c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease

Smith, Abigail O.; Jonassen, Julie A.; Preval, Kenley M; Davis, Roger J.; Pazour, Gregory J.

doi:10.33696/signaling.3.068

Cited by 2 publications

(3 citation statements)

References 179 publications

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“…Polycystic kidney disease (PKD) is a degenerative kidney disease wherein the renal tubules are filled with multiple fluid-filled cysts [198]. Autosomal dominant polycystic kidney disease (ADPKD) is one kind of PKD.…”

Section: Autosomal Dominant Polycystic Kidney Diseasementioning

confidence: 99%

“…ADPKD has been shown to be caused by mutations of the polycystin-1 (Pkd1) and Pkd2 genes. Smith et al recently found that the JNK pathway is involved in ADPKD as inhibition of JNK activity reduces cyst growth [198].…”

Section: Autosomal Dominant Polycystic Kidney Diseasementioning

confidence: 99%

“…In this review, we take several classic JNK inhibitors as examples to elucidate the application of these inhibitors in treating human diseases. and acute inflammatory insult [27,68,190,191,200] IB1/2 Type 2 diabetes [190,193] Natural phytochemicals C66 Diabetes; aortic damage; and atherosclerosis [27,[201][202][203] Lupeol Neuroinflammation; diabetes; and lipid metabolism [198,199] Gingerol Lipid metabolism [200]…”

Section: The Application Of Synthetic Jnk Inhibitors In Human Diseasesmentioning

confidence: 99%

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The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review

Yan,

He,

et al. 2024

Biomolecules

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JNK is named after c-Jun N-terminal kinase, as it is responsible for phosphorylating c-Jun. As a member of the mitogen-activated protein kinase (MAPK) family, JNK is also known as stress-activated kinase (SAPK) because it can be activated by extracellular stresses including growth factor, UV irradiation, and virus infection. Functionally, JNK regulates various cell behaviors such as cell differentiation, proliferation, survival, and metabolic reprogramming. Dysregulated JNK signaling contributes to several types of human diseases. Although the role of the JNK pathway in a single disease has been summarized in several previous publications, a comprehensive review of its role in multiple kinds of human diseases is missing. In this review, we begin by introducing the landmark discoveries, structures, tissue expression, and activation mechanisms of the JNK pathway. Next, we come to the focus of this work: a comprehensive summary of the role of the deregulated JNK pathway in multiple kinds of diseases. Beyond that, we also discuss the current strategies for targeting the JNK pathway for therapeutic intervention and summarize the application of JNK inhibitors as well as several challenges now faced. We expect that this review can provide a more comprehensive insight into the critical role of the JNK pathway in the pathogenesis of human diseases and hope that it also provides important clues for ameliorating disease conditions.

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Section: Autosomal Dominant Polycystic Kidney Diseasementioning

confidence: 99%

Section: Autosomal Dominant Polycystic Kidney Diseasementioning

confidence: 99%

Section: The Application Of Synthetic Jnk Inhibitors In Human Diseasesmentioning

confidence: 99%

See 1 more Smart Citation

The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review

Yan,

He,

et al. 2024

Biomolecules

View full text Add to dashboard Cite

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Illumination of understudied ciliary kinases

Flax,

Rosston,

Rocha

et al. 2024

Front. Mol. Biosci.

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Cilia are cellular signaling hubs. Given that human kinases are central regulators of signaling, it is not surprising that kinases are key players in cilia biology. In fact, many kinases modulate ciliogenesis, which is the generation of cilia, and distinct ciliary pathways. Several of these kinases are understudied with few publications dedicated to the interrogation of their function. Recent efforts to develop chemical probes for members of the cyclin-dependent kinase like (CDKL), never in mitosis gene A (NIMA) related kinase (NEK), and tau tubulin kinase (TTBK) families either have delivered or are working toward delivery of high-quality chemical tools to characterize the roles that specific kinases play in ciliary processes. A better understanding of ciliary kinases may shed light on whether modulation of these targets will slow or halt disease onset or progression. For example, both understudied human kinases and some that are more well-studied play important ciliary roles in neurons and have been implicated in neurodevelopmental, neurodegenerative, and other neurological diseases. Similarly, subsets of human ciliary kinases are associated with cancer and oncological pathways. Finally, a group of genetic disorders characterized by defects in cilia called ciliopathies have associated gene mutations that impact kinase activity and function. This review highlights both progress related to the understanding of ciliary kinases as well as in chemical inhibitor development for a subset of these kinases. We emphasize known roles of ciliary kinases in diseases of the brain and malignancies and focus on a subset of poorly characterized kinases that regulate ciliary biology.

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c-JUN n-Terminal Kinase (JNK) Signaling in Autosomal Dominant Polycystic Kidney Disease

Cited by 2 publications

References 179 publications

The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review

The Role of the Dysregulated JNK Signaling Pathway in the Pathogenesis of Human Diseases and Its Potential Therapeutic Strategies: A Comprehensive Review

Illumination of understudied ciliary kinases

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