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Microarrays: Human Disease Detection and Monitoring
Published in Attila Lorincz, Nucleic Acid Testing for Human Disease, 2016
Janet A. Warrington, Thomas B. Broudy
Li et al. developed a microarray-based salivary diagnostic system to identify cancer-associated RNAs from the saliva of oral squamous cell carcinoma (OSCC) patients.43 They profiled salivary mRNA and discovered 1,679 genes differentially expressed between cancer patient saliva and normal controls. Many of the genes in the expression signature may have little to do directly with cancer etiology, but accurately function as indirect markers for the underlying oral carcinoma.44 The team focused on seven of the most consistently expressed biomarkers, including transcripts of IL8, IL1B, DUSP1, HA3, OAZ1, S100P, and SAT.
Renal tubular gene biomarkers identification based on immune infiltrates in focal segmental glomerulosclerosis
Published in Renal Failure, 2022
JunYuan Bai, XiaoWei Pu, YunXia Zhang, Enlai Dai
Two specific genes were identified by the LASSO model and SVM-RFE, DUSP1 and NR4A1, and they were validated by an external dataset. DUSP1 is also called MKP1, and the protein encoded by this gene can dephosphorylate MAPK1/ERK2. DUSP1 has a decisive effect on the inflammatory reaction, appears to be a central mediator for resolving inflammation, and overexpression of DUSP1 has been proposed as a significant mechanism involved in GC actions [42]. Sheng J et al. showed that DUSP1 reduced mitochondrial damage caused by hyperglycemia, while a decrease in DUSP1 expression was related to glucose metabolism disorders, renal dysfunction, renal fibrosis and glomerular apoptosis [43]. Lu C et al. also showed that DUSP1 was decreased in HK-2 cells under hyperglycemic conditions, but in HG-treated HK-2 cells, overexpression of DUSP1 fractionally regenerated the autophagic flux and optimized the mitochondrial function. Meanwhile, by increasing parkin expression, the production of reactive oxygen species and cell apoptosis were decreased [44].
Dual Specific Phosphatase 14 Deletion Rescues Retinal Ganglion Cells and Optic Nerve Axons after Experimental Anterior Ischemic Optic Neuropathy
Published in Current Eye Research, 2021
Varun Kumar, Mohammad Ali Shariati, Louise Mesentier-Louro, Angela Jinsook Oh, Kristina Russano, Jeffrey L. Goldberg, Yaping Joyce Liao
We previously demonstrated that AAV2-mediated Dusp14 knockdown protected RGCs one week after rat optic nerve crush injury and promoted limited axonal regeneration.28 Dusp14 knockout also demonstrated significant RGC protection after optic nerve crush.28 Despite the many differences between the AION and optic crush models, inhibition of Dusp14 and activation of ERK1/2 using genetic (this study) or viral28 approaches rescues RGCs after optic nerve insult, suggesting a global role for Dusp14 in RGC death in optic neuropathies. Other Dusp family members such as Dusp6 and Dusp1 share homology with Dusp14, and in other model systems have been similarly linked to survival signaling. For example, embryonic fibroblasts from Dusp6 knockout mice have reduced apoptosis after myocardial infarction injury.44
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].