Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:4.1.2.13 (aldolase)
 3,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Under atherosclerosis the fractions corresponding to alpha-subunits are focused at a more alkaline pH than the same fractions in the norm. The curve of the enzymic activity of the fractions with atherosclerosis is higher. beta-subunits of aldolase from muscles of intact rabbits and those with sclerosis are identical in the amino acidic composition. In the enzyme alpha-subunits under conditions of atherosclerosis the content of lysine, serine, glycine, valine gets higher. On the basis of the previous research which reveals peptide having no analogs in the norm in the C-terminal fragment of aldolase molecule an assumption is advanced that under conditions of atherosclerosis the intermediate C-terminal site of the enzyme alpha-chain changes.
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PMID:[Amino acid composition and subunit structure of rabbit muscle aldolase in experimental atherosclerosis]. 721 Feb 25

This study offers proteomic elucidation of heat pretreatment-induced alleviation of UV-B toxicity in Anabaena doliolum. Heat-pretreated cells exposed to UV-B showed improved activity of PSI, PSII, whole chain, (14)C fixation, ATP and NADPH contents compared to UV-B alone. Proteomic analysis using two-dimensional gel electrophoresis (2-DE), MALDI-TOF MS/MS and reverse transcription polymerase chain reaction (RT-PCR) of UV-B and heat pretreatment followed by UV-B-treated cells exhibited significant and reproducible alterations in nine proteins homologous to phycocyanin-alpha-chain (PC-alpha-chain), phycoerythrocyanin-alpha-chain (PEC-alpha-chain), hypothetical protein alr0882, phycobilisome core component (PBS-CC), iron superoxide dismutase (Fe-SOD), fructose-1,6-bisphosphate aldolase (FBA), nucleoside diphosphate kinase (NDPK), phosphoribulokinase (PRK) and ribulose-1,5-bisphosphate carboxylase/oxygenase (RuBisCo) large chain. Except the PEC-alpha-chain, hypothetical protein alr0882 and PBS-CC, all other proteins showed upregulation at low doses of UV-B (U2) and significant downregulation at higher doses of UV-B (U5). The disruption of redox status, signaling, pentose phosphate pathway and Calvin cycle appears to be due to the downregulation of Fe-SOD, NDPK, FBA, PRK and RuBisCo thereby leading to the death of Anabaena. In contrast to this, the upregulation of all the above proteins in heat-pretreated cells, harboring different heat shock proteins (HSPs) like 60, 26 and 16.6, followed by UV-B treatment than only the UV-B-treated ones suggests a protective role of HSPs in mitigating UV-B toxicity.
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PMID:Heat pretreatment alleviates UV-B toxicity in the cyanobacterium Anabaena doliolum: A proteomic analysis of cross tolerance. 1907 3

The present study examines butachlor-induced inhibition of growth, photosynthetic pigments such as chlorophyll a, phycocyanin, allophycocyanin, phycoerythrin, photosystems I and II, whole chain electron transport, oxygen evolution, carbon fixation, ATP content, total thiol and glutathione contents of Aulosira fertilissima. For ascertaining if above mentioned changes are due to disturbance in plasma membrane integrity or proteins, fatty acid profiling and proteomics were done. Gas chromatographic (GC) analysis of fatty acid methyl esters (FAME) depicted a decrease in alpha-linolenic acid (C18:3) which appears responsible for plasma membrane instability. Enhanced lipid peroxidation and electrolyte leakage further attested the butachlor-induced cell damage. Butachlor-treated Aulosira exhibited significant and reproducible alternations in eight proteins as assessed by 2DE and LC-MS analysis of which phycocyanin alpha-chain, allophycocyanin beta-chain, C-phycocyanin alpha-subunit, ATP synthase beta-chain and FBP aldolase were associated with photosynthesis and respiration, peroxiredoxin with antioxidative defense system and GroES and NusB with protein folding and transcription termination respectively. However, a prolonged (15 d) butachlor treatment of Aulosira downregulated all the proteins except NusB. Reverse transcription PCR of the protein genes affirmed that aforesaid proteins were the gene products not artifacts. Downregulated GroES and over expressed NusB are critical proteins for cell death.
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PMID:Understanding butachlor toxicity in Aulosira fertilissima using physiological, biochemical and proteomic approaches. 1987 24