Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.11.1.7 (peroxidase)
 65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 72-year-old woman with deteriorated renal function underwent hemodialysis with a central venous double lumen catheter and was treated with predonisolone when diagnosed with MPO-ANCA associated rapidly progressive glomerulonephritis. She developed a high fever. On hospital day 64, the central venous catheter was removed immediately, and VCM and RFP were started. On hospital day 70, chest CT showed multiple nodular cavitated lesions, and she was diagnosed as septic pulmonary embolism (SPE). Six days later, chest radiography showed asymptomatic right hydropneumothorax. An intercostal tube was inserted and purulent fluid drained. Methicillin-resistant Staphylococcus aureus was isolated from blood culture, the central venous catheter, and pleural effusion. Her condition improved slowly, and she was discharged mobile on hospital day 129. Pneumothorax is reported to be a rare but possibly lethal complication of SPE in intravenous drug abusers. To our knowledge, this is the first case report of pneumothorax secondary to SPE due to central venous catheter infection. SPE related to intravascular devices or catheters has been increasing, and the significance of this SPE complication in the critically ill should be recognized.
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PMID:[A case of pneumothorax secondary to septic pulmonary embolism due to central venous catheter infection caused by methicillin-resistant Staphylococcus aureus]. 1830 81

A microparticle surface was designed by the unique method incorporating streptavidin-biotin affinity and sortase A (SrtA)-catalyzed transpeptidation. Leucine-proline-glutamate-threonine-glycine-tagged streptavidin (Stav-LPETG)was immobilized on the surface using streptavidin-biotin affinity, and GGGGG-tagged red fluorescent protein (Gly5-RFP) was conjugated with SrtA. Biotinylated fluorescein isothiocyanate (biotin-FITC) was then bound to residual biotin-binding sites in Stav-LPETG. The resulting particles had RFP and FITC immobilized on the surface via Stav-LPETG, and RFP- and FITC-associated fluorescence was observed using fluorescence microscopy. Finally, GGG-tagged glucose oxidase and biotinylated horseradish peroxidase were immobilized on the microparticle surface, resulting in a functional particle capable of detecting glucose. This particle can be repeatedly used and is more sensitive in detecting glucose than particles prepared using chemical modification. Our method provides a simple strategy for site-specific coimmobilization on molecular surfaces and expands the use of protein hybrid devices.
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PMID:Sortase A-catalyzed site-specific coimmobilization on microparticles via streptavidin. 2227 82

Autophagosome-lysosome fusion is a common critical step in various forms of macroautophagy/autophagy including mitophagy, the selective degradation of mitochondria. Regulations of this fusion process remain poorly defined. Here we have determined the role of SIGMAR1, a unique endoplasmic reticulum membrane protein. Knockout of Sigmar1 impaired mitochondrial clearance without altering the PINK1-PRKN/Parkin signaling, in mouse retinal explants and cultured cells treated with carbonyl cyanide m-chlorophenyl hydrazone (CCCP) for induction of mitophagy. SIGMAR1 depletion also caused accumulation of autophagosome markers LC3-II and SQSTM1, but did not change the levels of BECN1 and ATG7, proteins associated with autophagosome biogenesis. Lysosomal pH and protease activities were not negatively affected. However, sigmar1 knockout partially compromised autophagosome-lysosome fusion in CCCP-treated NSC34 cells, as revealed by reduced GFP fluorescence quenching of GFP-RFP-LC3-II puncta and co-localization of lysosomes with mitochondria. Furthermore, SIGMAR1 co-immunoprecipitated with ATG14, STX17, and VAMP8 (but not SNAP29), proteins key to autophagosome-lysosome membrane fusion. Re-expressing SIGMAR1 in the null background rescued clearance of mitochondria and autophagosomes. In summary, we started out finding that sigmar1 knockout impaired the clearance of mitochondria and autophagosomes, and then narrowed down the SIGMAR1 modulation to the autophagosome-lysosome fusion step. This study may shed new light on understanding autophagy-associated cyto-protection and disease mechanisms. Abbreviations: APEX2, a genetically engineered peroxidase; BiFC, bimolecule fluorescence complementation; CCCP, a mitophagy inducing compound; CRISPR, clustered regularly interspaced short palindromic repeats; EM, electron microscopy; ER, endoplasmic reticulum; MAP1LC3/LC3, microtubule-associated protein 1 light chain 3; SIGMAR1, sigma non-opioid intracellular receptor 1.
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PMID:SIGMAR1/Sigma-1 receptor ablation impairs autophagosome clearance. 3113 82