francischini, Suzane Q. Gomes, Mariana P. Barcelos, Rai C. Silva, Cleydson B. R. Santos, and Carlos H. T. P. Silva. "Revisiting the Proposition of Binding Pockets and Bioactive Poses for GSK-3β Allosteric Modulators Addressed to Neurodegenerative Diseases." International Journal of Molecular Sciences 22, no. 15 (July 31, 2021): 8252. http://dx.doi.org/10.3390/ijms22158252.

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Glycogen synthase kinase-3 beta (GSK-3β) is an enzyme pertinently linked to neurodegenerative diseases since it is associated with the regulation of key neuropathological features in the central nervous system. Among the different kinds of inhibitors of this kinase, the allosteric ones stand out due to their selective and subtle modulation, lowering the chance of producing side effects. The mechanism of GSK-3β allosteric modulators may be considered still vague in terms of elucidating a well-defined binding pocket and a bioactive pose for them. In this context, we propose to reinvestigate and reinforce such knowledge by the application of an extensive set of in silico methodologies, such as cavity detection, ligand 3D shape analysis and docking (with robust validation of corresponding protocols), and molecular dynamics. The results here obtained were consensually consistent in furnishing new structural data, in particular by providing a solid bioactive pose of one of the most representative GSK-3β allosteric modulators. We further applied this to the prospect for new compounds by ligand-based virtual screening and analyzed the potential of the two obtained virtual hits by quantum chemical calculations. All potential hits achieved will be subsequently tested by in vitro assays in order to validate our approaches as well as to unveil novel chemical entities as GSK-3β allosteric modulators.
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Kim, Nayoung, Mi Yeon Kim, Woo Seon Choi, Eunbi Yi, Hyo Jung Lee, and Hun Sik Kim. "GSK-3α Inhibition in Drug-Resistant CML Cells Promotes Susceptibility to NK Cell-Mediated Lysis in an NKG2D- and NKp30-Dependent Manner." Cancers 13, no. 8 (April 9, 2021): 1802. http://dx.doi.org/10.3390/cancers13081802.

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Natural killer (NK) cells are innate cytotoxic lymphocytes that provide early protection against cancer. NK cell cytotoxicity against cancer cells is triggered by multiple activating receptors that recognize specific ligands expressed on target cells. We previously demonstrated that glycogen synthase kinase (GSK)-3β, but not GSK-3α, is a negative regulator of NK cell functions via diverse activating receptors, including NKG2D and NKp30. However, the role of GSK-3 isoforms in the regulation of specific ligands on target cells is poorly understood, which remains a challenge limiting GSK-3 targeting for NK cell-based therapy. Here, we demonstrate that GSK-3α rather than GSK-3β is the primary isoform restraining the expression of NKG2D ligands, particularly ULBP2/5/6, on tumor cells, thereby regulating their susceptibility to NK cells. GSK-3α also regulated the expression of the NKp30 ligand B7-H6, but not the DNAM-1 ligands PVR or nectin-2. This regulation occurred independently of BCR-ABL1 mutation that confers tyrosine kinase inhibitor (TKI) resistance. Mechanistically, an increase in PI3K/Akt signaling in concert with c-Myc was required for ligand upregulation in response to GSK-3α inhibition. Importantly, GSK-3α inhibition improved cancer surveillance by human NK cells in vivo. Collectively, our results highlight the distinct role of GSK-3 isoforms in the regulation of NK cell reactivity against target cells and suggest that GSK-3α modulation could be used to enhance tumor cell susceptibility to NK cells in an NKG2D- and NKp30-dependent manner.
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Kehn-Hall, Kylene, Aarthi Narayanan, Lindsay Lundberg, Gavin Sampey, Chelsea Pinkham, Irene Guendel, Rachel Van Duyne, et al. "Modulation of GSK-3β Activity in Venezuelan Equine Encephalitis Virus Infection." PLoS ONE 7, no. 4 (April 4, 2012): e34761. http://dx.doi.org/10.1371/journal.pone.0034761.

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Tong, Yixin, Sohyun Park, Di Wu, Thurl E. Harris, Christopher A. Moskaluk, David L. Brautigan, and Zheng Fu. "Modulation of GSK 3β autoinhibition by Thr‐7 and Thr‐8." FEBS Letters 592, no. 4 (February 2018): 537–46. http://dx.doi.org/10.1002/1873-3468.12990.

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Dissertations / Theses on the topic "GSK-3β MODULATION"

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Harris, Jessica Lynn. "INVESTIGATIONS INTO MODULATION OF BRAIN OXIDATIVE STRESS BY VARIOUS INTERVENTIONS." UKnowledge, 2012. http://uknowledge.uky.edu/chemistry_etds/12.

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In this thesis study we examined glycogen synthase kinase-3β (GSK-3β) and its effects over Nrf2 and Pin 1 as it relates to Alzheimer’s disease (AD). AD is a neurodegenerative disease characterized by a prolonged high oxidative environment. Transcription factor Nrf2 is vital in the brain’s defense against oxidative insults through its up-regulation of over 100 antioxidants. Depletion of the brain’s antioxidant defense system results in intolerance to an oxidative environment, contributing to the progression of AD. The regulatory Pin 1 protein promotes cellular homeostasis, and when down-regulated results in increased deposits of neurofibrillary tangles (NFTs) and amyloid-β (Aβ) plaques, the two pathological hallmarks of AD. Using aged SAMP8 mice treated with antisense oligonucleotide (AO) directed at GSK-3β and random AO, the data presented here demonstrate decreased oxidative stress and increased Nrf2 transcriptional activity and Pin 1 levels as a result of the down-regulation of GSK-3β. Collectively, these results implicate GSK-3β activity in the increased oxidative stress of AD and support its inhibition as a possible therapeutic treatment for the disease. Further, we elucidate a possible mechanism connecting GSK-3β to the loss of tolerance to an oxidative environment and increased deposits of NFTs and Aβ plaques observed in AD.
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Schleithoff, Lisa-Marie [Verfasser], Michael [Gutachter] Naumann, and Stefan [Gutachter] Frantz. "Modulation der NF--κB-Aktivität durch NEMO und GSK-3β in multivesikulären bodies / Lisa-Marie Schleithoff ; Gutachter: Michael Naumann, Stefan Frantz." Magdeburg : Universitätsbibliothek Otto-von-Guericke-Universität, 2019. http://d-nb.info/1220035351/34.

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Schleithoff, Lisa-Marie [Verfasser], Michael Gutachter] Naumann, and Stefan [Gutachter] [Frantz. "Modulation der NF--κB-Aktivität durch NEMO und GSK-3β in multivesikulären bodies / Lisa-Marie Schleithoff ; Gutachter: Michael Naumann, Stefan Frantz." Magdeburg : Universitätsbibliothek Otto-von-Guericke-Universität, 2019. http://nbn-resolving.de/urn:nbn:de:gbv:ma9:1-1981185920-141298.

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Book chapters on the topic "GSK-3β MODULATION"

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Li, Yan-Chun, Min-Juan Wang, and Wen-Jun Gao. "Hyperdopaminergic Modulation of Inhibitory Transmission is Dependent on GSK-3β Signaling-Mediated Trafficking of GABAA Receptors." In Catecholamine Research in the 21st Century, 100–101. Elsevier, 2014. http://dx.doi.org/10.1016/b978-0-12-800044-1.00087-8.

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Conference papers on the topic "GSK-3β MODULATION"

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Ghadimi, D., A. Nielsen, M. Farghaly Yoness Hassan, R. Fölster-Holst, M. de Vrese, and KJ Heller. "Modulation of GSK – 3β/β – catenin cascade by commensal bifidobateria plays an important role for the inhibition of metaflammation-related biomarkers in response to LPS or non-physiological concentrations of fructose: An in vitro study." In 47. Jahrestagung der Gesellschaft für Gastroenterologie in Bayern e.V. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688867.

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