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Article ; Online: Promising small molecule anti-fibrotic agents: Newly developed or repositioned drugs targeting myofibroblast transdifferentiation.

Ishikane, Shin / Arioka, Masaki / Takahashi-Yanaga, Fumi

2023 Volume 214, Page(s) 115663

Abstract: Fibrosis occurs in all organs and tissues except the brain, and its progression leads to dysfunction of affected organs. Fibrosis-induced organ dysfunction results from the loss of elasticity, strength, and functionality of tissues due to the ... ...

Abstract	Fibrosis occurs in all organs and tissues except the brain, and its progression leads to dysfunction of affected organs. Fibrosis-induced organ dysfunction results from the loss of elasticity, strength, and functionality of tissues due to the extracellular matrix secreted by myofibroblasts that express smooth muscle-type actin as a marker. Myofibroblasts, which play a major role in fibrosis, were once thought to originate exclusively from activated fibroblasts; however, it is now clear that myofibroblasts are diverse in origin, from epithelial cells, endothelial cells, adipocytes, macrophages, and other cells. Fibrosis of vital organs, such as the heart, lungs, kidneys, and liver, is a serious chronic disease that ultimately leads to death. Currently, anti-cancer drugs have made remarkable progress, as evidenced by the development of many molecular-targeted drugs, and are making a significant contribution to improving the prognosis of cancer treatment. However, the development of anti-fibrotic agents, which also play an important role in prognosis, has lagged. In this review, the current knowledge regarding myofibroblasts is summarized, with particular attention given to their origin and transdifferentiation signaling pathways (e.g., TGF-β, Wnt/β-catenin, YAP/TAZ and AMPK signaling pathways). The development of new small molecule anti-fibrotic agents and the repositioning of existing drugs targeting myofibroblast transdifferentiation are discussed.
MeSH term(s)	Antifibrotic Agents/chemistry ; Antifibrotic Agents/pharmacology ; Drug Development ; Drug Repositioning ; Myofibroblasts/drug effects ; Myofibroblasts/pathology ; Cell Transdifferentiation/drug effects ; Humans ; Fibrosis
Chemical Substances	Antifibrotic Agents
Language	English
Publishing date	2023-06-17
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2023.115663
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Article ; Online: 2,5-Dimethyl-celecoxib induces early termination of inflammatory responses by transient macrophage accumulation and inhibits the progression of cardiac remodeling in a mouse model of cryoinjury-induced myocardial infarction.

Kishigami, Takehiro / Ishikane, Shin / Arioka, Masaki / Igawa, Kazunobu / Nishimura, Yosuke / Takahashi-Yanaga, Fumi

Journal of pharmacological sciences

2024 Volume 154, Issue 2, Page(s) 97–107

Abstract: In our previous study, we reported that 2, 5-dimethyl-celecoxib (DM-C), a derivative of celecoxib, prevents cardiac remodeling in different mouse models of heart failure, including myocardial infarction (MI). The inflammatory response after MI affects ... ...

Abstract	In our previous study, we reported that 2, 5-dimethyl-celecoxib (DM-C), a derivative of celecoxib, prevents cardiac remodeling in different mouse models of heart failure, including myocardial infarction (MI). The inflammatory response after MI affects the progression of cardiac remodeling, wherein the immune cells, mainly macrophages, play crucial roles. Therefore, we evaluated the effect of DM-C on macrophages in a cryoinjury-induced myocardial infarction (CMI) mouse model. We observed that DM-C attenuated the deterioration of left ventricular ejection fraction and cardiac fibrosis 14 d after CMI. Gene expression of pro-inflammatory cytokines at the infarct site was reduced by DM-C treatment. Analysis of macrophage surface antigens revealed that DM-C induced transient accumulation of macrophages at the infarct site without affecting their polarization. In vitro experiments using peritoneal monocytes/macrophages revealed that DM-C did not directly increase the phagocytic ability of the macrophages but increased their number, thereby upregulating the clearance capacity. Moreover, DM-C rapidly excluded the cells expressing necrotic cell marker from the infarct site. These results suggested that DM-C enhanced the clearance capacity of macrophages by transiently increasing their number at the infarct site, and terminated the escape from the inflammatory phase earlier, thereby suppressing excessive cardiac remodeling and ameliorating cardiac dysfunction.
MeSH term(s)	Animals ; Mice ; Celecoxib/pharmacology ; Celecoxib/therapeutic use ; Stroke Volume ; Ventricular Remodeling ; Ventricular Function, Left ; Myocardial Infarction/drug therapy ; Macrophages ; Disease Models, Animal ; Pyrazoles ; Sulfonamides
Chemical Substances	Celecoxib (JCX84Q7J1L) ; 2,5-dimethylcelecoxib ; Pyrazoles ; Sulfonamides
Language	English
Publishing date	2024-01-03
Publishing country	Japan
Document type	Journal Article
ZDB-ID	2104264-0
ISSN	1347-8648 ; 1347-8613
ISSN (online)	1347-8648
ISSN	1347-8613
DOI	10.1016/j.jphs.2024.01.001
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Article: Roles of Glycogen Synthase Kinase-3 (GSK-3) in Cardiac Development and Heart Disease.

Takahashi-Yanaga, Fumi

Journal of UOEH

2018 Volume 40, Issue 2, Page(s) 147–156

Abstract: Glycogen synthase kinase-3 (GSK-3) is a cytoplasmic serine/threonine protein kinase which is known to regulate a variety of cellular processes through a number of signaling pathways important for cell proliferation, stem cell renewal, apoptosis and ... ...

Abstract	Glycogen synthase kinase-3 (GSK-3) is a cytoplasmic serine/threonine protein kinase which is known to regulate a variety of cellular processes through a number of signaling pathways important for cell proliferation, stem cell renewal, apoptosis and development. Although GSK-3 exists in a variety of tissues, this kinase plays very important roles in the heart to control its development through the formation of heart and cardiomyocyte proliferation. GSK-3 is also recognized as one of the main molecules that control cardiac hypertrophy and fibrosis. Therefore, GSK-3 could be an attractive target for the development of new drugs to cure cardiac diseases. The present review summarizes the roles of GSK-3 in the signaling pathways and the heart, and discusses the possibility of new drug development targeting this kinase.
MeSH term(s)	Animals ; Glycogen Synthase Kinase 3/metabolism ; Heart/embryology ; Heart/growth & development ; Heart Diseases/enzymology ; Humans ; Myocardium/enzymology ; Signal Transduction
Chemical Substances	Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2018-06-28
Publishing country	Japan
Document type	Journal Article ; Review
ZDB-ID	632724-2
ISSN	2187-2864 ; 0387-821X
ISSN (online)	2187-2864
ISSN	0387-821X
DOI	10.7888/juoeh.40.147
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Article ; Online: Glycogen synthase kinase-3 inhibitor as a multi-targeting anti-rheumatoid drug.

Arioka, Masaki / Takahashi-Yanaga, Fumi

Biochemical pharmacology

2019 Volume 165, Page(s) 207–213

Abstract: Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that causes swelling, bone erosion, and joint disorder. Patients with RA therefore suffer from pain and physiological disability, and have a decreased quality of life. During the ... ...

Abstract	Rheumatoid arthritis (RA) is a chronic inflammatory joint disease that causes swelling, bone erosion, and joint disorder. Patients with RA therefore suffer from pain and physiological disability, and have a decreased quality of life. During the progression of RA, many different types of cells and inflammatory factors influence each other with an important role. A better understanding of the pathology of RA should therefore lead to the development of effective anti-rheumatoid drugs, such as the anti-TNFα antibody. Glycogen synthase kinase-3 (GSK-3) is a cytoplasmic serine/threonine protein kinase that is involved in a large number of key cellular processes and is dysregulated in a wide variety of diseases, including inflammation and osteoporosis. The accumulated evidence has suggested that GSK-3 could be involved in multiple steps in the progression of RA. In the present review, the mechanisms of the pathogenesis of RA are summarized, and recent developments and potential new drugs targeting GSK-3 are discussed.
MeSH term(s)	Animals ; Antirheumatic Agents/pharmacology ; Bone Regeneration/physiology ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/physiology ; Humans ; Inflammation/etiology ; Osteoclasts/physiology ; Osteogenesis/physiology ; Th17 Cells/immunology
Chemical Substances	Antirheumatic Agents ; Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2019-02-15
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2019.02.020
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Article ; Online: Differentiation-inducing factor-1 reduces lipopolysaccharide-induced vascular cell adhesion molecule-1 by suppressing mTORC1-S6K signaling in vascular endothelial cells.

Arioka, Masaki / Seto-Tetsuo, Fumi / Inoue, Takeru / Miura, Koichi / Ishikane, Shin / Igawa, Kazunobu / Tomooka, Katsuhiko / Takahashi-Yanaga, Fumi / Sasaguri, Toshiyuki

Life sciences

2023 Volume 335, Page(s) 122278

Abstract: Aims: Differentiation-inducing factor-1 (DIF-1), a compound in Dictyostelium discoideum, exhibits anti-cancer effects by inhibiting cell proliferation and motility of various mammalian cancer cells in vitro and in vivo. In addition, DIF-1 suppresses ... ...

Abstract	Aims: Differentiation-inducing factor-1 (DIF-1), a compound in Dictyostelium discoideum, exhibits anti-cancer effects by inhibiting cell proliferation and motility of various mammalian cancer cells in vitro and in vivo. In addition, DIF-1 suppresses lung colony formation in a mouse model, thus impeding cancer metastasis. However, the precise mechanism underlying its anti-metastatic effect remains unclear. In the present study, we aim to elucidate this mechanism by investigating the adhesion of circulating tumor cells to blood vessels using in vitro and in vivo systems. Main methods: Melanoma cells (1.0 × 10 Key findings: Intragastric administration of DIF-1 suppressed lung colony formation. DIF-1 also substantially inhibited the adhesion of cancer cells to human umbilical vein endothelial cells. Notably, DIF-1 did not affect the expression level of adhesion-related proteins in cancer cells, but it did decrease the expression of vascular cell adhesion molecule-1 (VCAM-1) in human umbilical vein endothelial cells by suppressing its mRNA-to-protein translation through inhibition of mTORC1-p70 S6 kinase signaling. Significance: DIF-1 reduced tumor cell adhesion to blood vessels by inhibiting mTORC1-S6K signaling and decreasing the expression of adhesion molecule VCAM-1 on vascular endothelial cells. These findings highlight the potential of DIF-1 as a promising compound for the development of anti-cancer drugs with anti-metastatic properties.
MeSH term(s)	Mice ; Animals ; Male ; Humans ; Vascular Cell Adhesion Molecule-1/metabolism ; Lipopolysaccharides/pharmacology ; Dictyostelium/metabolism ; Mice, Inbred C57BL ; Proteins ; Human Umbilical Vein Endothelial Cells/metabolism ; Mechanistic Target of Rapamycin Complex 1 ; Cell Differentiation ; Cell Adhesion ; Mammals/metabolism
Chemical Substances	Vascular Cell Adhesion Molecule-1 ; Lipopolysaccharides ; Proteins ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1)
Language	English
Publishing date	2023-11-18
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	3378-9
ISSN	1879-0631 ; 0024-3205
ISSN (online)	1879-0631
ISSN	0024-3205
DOI	10.1016/j.lfs.2023.122278
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Article ; Online: The role of angiotensin II in cancer metastasis: Potential of renin-angiotensin system blockade as a treatment for cancer metastasis.

Ishikane, Shin / Takahashi-Yanaga, Fumi

Biochemical pharmacology

2018 Volume 151, Page(s) 96–103

Abstract: Hypertension, which often exists as a comorbid condition in cancer patients, is considered as a factor affecting cancer progression. The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure, and angiotensin II (Ang ... ...

Abstract	Hypertension, which often exists as a comorbid condition in cancer patients, is considered as a factor affecting cancer progression. The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure, and angiotensin II (Ang II) is a well-known pressor peptide in RAS. There is also accumulated evidence indicating that Ang II plays a critical role in the metastasis of various cancers by modulating adhesion, migration invasion, proliferation, and angiogenesis. Consistent with this, large epidemiological studies have reported the potential beneficial effects of angiotensin-converting enzyme (ACE) inhibitors and Ang II type 1 receptor blockers (ARBs) against cancer metastasis; however, some of the results remain controversial. Although the precise Ang II-related mechanisms involved in cancer metastasis are not completely clear yet, a number of basic and meta-analytic studies have shown that ACE inhibitors and ARBs reduce the metastatic potential of tumors. In this review, we summarize the relationships among hypertension, RAS, and metastasis as demonstrated in basic and clinical studies. Finally, we discuss the possibility of using RAS inhibitors as anti-metastatic drugs.
MeSH term(s)	Angiotensin II/metabolism ; Angiotensin II Type 1 Receptor Blockers/therapeutic use ; Angiotensin-Converting Enzyme Inhibitors/therapeutic use ; Cell Adhesion/drug effects ; Cell Movement/drug effects ; Humans ; Neoplasm Metastasis/drug therapy ; Neoplasm Metastasis/pathology ; Renin-Angiotensin System/drug effects
Chemical Substances	Angiotensin II Type 1 Receptor Blockers ; Angiotensin-Converting Enzyme Inhibitors ; Angiotensin II (11128-99-7)
Language	English
Publishing date	2018-03-10
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2018.03.008
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Article ; Online: DIF-1 inhibits growth and metastasis of triple-negative breast cancer through AMPK-mediated inhibition of the mTORC1-S6K signaling pathway.

Seto-Tetsuo, Fumi / Arioka, Masaki / Miura, Koichi / Inoue, Takeru / Igawa, Kazunobu / Tomooka, Katsuhiko / Takahashi-Yanaga, Fumi / Sasaguri, Toshiyuki

Oncogene

2021 Volume 40, Issue 37, Page(s) 5579–5589

Abstract: We have previously reported that the differentiation-inducing factor-1 (DIF-1), a compound identified in Dictyostelium discoideum, suppresses the growth of MCF-7 breast cancer cells by inactivating p70 ribosomal protein S6 kinase ( ... ...

Abstract	We have previously reported that the differentiation-inducing factor-1 (DIF-1), a compound identified in Dictyostelium discoideum, suppresses the growth of MCF-7 breast cancer cells by inactivating p70 ribosomal protein S6 kinase (p70
MeSH term(s)	AMP-Activated Protein Kinases ; Animals ; Humans ; Mechanistic Target of Rapamycin Complex 1 ; Mice ; Ribosomal Protein S6 Kinases, 70-kDa ; Signal Transduction ; Triple Negative Breast Neoplasms
Chemical Substances	Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Ribosomal Protein S6 Kinases, 70-kDa (EC 2.7.11.1) ; ribosomal protein S6 kinase, 70kD, polypeptide 2 (EC 2.7.11.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
Language	English
Publishing date	2021-07-24
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639046-8
ISSN	1476-5594 ; 0950-9232
ISSN (online)	1476-5594
ISSN	0950-9232
DOI	10.1038/s41388-021-01958-4
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Article ; Online: Angiotensin II promotes primary tumor growth and metastasis formation of murine TNBC 4T1 cells through the fibroblasts around cancer cells.

Takiguchi, Tomohiro / Takahashi-Yanaga, Fumi / Ishikane, Shin / Tetsuo, Fumi / Hosoda, Hiroshi / Arioka, Masaki / Kitazono, Takanari / Sasaguri, Toshiyuki

European journal of pharmacology

2021 Volume 909, Page(s) 174415

Abstract: Angiotensin II (Ang II) reportedly facilitates primary tumor growth and distal hematogenous metastasis formation in various murine intravenous metastasis models. However, it is unclear whether Ang II accelerates the initial processes of metastasis ... ...

Abstract	Angiotensin II (Ang II) reportedly facilitates primary tumor growth and distal hematogenous metastasis formation in various murine intravenous metastasis models. However, it is unclear whether Ang II accelerates the initial processes of metastasis formation that begins in primary tumors surrounded by tumor microenvironment. We examined the effects of Ang II on primary tumors and lung metastasis lesions using a murine spontaneous metastasis model, in which triple negative breast cancer 4T1 cells constitutively expressing luciferase (4T1-Luc cells) were injected into the mammary fat pad of BALB/c mice. Subcutaneous injection of Ang II significantly accelerated primary tumor growth and lung metastasis formation. Ang II increased the protein expression levels of c-Myc, cyclin D1, fibronectin, vimentin, αSMA and Snail, and the treatment with the Ang II type 1 receptor blocker valsartan significantly suppressed the Ang II-induced increases of fibronectin and vimentin. Valsartan also significantly reduced lung metastatic lesions. However, Ang II did not have significant effects on 4T1-Luc cells including the proliferation, migration, invasion, or the expressions of proteins related to cell proliferation and epithelial-to-mesenchymal transition. In contrast, when 4T1-Luc cells were co-cultured with dermal fibroblasts, Ang II significantly accelerated cell migration and increased the expressions of fibronectin, vimentin, αSMA and Snail in 4T1-Luc cells. And moreover, Ang II significantly increased the mRNA expression of IL-6 in fibroblasts co-cultured with 4T1-Luc cells. These results suggested that Ang II accelerates surrounding fibroblasts by soluble factors such as IL-6 to promote epithelial-to-mesenchymal transition, which result in the initiation of cancer metastasis.
MeSH term(s)	Angiotensin II/metabolism ; Animals ; Cancer-Associated Fibroblasts/metabolism ; Cancer-Associated Fibroblasts/pathology ; Cell Line, Tumor ; Disease Models, Animal ; Epithelial-Mesenchymal Transition ; Female ; Humans ; Lung/pathology ; Lung Neoplasms/secondary ; Mammary Glands, Animal/pathology ; Mice ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment
Chemical Substances	Angiotensin II (11128-99-7)
Language	English
Publishing date	2021-08-08
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	80121-5
ISSN	1879-0712 ; 0014-2999
ISSN (online)	1879-0712
ISSN	0014-2999
DOI	10.1016/j.ejphar.2021.174415
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Article ; Online: Activator or inhibitor? GSK-3 as a new drug target.

Takahashi-Yanaga, Fumi

Biochemical pharmacology

2013 Volume 86, Issue 2, Page(s) 191–199

Abstract: Glycogen synthase kinase-3 (GSK-3) is a cytoplasmic serine/threonine protein kinase that phosphorylates and inhibits glycogen synthase, thereby inhibiting glycogen synthesis from glucose. However, this serine/threonine kinase is now known to regulate ... ...

Abstract	Glycogen synthase kinase-3 (GSK-3) is a cytoplasmic serine/threonine protein kinase that phosphorylates and inhibits glycogen synthase, thereby inhibiting glycogen synthesis from glucose. However, this serine/threonine kinase is now known to regulate numerous cellular processes through a number of signaling pathways important for cell proliferation, stem cell renewal, apoptosis and development. Because of these diverse roles, malfunction of this kinase is also known to be involved in the pathogenesis of human diseases, such as nervous system disorders, diabetes, bone formation, inflammation, cancer and heart failure. Therefore, GSK-3 is recognized as an attractive target for the development of new drugs. The present review summarizes the roles of GSK-3 in the insulin, Wnt/β-catenin and hedgehog signaling pathways including the regulation of their activities. The roles of GSK-3 in the development of human diseases within the context of its participation in various signaling pathways are also summarized. Finally, the possibility of new drug development targeting this kinase is discussed with recent information about inhibitors and activators of GSK-3.
MeSH term(s)	Animals ; Enzyme Activation ; Glycogen Synthase Kinase 3/antagonists & inhibitors ; Glycogen Synthase Kinase 3/drug effects ; Glycogen Synthase Kinase 3/metabolism ; Humans ; Signal Transduction
Chemical Substances	Glycogen Synthase Kinase 3 (EC 2.7.11.26)
Language	English
Publishing date	2013-07-15
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2013.04.022
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Article ; Online: 2,5-Dimethylcelecoxib attenuates cardiac fibrosis caused by cryoinjury-induced myocardial infarction by suppressing the fibroblast-to-myofibroblast transformation via inhibition of the TGF-β signaling pathway.

Ikushima, Eigo / Ishikane, Shin / Kishigami, Takehiro / Matsunaga, Hiroaki / Igawa, Kazunobu / Tomooka, Katsuhiko / Nishimura, Yosuke / Takahashi-Yanaga, Fumi

Biochemical pharmacology

2022 Volume 197, Page(s) 114950

Abstract: We previously reported that 2,5-dimethylcelecoxib (DM-C), a derivative of celecoxib, lacks cyclooxygenase-2 inhibitory effects and suppresses cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3). However, it remains unclear whether DM-C ... ...

Abstract	We previously reported that 2,5-dimethylcelecoxib (DM-C), a derivative of celecoxib, lacks cyclooxygenase-2 inhibitory effects and suppresses cardiac remodeling by activating glycogen synthase kinase-3 (GSK-3). However, it remains unclear whether DM-C attenuates fibroblast-to-myofibroblast transformation (FMT), which plays a key role in cardiac fibrosis. Therefore, we evaluated the effect of DM-C on FMT using a cryoinjury-induced myocardial infarction (CMI) mouse model. We found that DM-C attenuated the deterioration of left ventricular ejection fraction after CMI by decreasing cardiac fibrosis. Analysis of the expression level of α-smooth muscle actin (α-SMA), a marker for myofibroblasts, indicated that DM-C decreased FMT at the cardiac injury site. To investigate the mechanism by which DM-C attenuated FMT, fibroblasts obtained from the heart were stimulated with TGF-β to induce FMT, and the effect of DM-C was analyzed. DM-C suppressed the expression of α-SMA and the phosphorylation levels of Smad 2/3 and GSK-3, indicating that DM-C suppressed α-SMA expression by inhibiting the transforming growth factor (TGF)-β signaling pathway via activation of GSK-3. DM-C decreased the expression of collagen, connective tissue growth factor (CTGF) and Snail, which are also known to accelerate cardiac fibrosis. These results suggested that DM-C attenuated cardiac fibrosis by suppressing FMT at the injured site after CMI by inhibiting the TGF-β signaling pathway via activation of GSK-3. Thus, DM-C has potential against cardiac disease as a novel anti-fibrotic agent.
MeSH term(s)	Animals ; Cells, Cultured ; Fibroblasts/drug effects ; Fibroblasts/enzymology ; Fibroblasts/pathology ; Fibrosis ; Freezing/adverse effects ; Glycogen Synthase Kinase 3/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Myocardial Infarction/drug therapy ; Myocardial Infarction/enzymology ; Myocardial Infarction/etiology ; Myocardial Infarction/pathology ; Myofibroblasts/drug effects ; Myofibroblasts/enzymology ; Myofibroblasts/pathology ; Nitrogen/toxicity ; Pyrazoles/pharmacology ; Pyrazoles/therapeutic use ; Rats ; Rats, Inbred Lew ; Signal Transduction/drug effects ; Signal Transduction/physiology ; Sulfonamides/pharmacology ; Sulfonamides/therapeutic use
Chemical Substances	2,5-dimethylcelecoxib ; Pyrazoles ; Sulfonamides ; Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Nitrogen (N762921K75)
Language	English
Publishing date	2022-02-07
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	208787-x
ISSN	1873-2968 ; 0006-2952
ISSN (online)	1873-2968
ISSN	0006-2952
DOI	10.1016/j.bcp.2022.114950
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