Role of c‐Jun N‐terminal kinase activation in apoptosis induced by removal of the growth factors

Ning, Yue-Bao; Du, Zhiqiang

doi:10.1002/cbin.10425

Cited by 6 publications

(3 citation statements)

References 30 publications

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“…C-Jun NH 2-terminal kinase, also known as JNK, is a protein kinase that, along with ERK and MAPK p38, belongs to the family of enzymes known as mitogen-activated protein kinases (MAPKs) [ 27 ]. As illustrated in Figure 2 , MAPKs are known to play a role in the regulation of a variety of cellular functions and Activation of c-Jun can be induced by JNK, and the phosphorylation and continued expression of c-Jun is a necessary step in the pathway that leads to the induction of apoptosis [ 28 ]. To date, three identically structured isoforms of JNK have been identified in humans, namely JNK1, JNK2, and JNK3.…”

Section: Jnk3 and Neuroprotectionmentioning

confidence: 99%

JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties

Wu,

Zhao,

Guan

et al. 2024

Cell Adhesion & Migration

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The intensive study and investigation of neuroprotective therapy for central nervous system (CNS) diseases is ongoing. Due to shared mechanisms of neurodegeneration, a neuroprotective approach might offer benefits across multiple neurological disorders, despite variations in symptoms or injuries. C-Jun N-terminal Kinase 3 (JNK3) is found primarily in the CNS and is involved in physiological processes such as brain development, synapse formation, and memory formation. The potential of JNK3 as a target for pharmacological development holds promise for advancing neuroprotective therapies. Developing small molecule JNK3 inhibitors into drugs with neuroprotective qualities could facilitate neuronal restoration and self-repair. This review focuses on elucidating key neuroprotective mechanisms, exploring the interplay between neurodegenerative diseases and neuroprotection, and discussing advancements in JNK3 inhibitor drug development.

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Section: Jnk3 and Neuroprotectionmentioning

confidence: 99%

JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties

Wu,

Zhao,

Guan

et al. 2024

Cell Adhesion & Migration

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“…Interleukin-3 (IL3), Interleukin 3 Receptor Subunit Alpha (IL3RA), and Colony Stimulating Factor 2 Receptor Beta Common Subunit (CSF2RB) are all involved in the IL3 cytokine activity [46,47]. IL3 is involved in JAK-STAT activation and progenitor blood cells maintenance and development [7,48], being related to apoptosis by its absence and not by direct activation [49]. PI3K/AKT pathway and BCL2 protein family are involved in apoptosis, cell growth and cell survival [50].…”

Section: Disjoint Gene Assignment Between Pathwaysmentioning

confidence: 99%

PALMER: improving pathway annotation based on the biomedical literature mining with a constrained latent block model

et al. 2020

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Background In systems biology, it is of great interest to identify previously unreported associations between genes. Recently, biomedical literature has been considered as a valuable resource for this purpose. While classical clustering algorithms have popularly been used to investigate associations among genes, they are not tuned for the literature mining data and are also based on strong assumptions, which are often violated in this type of data. For example, these approaches often assume homogeneity and independence among observations. However, these assumptions are often violated due to both redundancies in functional descriptions and biological functions shared among genes. Latent block models can be alternatives in this case but they also often show suboptimal performances, especially when signals are weak. In addition, they do not allow to utilize valuable prior biological knowledge, such as those available in existing databases. Results In order to address these limitations, here we propose PALMER, a constrained latent block model that allows to identify indirect relationships among genes based on the biomedical literature mining data. By automatically associating relevant Gene Ontology terms, PALMER facilitates biological interpretation of novel findings without laborious downstream analyses. PALMER also allows researchers to utilize prior biological knowledge about known gene-pathway relationships to guide identification of gene–gene associations. We evaluated PALMER with simulation studies and applications to studies of pathway-modulating genes relevant to cancer signaling pathways, while utilizing biological pathway annotations available in the KEGG database as prior knowledge. Conclusions We showed that PALMER outperforms traditional latent block models and it provides reliable identification of novel gene–gene associations by utilizing prior biological knowledge, especially when signals are weak in the biomedical literature mining dataset. We believe that PALMER and its relevant user-friendly software will be powerful tools that can be used to improve existing pathway annotations and identify novel pathway-modulating genes.

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“…The latter leads to apoptosis in the system studied. Although the studies were not extensively expanded, the hypothesis provides a potential molecular mechanism for the apoptosis induction by JNK1 in many systems [Jia et al, ; Benzina et al, ; Ning and Du, ].…”

Section: Dna Damage Dna Damage Response (Ddr) and Dna Repairmentioning

confidence: 99%

DNA Repair in Despair—Vitamin D Is Not Fair

Gocek

Studzinski

2016

J of Cellular Biochemistry

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The role of vitamin D as a treatment option for neoplastic diseases, once considered to have a bright future, remains controversial. The preclinical studies discussed herein show compelling evidence that Vitamin D Derivatives (VDDs) can convert some cancer and leukemia cells to a benign phenotype, by differentiation/maturation, cell cycle arrest, or induction of apoptosis. Furthermore, there is considerable, though still evolving, knowledge of the molecular mechanisms underlying these changes. However, the attempts to clearly document that the treatment outcomes of human neoplastic diseases can be positively influenced by VDDs have been, so far, disappointing. The clinical trials to date of VDDs, alone or combined with other agents, have not shown consistent results. It is our contention, shared by others, that there were limitations in the design or execution of these trials which have not yet been fully addressed. Based on the connection between upregulation of JNK by VDDs and DNA repair, we propose a new avenue of attack on cancer cells by increasing the toxicity of the current, only partially effective, cancer chemotherapeutic drugs by combining them with VDDs. This can impair DNA repair and thus kill the malignant cells, warranting a comprehensive study of this novel concept. J. Cell. Biochem. 117: 1733-1744, 2016. © 2016 Wiley Periodicals, Inc.

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Role of c‐Jun N‐terminal kinase activation in apoptosis induced by removal of the growth factors

Cited by 6 publications

References 30 publications

JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties

JNK3 inhibitors as promising pharmaceuticals with neuroprotective properties

PALMER: improving pathway annotation based on the biomedical literature mining with a constrained latent block model

DNA Repair in Despair—Vitamin D Is Not Fair

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