Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P62988 (Ubiquitin)
 4,326 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

AMP-activated protein kinase (AMPK) is a ubiquitous eukaryotic protein kinase regulating cellular metabolism and energy demand. In brain AMPK plays a role as a multidimensional energy sensor and AMPK alpha2 subunit is expressed at higher levels than AMPK alpha1 subunit. In order to identify potential targets of AMPK in brain, we perform bacterial two-hybrid screening of a rat fetal brain cDNA library using AMPK alpha2 subunit as bait. Here, we present seven potential AMPK alpha2 subunit interacting proteins, including 6-phosphofructo-1-kinase (PFK-1), polyubiquitin, cytochrome c oxidase subunit I (COX I), heat shock protein 8 (HSP8), HLA-B-associated transcript 3 (BAT3) isoform 1, protein tyrosine phosphatase receptor type D (PTPRD) and islet-brain 1 (IB1). They are involved in glycolysis, protein degradation, mitochondrial electron transport and apoptosis pathways participating in energy regulation directly or indirectly. These data may provide new insight into further studying the pathways of AMPK energy regulation in brain and possible mechanisms of AMPK-mediated neuroprotective effect.
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PMID:Screening of AMP-activated protein kinase alpha2 subunit interacting proteins by bacterial two-hybrid system. 1803 17

Highly upregulated in liver cancer (HULC), a lncRNA overexpressed in hepatocellular carcinoma (HCC), has been demonstrated to be involved in the carcinogenesis and progression of HCC. However, the mechanisms of HULC promoting the abnormal growth of HCC cells are still not well elucidated. In the present study, we for the first time demonstrated that HULC promoted the growth of HCC cells through elevating COX-2 protein. Moreover, the study of the corresponding mechanism by which HULC upregulated COX-2 showed that HULC enhanced the level of ubiquitin-specific peptidase 22 (USP22), which decreased ubiquitin-mediated degradation of COX-2 protein by removing the conjugated polyubiquitin chains from COX-2 and finally stabilized COX2 protein. In addition, knockdown of USP22 or COX-2 attenuated HULC-mediated abnormal growth of HCC cells. In conclusion, our results demonstrated that "USP22/COX-2" axis played an important role in HULC promoting growth of HCC cells. The identification of this novel pathway may pave a road for developing new potential anti-HCC strategies.
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PMID:lncRNA HULC promotes the growth of hepatocellular carcinoma cells via stabilizing COX-2 protein. 2863 76