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Chemopreventive Agents
Published in David E. Thurston, Ilona Pysz, Chemistry and Pharmacology of Anticancer Drugs, 2021
NF-κB is a major transcription factor which tightly controls DNA transcription, cell survival, and immune responses to infection, and controls many genes involved in inflammatory processes. Up-regulated expression of NF-κB is common in chronic inflammation which can promote the initiation of cancer. Some chemopreventive agents are thought to work by down-regulating NF-κB expression thus leading to cellular protection from DNA damage caused by inflammation. Another example is Nrf2, a dual-specificity phosphatase that plays a key role in inactivating several MAP kinase isoforms during inflammatory processes. Some chemopreventive agents are thought to work by inhibiting NF-κB or Nrf2.
Epigenetic Alterations in Alzheimer’s Disease and Its Therapeutic and Dietary Interventions
Published in Atanu Bhattacharjee, Akula Ramakrishna, Magisetty Obulesu, Phytomedicine and Alzheimer’s Disease, 2020
P. M. Aswathy, C. M. Shafeeque, Moinak Banerjee
DNA methylation profiles of hippocampal tissues from control and AD patients have identified the presence of promoter hypermethylation of the gene Dual‐Specificity Phosphatase 22 (DUSP22), that inhibits protein kinase A (PKA) activity and, thereby determines tau phosphorylation status and cyclic AMP-responsive element-binding protein (CREB) signaling in AD (Sanchez-Mut et al. 2014). The methylation status of DUSP22 correlated positively with the Braak stages of the patient (Sanchez-Mut et al. 2014). Decreased expression of another phosphatase, DUSP6, that regulates tau production, through hypermethylation, was recently shown in AD brains (Watson et al. 2016). The Bridging Integrator1 (BIN1), which mediates AD risk by modulating tau pathology (Chapuis et al. 2013), was shown to be aberrantly hypermethylated in AD, resulting in Aβ load (De Jager et al. 2014; Yu et al. 2015).
Bannayan–Riley–Ruvalcaba Syndrome
Published in Dongyou Liu, Handbook of Tumor Syndromes, 2020
Gabriela Maria Abreu Gontijo, Clóvis Antônio Lopes Pinto
The PTEN gene (also known as TEP1 [TGF-b regulated and epithelial cell-enriched phosphatase], or MMAC1 [mutated in multiple advanced cancers]) is located on chromosome 10q23.31 and contains nine exons that span a genome distance of >120 kb [1]. Its coding sequence of 1209-bp is predicted to generate a 403-aa, 47 kDa dual-specificity phosphatase (PTEN), which consists of two major functional domains, an N-terminal domain from exons 1–6 and a C-terminal domain from exons 6–9.
The mechanism of miR-363-3p/DUSP10 signaling pathway involved in the gastric mucosal injury induced by clopidogrel
Published in Toxicology Mechanisms and Methods, 2021
Jiang Zongdan, Lu Yuyu, Wang Zhibing, Li Chao, Zhang Zhenyu, Sun Weihao
Our recent study (Wu et al. 2013) had concluded that attenuated expression of the TJ proteins occludin and ZO-1 in human gastric epithelial cells could be involved in clopidogrel-induced gastric mucosal injury through activation of the p38 MAPK pathway. P38 is a kinase that regulates multiple cellular functions, including cell apoptosis, differentiation, stress response, proliferation, and so on (Cuenda and Sanz-Ezquerro 2017). Negative regulation of MAPK activity is mediated by MAPK phosphatase (MKP) (Farooq and Zhou 2004). The dual-specificity phosphatase 10 (DUSP10) also called MKP5 was identified as a phosphatase that selectively inactivates JNK and p38 MAPK (Tanoue et al. 1999). Interestingly, different groups have described how the DUSP10 gene is negatively regulated by miRNAs, which are induced in different diseases and cancers. In hepatocellular cancer and pancreatic cancer, miR-181 and miR-92a, respectively, negatively regulate the DUSP10 expression, affecting the proliferation and migration of tumorigenic cells (Song et al. 2013; He et al. 2014).
New insights into the novel anti-inflammatory mode of action of glucocorticoids
Published in Immunopharmacology and Immunotoxicology, 2020
Deepa K. Ingawale, Satish K. Mandlik
It is also called as Dual specificity phosphatase 1 (DUSP1). It is member of phosphatases family that catalyzes the removal of phosphate group from threonine, serine or tyrosine amino acid residues [110]. It is an inducible nuclear phosphatase that dephosphorylates Mitogen-activated protein kinases (MAPKs) [111]. MKP-1 proteins are important regulators of immune responses and inflammatory process and were found to regulate p38 MAPK and JNK signaling [112]. MKP-1 proteins are activated by phosphorylation process and linked to many physiological and pathophysiological processes, such as CNS disorders, skeletal muscle metabolism, malignancy, atherosclerosis, asthma, psoriasis and rheumatoid arthritis [113–119]. The GC-induced expression of MKP-1 has also been associated with inhibition of extracellular signal-regulated kinase (ERK) pathway in certain cells [120]. The phosphorylation of transcription factors and RNA-binding proteins regulates the expression of inflammatory gene at both transcriptional and post-transcriptional levels [121]. MKP-1 is induced by pro-inflammatory stimuli and forms a negative feedback loop to limit MAPK signaling and the expression of inflammatory mediators. Hence, over expression of MKP-1 protein attenuates JNK and p38 MAPK pathways signaling and inhibits the expression of several inflammatory genes [122,123].
Role and molecular mechanism of stem cells in colorectal cancer initiation
Published in Journal of Drug Targeting, 2020
Meng-Yan Wang, Yu-Han Qiu, Mei-Lian Cai, Cong-Hui Zhang, Xiao-Wei Wang, Hong Liu, Yi- Chen, Wu-Li Zhao, Jing-Bo Liu, Rong-Guang Shao
In recent years, scientists have discovered a negative correlation between the dual-specificity phosphatase 2 (DUSP2) and the CSC phenotype [70]. The ERK pathway has been shown to play an important role in the maintenance of CSC phenotypes [71]. Scientists isolated primary CD133 high and CD133 low cells from patients with colorectal cancer. The results from the experiment revealed that enhanced ERK activation was observed in CD133 high cells compared to CD133 low cells. This finding proved that ERK activation was critical for the maintenance of tumour stem cells and the proliferation of tumours. As a phosphatase, DUSP2 mediated dephosphorylation of ERK, thereby interrupting the proliferation of cancer cells and disrupting the maintenance of tumour stem cell characteristics [70].