14-3-3η inhibits chondrogenic differentiation of ATDC5 cell

Yoon, Hee Eun; Kim, Ki Soon; Kim, Ick Young

doi:10.1016/j.bbrc.2011.01.107

Cited by 4 publications

(4 citation statements)

References 28 publications

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“…Moreover, the protein 14-3-3η is induced by TNF-alpha and found in the serum and synovial fluid of patients with joint inflammation [59]. Chondrogenesis of ATDC5 cells was inhibited by TNF but also by overexpression of 14-3-3η, while silencing of 14-3-3η stimulated chondrogenesis [59]. As similar a effect was observed by IL-6, a factor highly elevated under inflammatory conditions.…”

Section: Inflammation and Cartilage Repairmentioning

confidence: 87%

“…Incubation of ATDC5 cells, a clonal murine chondrogenic cell line, in a chondrogenic culture system with IL-1 results in inhibition of chondrogenesis [58]. Moreover, the protein 14-3-3η is induced by TNF-alpha and found in the serum and synovial fluid of patients with joint inflammation [59]. Chondrogenesis of ATDC5 cells was inhibited by TNF but also by overexpression of 14-3-3η, while silencing of 14-3-3η stimulated chondrogenesis [59].…”

Section: Inflammation and Cartilage Repairmentioning

confidence: 99%

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The Interaction between Joint Inflammation and Cartilage Repair

Kraan

2019

Tissue Eng Regen Med

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Background: Articular cartilage lesions occur frequently but unfortunately damaged cartilage has a very limited intrinsic repair capacity. Therefore, there is a high need to develop technology that makes cartilage repair possible. Since joint damage will lead to (sterile) inflammation, development of this technology has to take into account the effects of inflammation on cartilage repair. Methods: A literature search has been performed including combinations of the following keywords; cartilage repair, fracture repair, chondrogenesis, (sterile) inflammation, inflammatory factors, macrophage, innate immunity, and a number of individual cytokines. Papers were selected that described how inflammation or inflammatory factors affect chondrogenesis and tissue repair. A narrative review is written based on these papers focusing on the role of inflammation in cartilage repair and what we can learn from findings in other organs, especially fracture repair. Results: The relationship between inflammation and tissue repair is not straightforward. Acute, local inflammation stimulates fracture repair but appears to be deleterious for chondrogenesis and cartilage repair. Systemic inflammation has a negative effect on all sorts of tissue repair. Conclusion: Findings on the role of inflammation in fracture repair and cartilage repair are not in line. The currently widely used models of chondrogenesis, using high differentiation factor concentrations and corticosteroid levels, are not optimal. To make it possible to draw more valid conclusions about the role of inflammation and inflammatory factors on cartilage repair, model systems must be developed that better mimic the real conditions in a joint with damaged cartilage.

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Section: Inflammation and Cartilage Repairmentioning

confidence: 87%

Section: Inflammation and Cartilage Repairmentioning

confidence: 99%

The Interaction between Joint Inflammation and Cartilage Repair

Kraan

2019

Tissue Eng Regen Med

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“…YWHAH gene products belong to the highly conserved 14-3-3 family of proteins, which are mediated by binding to phosphoserine proteins. Signal transduction inhibits cell division 26 . The BIRC5 gene is a member of the inhibitor of apoptosis (IAP) gene family, and the IAP gene family encodes negative regulatory proteins that inhibit apoptotic cells 27 .…”

Section: Resultsmentioning

confidence: 99%

Comparative transcriptome analysis revealed omnivorous adaptation of the small intestine of Melinae

Wang

Yang

Zhou

et al. 2021

Sci Rep

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As the main digestive organ, the small intestine plays a vital role in the digestion of animals. At present, most of the research on animal feeding habits focuses on carnivores and herbivores. However, the mechanism of feeding and digestion in omnivores remains unclear. This study aims to reveal the molecular basis of the omnivorous adaptive evolution of Melinae by comparing the transcriptome of the small intestines of Asian Badgers (Meles leucurus) and Northern Hog Badgers (Arctonyx albogularis). We obtained high-quality small intestinal transcriptome data from these two species. Key genes and signalling pathways were analysed through Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) and other databases. Research has mainly found that orthologous genes related to six enzymes have undergone adaptive evolution. In addition, the study also found three digestion-related pathways (cGMP-PKG, cAMP, and Hippo). They are related to the digestion and absorption of nutrients, the secretion of intestinal fluids, and the transport of food through the small intestine, which may help omnivorous animals adapt to an omnivorous diet. Our study provides insight into the adaptation of Melinae to omnivores and affords a valuable transcriptome resource for future research.

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“…Plasmids are given in Supplementary Table S1. Lipofectamine LTX with PLUS reagents were used for transfection of 14-3-3 isoforms, , sc138, and sc174 into cancer cells. For the reporter assay, HEK293T was plated in a 24-well plate, left to attach, and then transfected with 100 ng of reporters (STAT3-luc, AP1-luc, and NF-kB-luc plasmid) and 100 ng of 14-3-3 isoform plasmids or sc138 along with 2 ng of Renilla-luc (pRL-TK) plasmid.…”

Section: Methodsmentioning

confidence: 99%

Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction

Varlı,

Bhosle,

Kim

et al. 2024

JACS Au

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The anticancer therapeutic effects of usnic acid (UA), a lichen secondary metabolite, have been demonstrated in vitro and in vivo. However, the mechanism underlying the anticancer effect of UA remains to be clarified. In this study, the target protein of UA was identified using a UA-linker-Affi-Gel molecule, which showed that UA binds to the 14-3-3 protein. UA binds to 14-3-3, causing the degradation of proteasomal and autophagosomal proteins. The interaction of UA with 14-3-3 isoforms modulated cell invasion, cell cycle progression, aerobic glycolysis, mitochondrial biogenesis, and the Akt/mTOR, JNK, STAT3, NF-κB, and AP-1 signaling pathways in colorectal cancer. A peptide inhibitor of 14-3-3 blocked or regressed the activity of UA and inhibited its effects. The results suggest that UA binds to 14-3-3 isoforms and suppresses cancer progression by affecting 14-3-3 targets and phosphorylated proteins.

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14-3-3η inhibits chondrogenic differentiation of ATDC5 cell

Cited by 4 publications

References 28 publications

The Interaction between Joint Inflammation and Cartilage Repair

The Interaction between Joint Inflammation and Cartilage Repair

Comparative transcriptome analysis revealed omnivorous adaptation of the small intestine of Melinae

Usnic Acid Targets 14-3-3 Proteins and Suppresses Cancer Progression by Blocking Substrate Interaction

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