Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.24 (mitogen-activated protein kinase)
 95,810 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathogen-associated molecular pattern (PAMP) recognition occurs by plasma membrane located receptors that induce among other processes nuclear gene expression. However, signaling to the nuclear compartment is restricted by the nuclear envelope and nuclear pore complexes. We show here that among the four Arabidopsis lamin homologs LITTLE NUCLEI/CROWDED NUCLEI (LINC/CRWN), LINC1 plays an important role in PTI and jasmonic acid (JA) signaling. We show that linc1 knock out mutants affect PAMP-triggered MAPK activation and growth inhibition, but not reactive oxygen species or callose accumulation. We also demonstrate that linc1 mutants are compromised in regulating PAMP-triggered pathogen-related genes, in particular encoding factors involved in JA signaling and responses. Expression of a number of JAZ domain proteins, the key JA-related transcription factor MYC2 as well as key MYB transcription factors and biosynthesis genes of both the indole and aliphatic glucosinolate pathways are changed in linc1 mutants. Moreover, PAMP triggers JA and JA-Ile accumulation in linc1 mutants, whereas salicylic acid levels are unchanged. Despite impairment in PAMP-triggered immunity, linc1 mutants still show basal immunity towards Pseudomonas syringae DC3000 strains. High JA levels usually render plants resistant to necrotrophic pathogen. Thus, linc1 mutants show enhanced resistance to Botrytis cinerea infection. In accordance with a general role of LINC1 in JA signaling, linc1 mutants are hypersensitive to growth inhibition to external JA. In summary, our findings show that the lamin-like LINC1 protein plays a key role in JA signaling and regulation of PTI responses in Arabidopsis.
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PMID:The Lamin-Like LITTLE NUCLEI 1 (LINC1) Regulates Pattern-Triggered Immunity and Jasmonic Acid Signaling. 3199 32

Bekhogainsam decoction (BHID), a representative prescription for the treatment of diabetes mellitus (DM) and diabetic complications in both traditional Korean and Chinese medicine, was examined for its ability to ameliorate diabetic nephropathy (DN), and its mechanism of action was evaluated by metabolomics, gut microbiota, and network pharmacology. In this study, male specific pathogen-free C57BL/6 mice were intraperitoneally injected with streptozotocin (STZ, 100 mg/kg) once per day for 3 days consecutively, and were then orally administered BHID at 100 and 500 mg/kg, and metformin at 250 mg/kg once per day for 4 weeks. Our results showed that the administration of BHID to mice with STZ-induced DN prevented physiological and serological changes, structural damage, and kidney dysfunction. Based on a metabolomics test with serum, the profoundly altered metabolites in the BHID treatment group were identified. Thirty-six BHID-related proteins and four signaling pathways, including valine, leucine, and isoleucine biosynthesis, nicotinate and nicotinamide metabolism, tryptophan metabolism, and alanine, aspartate, and glutamate metabolism pathways, were explored. Principal coordinates analysis (PCoA) of the gut microbiota revealed that BHID treatment significantly affected the flora composition. In addition, the network pharmacology analysis revealed that BHID acted through phosphatidylinositol-3-kinase/protein kinase B (PI3K/Akt) and MAPK-related protein targets. Our findings on the anti-DN effects of BHID and its mechanism of action, from the perspective of systems biology, have provided scientific evidence to support the clinical treatment of patients with diabetes, and implied that BHID has the potential to prevent the progression of DN.
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PMID:A Novel Approach Based on Metabolomics Coupled With Intestinal Flora Analysis and Network Pharmacology to Explain the Mechanisms of Action of Bekhogainsam Decoction in the Improvement of Symptoms of Streptozotocin-Induced Diabetic Nephropathy in Mice. 3250 32


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