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  1. Article ; Online: c-Jun NH

    Chen, Yiping / Liu, Kaihua / Zhang, Jingwen / Hai, Yan / Wang, Peng / Wang, Hongyan / Liu, Qiuyan / Wong, Catherine C L / Yao, Jun / Gao, Yang / Liao, Yijiao / Tang, Xiuwen / Wang, Xiu Jun

    Hepatology (Baltimore, Md.)

    2020  Volume 71, Issue 5, Page(s) 1787–1801

    Abstract: ... While the activation of c-Jun NH: Approach and results: In this study, we demonstrated that the activation of JNK ...

    Abstract Background and aims: Acetaminophen (APAP) overdose induces severe liver injury and hepatic failure. While the activation of c-Jun NH
    Approach and results: In this study, we demonstrated that the activation of JNK in mouse liver following exposure to APAP was correlated with the phosphorylation of Nrf2 and down-regulation of the antioxidant response element (ARE)-driven genes, NAD(P)H:quinone dehydrogenase 1, glutathione S-transferase α3, glutathione S-transferase M1, glutathione S-transferase M5, and aldo-keto reductase 1C. The JNK inhibitor, SP600125, or knockdown of JNK by infection of adenovirus expressing JNK small interfering RNA, ameliorated the APAP induced liver toxicity, and inhibited the phosphorylation of Nrf2 and down-regulation of detoxifying enzymes by stabilizing the transcription factor. Mechanistically, JNK antagonized Nrf2- and ARE-driven gene expression in a Kelch-like ECH-associated protein 1-independent manner. Biochemical analysis revealed that phosphorylated JNK (P-JNK) directly interacted with the Nrf2-ECH homology (Neh) 1 domain of Nrf2 and phosphorylated the serine-aspartate-serine motif 1 (SDS1) region in the Neh6 domain of Nrf2.
    Conclusions: Mass spectrometric analysis identified serine 335 in the SDS1 region of mNrf2 as the major phosphorylation site for modulation of Nrf2 ubiquitylation by P-JNK. This study demonstrates that Nrf2 is a target of P-JNK in AILI. Our finding may provide a strategy for the treatment of AILI.
    MeSH term(s) Acetaminophen/toxicity ; Analgesics, Non-Narcotic/toxicity ; Animals ; Anthracenes/pharmacology ; Chemical and Drug Induced Liver Injury/genetics ; Chemical and Drug Induced Liver Injury/metabolism ; Chemical and Drug Induced Liver Injury/pathology ; Cytoprotection/drug effects ; Cytoprotection/genetics ; Disease Models, Animal ; Down-Regulation ; Enzyme Inhibitors/pharmacology ; Liver/drug effects ; Liver/metabolism ; Liver/pathology ; Male ; Mice ; Mice, Inbred C57BL ; Mitogen-Activated Protein Kinase 8/metabolism ; NF-E2-Related Factor 2 ; Phosphorylation/drug effects ; Protein Domains ; Ubiquitination
    Chemical Substances Analgesics, Non-Narcotic ; Anthracenes ; Enzyme Inhibitors ; NF-E2-Related Factor 2 ; Nfe2l2 protein, mouse ; pyrazolanthrone (1TW30Y2766) ; Acetaminophen (362O9ITL9D) ; Mitogen-Activated Protein Kinase 8 (EC 2.7.11.24)
    Language English
    Publishing date 2020-02-05
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 604603-4
    ISSN 1527-3350 ; 0270-9139
    ISSN (online) 1527-3350
    ISSN 0270-9139
    DOI 10.1002/hep.31116
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  2. Article: c-Jun as a one-way valve at the naive to primed interface.

    Li, Dongwei / Luo, Ling / Guo, Lin / Wu, Chuman / Zhang, Ran / Peng, Yuling / Wu, Menghua / Kuang, Junqi / Li, Yan / Zhang, Yudan / Xie, Jun / Xie, Wenxiu / Mao, Rui / Ma, Gang / Fu, Xiuling / Chen, Jiekai / Hutchins, Andrew P / Pei, Duanqing

    Cell & bioscience

    2023  Volume 13, Issue 1, Page(s) 191

    Abstract: Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene ... However, its role in early embryonic development remains unknown.: Results: Here, we show that c-Jun acts ... as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced ...

    Abstract Background: c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown.
    Results: Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient.
    Conclusions: The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
    Language English
    Publishing date 2023-10-14
    Publishing country England
    Document type Journal Article
    ZDB-ID 2593367-X
    ISSN 2045-3701
    ISSN 2045-3701
    DOI 10.1186/s13578-023-01141-0
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  3. Article ; Online: The chromatin remodeling factor Arid1a cooperates with Jun/Fos to promote osteoclastogenesis by epigenetically upregulating Siglec15 expression.

    Zhang, Yongxing / Sun, Hangxiang / Huang, Fei / Chen, Yang / Ding, Xiying / Zhou, Chenhe / Wu, Yan / Zhang, Qing / Ma, Xiao / Wang, Jun / Yue, Rui / Shen, Li / Sun, Xuxu / Ye, Zhaoming

    Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research

    2024  

    Abstract: ... Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion ...

    Abstract Osteoporosis is characterized by an imbalance between osteoclast-mediated bone resorption and osteoblast-related bone formation, particularly increased osteoclastogenesis. However, the mechanisms by which epigenetic factors regulate osteoclast precursor differentiation during osteoclastogenesis remain poorly understood. Here, we show that the specific knockout of the chromatin remodeling factor Arid1a in bone marrow-derived macrophages (BMDMs) results in increased bone mass. The loss of Arid1a in BMDM inhibits cell-cell fusion and maturation of osteoclast precursors, thereby suppressing osteoclast differentiation. Mechanistically, Arid1a increases the chromatin access in the gene promoter region of sialic acid-binding Ig-like lectin 15 (Siglec15) by transcription factor Jun/Fos, which results in the upregulation of Siglec15 and promotion of osteoclast differentiation. However, the loss of Arid1a reprograms the chromatin structure to restrict Siglec15 expression in osteoclast precursors, thereby inhibiting BMDM differentiation into mature osteoclasts. Deleting Arid1a after ovariectomy (a model for postmenopausal bone loss) alleviated bone loss and maintained bone mass. In summary, epigenetic reprogramming mediated by Arid1a loss suppresses osteoclast differentiation and may serve as a promising therapeutic strategy for treating bone loss diseases.
    Language English
    Publishing date 2024-03-11
    Publishing country England
    Document type Journal Article
    ZDB-ID 632783-7
    ISSN 1523-4681 ; 0884-0431
    ISSN (online) 1523-4681
    ISSN 0884-0431
    DOI 10.1093/jbmr/zjae042
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  4. Article ; Online: c-Jun as a one-way valve at the naive to primed interface

    Dongwei Li / Ling Luo / Lin Guo / Chuman Wu / Ran Zhang / Yuling Peng / Menghua Wu / Junqi Kuang / Yan Li / Yudan Zhang / Jun Xie / Wenxiu Xie / Rui Mao / Gang Ma / Xiuling Fu / Jiekai Chen / Andrew P. Hutchins / Duanqing Pei

    Cell & Bioscience, Vol 13, Iss 1, Pp 1-

    2023  Volume 16

    Abstract: Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor ... However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way ... valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during ...

    Abstract Abstract Background c-Jun is a proto-oncogene functioning as a transcription factor to activate gene expression under many physiological and pathological conditions, particularly in somatic cells. However, its role in early embryonic development remains unknown. Results Here, we show that c-Jun acts as a one-way valve to preserve the primed state and impair reversion to the naïve state. c-Jun is induced during the naive to primed transition, and it works to stabilize the chromatin structure and inhibit the reverse transition. Loss of c-Jun has surprisingly little effect on the naïve to primed transition, and no phenotypic effect on primed cells, however, in primed cells the loss of c-Jun leads to a failure to correctly close naïve-specific enhancers. When the primed cells are induced to reprogram to a naïve state, these enhancers are more rapidly activated when c-Jun is lost or impaired, and the conversion is more efficient. Conclusions The results of this study indicate that c-Jun can function as a chromatin stabilizer in primed EpiSCs, to maintain the epigenetic cell type state and act as a one-way valve for cell fate conversions.
    Keywords EpiSCs ; c-Jun ; Naïve to primed transition ; Primed to naïve transition ; Biotechnology ; TP248.13-248.65 ; Biology (General) ; QH301-705.5 ; Biochemistry ; QD415-436
    Language English
    Publishing date 2023-10-01T00:00:00Z
    Publisher BMC
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: TRIB3 promotes the growth of oral squamous cell carcinoma by regulating JNK/JUN-mediated aerobic glycolysis.

    Meng, Zhaolun / Wang, Yan / Wang, Xiao / Han, Xuefeng

    Archives of oral biology

    2024  Volume 164, Page(s) 105977

    Abstract: ... TRIB3 and the JNK/JUN pathway and whether it regulates glycolytic processes in OSCC cells ... through the JNK/JUN pathway. Finally, tumor growth in vivo was tested using Xenograft models to observe the effect ... In addition, these effects are regulated by the JNK/JUN pathway. The use of JNK inhibitor inhibited the pro-growth and ...

    Abstract Objective: The potentiation of glycolysis is a leading driver of squamous cell carcinoma. Targeted modulation of the glycolytic process might be a pivotal tool for treating squamous cell carcinoma. Tribble homolog 3 (TRIB3) expression is elevated in some squamous cell carcinomas and correlates with poor prognosis. We investigated whether increased TRIB3 expression contributes to the progression of oral squamous cell carcinoma (OSCC) by modulating glycolysis.
    Methods: We analyzed the expression of TRIB3 in the TCGA database for clinical tissue samples, in vitro, and in vivo. Cell proliferation, migration, invasion, and apoptosis were observed by overexpressing or knocking down TRIB3. Crucially, the impact of TRIB3 on aerobic glycolysis in OSCC was also probed in our study, including glucose uptake, lactate content, ATP production, extracellular acidification rate, and oxygen consumption rate. Importantly, we examined the relationship between TRIB3 and the JNK/JUN pathway and whether it regulates glycolytic processes in OSCC cells through the JNK/JUN pathway. Finally, tumor growth in vivo was tested using Xenograft models to observe the effect of knockdown TRIB3.
    Results: Our study identified TRIB3 as the most variable and prognostic in OSCC. A significant high expression of TRIB3 in OSCC cells was determined in vitro and promoted cell proliferation, migration, invasion, apoptosis, and aerobic glycolysis. Knockdown of TRIB3 produced opposite effects. In addition, these effects are regulated by the JNK/JUN pathway. The use of JNK inhibitor inhibited the pro-growth and glycolytic effects of TRIB3 on OSCC cells. Finally, we further determined that TRIB3 knockdown would effectively suppress tumor growth in vivo.
    Conclusion: This study reveals that TRIB3 promotes OSCC growth by regulating JNK/JUN pathway-mediated aerobic glycolysis, and TRIB3 may be a potential target for treating OSCC.
    Language English
    Publishing date 2024-04-21
    Publishing country England
    Document type Journal Article
    ZDB-ID 80227-x
    ISSN 1879-1506 ; 0003-9969
    ISSN (online) 1879-1506
    ISSN 0003-9969
    DOI 10.1016/j.archoralbio.2024.105977
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  6. Article ; Online: Corrigendum to "Hemoporfin-mediated photodynamic therapy for the treatment of port-wine stain: A multicenter, retrospective study" [Photodiagnosis Photodyn Ther. 2023 Jun;42:103545].

    Zhang, Xiaofeng / Yuan, Chen / Xiao, Xuemin / Yin, Rui / Lei, Hongzhao / Li, Yan / Zheng, Shumao / Wen, Sijian / Li, Dongsheng / Wang, Xuejun / Lu, Zhong / Zhang, Yunfeng / Zeng, Weihui / He, Sijin / Li, Yuzhen / Jian, Dan / Yang, Jun / Zhong, Hua / Han, Dawei /
    Chen, Xiaoying / Zhou, Junfeng / Cai, Yantao / Peng, Xi / Li, Zhiming / Liu, Xueying / Lin, Tong / Zhang, Ruzhi / Li, Guang / Zhuang, Yin / Liu, Ling / Yan, Yan / Wang, Baoxi

    Photodiagnosis and photodynamic therapy

    2023  Volume 45, Page(s) 103931

    Language English
    Publishing date 2023-12-26
    Publishing country Netherlands
    Document type Published Erratum
    ZDB-ID 2149918-4
    ISSN 1873-1597 ; 1572-1000
    ISSN (online) 1873-1597
    ISSN 1572-1000
    DOI 10.1016/j.pdpdt.2023.103931
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  7. Article ; Online: Correction: Ubiquitous mitochondrial creatine kinase promotes the progression of gastric cancer through a JNK-MAPK/JUN/HK2 axis regulated glycolysis.

    Mi, Yushuai / Li, Quanhui / Liu, Bingtian / Wang, Dehai / Liu, Ziping / Wang, Tianshi / Wang, Yuan / Zang, Yifeng / Zhou, Yan / Wen, Yugang / Ding, Yinlu

    Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association

    2024  Volume 27, Issue 3, Page(s) 646–648

    Language English
    Publishing date 2024-03-22
    Publishing country Japan
    Document type Published Erratum
    ZDB-ID 1463526-4
    ISSN 1436-3305 ; 1436-3291
    ISSN (online) 1436-3305
    ISSN 1436-3291
    DOI 10.1007/s10120-024-01490-w
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    Zs.A 5290: Show issues Location:
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  8. Article ; Online: Shengjihuayu formula ameliorates the oxidative injury in human keratinocytes via blocking JNK/c-Jun/MMPs signaling pathway.

    Sun, Lu / Yin, Hao / Li, Yu-Ting / Qiao, Yun-Xiao / Wang, Jie / He, Qing-Yi / Xiao, Zhen-Wei / Kuai, Le / Xiang, Yan-Wei

    Journal of ethnopharmacology

    2024  Volume 326, Page(s) 117938

    Abstract: ... PRDX1, HSP90AA1, HSP90AB1, HSPA8, and TNF-α. Western blot revealed the presence of the JNK/c-Jun/MMPs ...

    Abstract Ethnopharmacological relevance: The reactive oxygen species (ROS) surge in the chronic wound tissue of diabetic ulcers (DUs) aggravates the inflammatory response. The oxidative stress state during inflammation will exacerbate inflammation and cause tissue damage, resulting in prolonged wound healing. Shengjihuayu Formula (SJHYF) is a renowned Chinese medicine prescription for treating chronic wounds in diabetic ulcers. Growing clinical evidence has demonstrated that SJHYF exhibits superior therapeutic efficacy and has a favorable safety profile. However, the underlying mechanisms by which SJHYF ameliorates oxidative damage under pathological conditions of DUs remain unclear.
    Objective: To investigate the cytoprotective properties of SJHYF on hydrogen peroxide (H
    Methods: HaCaT cells were incubated with H
    Results: The application of SJHY at a concentration of 0.25 mg/mL promoted cell proliferation, cell migration, and reduced ROS production. In addition, SJHYF was detected to have a total of 93 active compounds, including key components such as Galloyl-beta-D-glucose, Danshensu, Procyanidin B2, Catechin, and Alkannin. The RNA-seq analysis identified several core targets namely KRT17, TGM1, JUNB, PRDX5, TXNIP, PRDX1, HSP90AA1, HSP90AB1, HSPA8, and TNF-α. Western blot revealed the presence of the JNK/c-Jun/MMPs pathway and its related transcription factors.
    Conclusion: SJHYF displays significant protective effects on H
    MeSH term(s) Humans ; Reactive Oxygen Species/metabolism ; Hydrogen Peroxide/metabolism ; Ulcer ; Oxidative Stress ; Keratinocytes ; MAP Kinase Signaling System ; Inflammation/metabolism ; Diabetes Mellitus/metabolism ; Apoptosis ; Glucose
    Chemical Substances Reactive Oxygen Species ; Hydrogen Peroxide (BBX060AN9V) ; beta-d-glucose ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2024-02-22
    Publishing country Ireland
    Document type Journal Article
    ZDB-ID 134511-4
    ISSN 1872-7573 ; 0378-8741
    ISSN (online) 1872-7573
    ISSN 0378-8741
    DOI 10.1016/j.jep.2024.117938
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    Zs.A 1494: Show issues Location:
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  9. Article ; Online: Notch-mediated lactate metabolism regulates MDSC development through the Hes1/MCT2/c-Jun axis.

    Zhao, Jun-Long / Ye, Yu-Chen / Gao, Chun-Chen / Wang, Liang / Ren, Kai-Xi / Jiang, Ru / Hu, Si-Jun / Liang, Shi-Qian / Bai, Jian / Liang, Jia-Long / Ma, Peng-Fei / Hu, Yi-Yang / Li, Ben-Chang / Nie, Yong-Zhan / Chen, Yan / Li, Xiao-Fei / Zhang, Wei / Han, Hua / Qin, Hong-Yan

    Cell reports

    2022  Volume 38, Issue 10, Page(s) 110451

    Abstract: ... Jun as a novel intracellular sensor of lactate in myeloid cells using liquid-chromatography ... mass spectrometry (LC-MS) followed by CRISPR-Cas9-mediated gene disruption. Meanwhile, lactate interacts with c-Jun ... between the Notch-MCT2/lactate-c-Jun axis in myeloid cells and tumorigenesis is also confirmed in clinical ...

    Abstract Myeloid-derived suppressor cells (MDSCs) and tumor-associated macrophages (TAMs) play critical roles in tumorigenesis. However, the mechanisms underlying MDSC and TAM development and function remain unclear. In this study, we find that myeloid-specific activation of Notch/RBP-J signaling downregulates lactate transporter MCT2 transcription via its downstream molecule Hes1, leading to reduced intracellular lactate levels, blunted granulocytic MDSC (G-MDSC) differentiation, and enhanced TAM maturation. We identify c-Jun as a novel intracellular sensor of lactate in myeloid cells using liquid-chromatography-mass spectrometry (LC-MS) followed by CRISPR-Cas9-mediated gene disruption. Meanwhile, lactate interacts with c-Jun to protect from FBW7 ubiquitin-ligase-mediated degradation. Activation of Notch signaling and blockade of lactate import repress tumor progression by remodeling myeloid development. Consistently, the relationship between the Notch-MCT2/lactate-c-Jun axis in myeloid cells and tumorigenesis is also confirmed in clinical lung cancer biopsies. Taken together, our current study shows that lactate metabolism regulated by activated Notch signaling might participate in MDSC differentiation and TAM maturation.
    MeSH term(s) Carcinogenesis/genetics ; Humans ; Lactic Acid ; Myeloid Cells ; Myeloid-Derived Suppressor Cells ; Signal Transduction ; Transcription Factor HES-1
    Chemical Substances Transcription Factor HES-1 ; HES1 protein, human (149348-15-2) ; Lactic Acid (33X04XA5AT)
    Language English
    Publishing date 2022-03-19
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110451
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  10. Article ; Online: Evaluation of JUN, FN1 and LAMB1 polymorphisms in pterygium in a Chinese Han population.

    Wu, Xiying / Dong, Shiqi / Xu, Yuting / Zhu, Ge / Yan, Ming

    Ophthalmic genetics

    2022  Volume 43, Issue 4, Page(s) 488–495

    Abstract: ... meaningful, among which JUN, FN1, and LAMB1 were verified to significantly differentially express ... rs11688, rs3748814 in JUN; rs1263, rs1132741, rs1250259 in FN1; rs20556, rs35710474, rs25659, rs4320486 ... that JUN, FN1, and LAMB1 polymorphisms were not associated with susceptibility to pterygium in Chinese Han ...

    Abstract Purpose: To explore the underlying molecular mechanism of pterygium and identify the key genes regulating the development of pterygium.
    Methods: Differentially expressed mRNAs were obtained from the Gene Expression Omnibus (GEO) database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed using the DAVID (http://david.abcc.ncifcrf.gov/). The differential expressions of hub genes were verified using the reverse transcription-real-time fluorescent quantitative PCR (RT-qPCR). The function of the hub genes was further confirmed based on associations between the single nucleotide polymorphisms (SNPs) in hub genes and pterygium. The genotyping results were analyzed using SNPStats online software in five gene models, including codominant, dominant, recessive, overdominant, and log-additive. Five gene models were analyzed using SNPStats.
    Results: We found that 240 genes were significantly differentially expressed. Functional enrichment analysis showed that focal adhesion pathway is extremely meaningful, among which JUN, FN1, and LAMB1 were verified to significantly differentially express in pterygium (P = 0.0011, P = 0.0018, and P = 0.0050, respectively). However, the all nine candidate SNPs (rs11688, rs3748814 in JUN; rs1263, rs1132741, rs1250259 in FN1; rs20556, rs35710474, rs25659, rs4320486 in LAMB1), were not statistically associated with pterygium.
    Conclusion: Our results demonstrated that JUN, FN1, and LAMB1 polymorphisms were not associated with susceptibility to pterygium in Chinese Han population. Considering the fact that these three genes are differentially expressed in pterygium, further research is needed to explain its involvement in pterygium.
    MeSH term(s) China ; Conjunctiva/abnormalities ; Fibronectins/genetics ; Gene Expression Profiling/methods ; Gene Ontology ; Humans ; Laminin/genetics ; Proto-Oncogene Proteins c-jun/genetics ; Pterygium/genetics
    Chemical Substances FN1 protein, human ; Fibronectins ; JUN protein, human ; LAMB1 protein, human ; Laminin ; Proto-Oncogene Proteins c-jun
    Language English
    Publishing date 2022-04-21
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1199279-7
    ISSN 1744-5094 ; 0167-6784 ; 1381-6810
    ISSN (online) 1744-5094
    ISSN 0167-6784 ; 1381-6810
    DOI 10.1080/13816810.2022.2065511
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