scholarly journals MS for investigation of time-dependent protein adsorption on surfaces in complex biological samples

2015 ◽  
Vol 1 (4) ◽  
Author(s):  
Torgny Undin ◽  
Sara Bergström Lind ◽  
Andreas P Dahlin
2017 ◽  
Vol 37 (suppl_1) ◽  
Author(s):  
Deanna Plubell ◽  
Alexandra Fenton ◽  
Clark Wayne ◽  
Neil A Zakai ◽  
Joseph F Quinn ◽  
...  

Background: Prospective cohort studies and meta-analyses examining the relationship between HDL-cholesterol (C) and stroke are discordant and question the value of HDL-C as a marker for stroke risk prediction. Other properties of HDL-C such as cholesterol efflux capacity (CEC) and proteome, are less studied. Methods: We investigated the changes in HDL CEC and proteome to determine if they are associated with improved stroke recovery. Plasma from age- and lipid profile-matched healthy controls (N = 35) and stroke patients were collected at 24 (early, N = 35) and 96 hour (late, N = 20) post stroke, and analyzed with three independent assays to measure macrophage-mediated, ABCA1 and ABCG1-specific sterol efflux, and HDL proteome. Stroke recovery was assessed at 3 months using the Modified Rankin Scores (MRS) and the NIH Stroke Scale (NIHSS). Results: Both macrophage- and ABCG1-mediated CEC were reduced by 50% ( P <0.0001) and 20% ( P <0.038) in early and late post stroke samples, respectively, compared to the control group. Patients who had comparable or increased CEC between the two-time points exhibited lower NIHSS and MRS indicating better recovery. Proteomic analysis of HDL indicated a distinct time-dependent remodeling post stroke. Coagulation complement cascade proteins (FGB, FGA, A2M, C3) significantly increased (FDR>0.01) early and returned to control levels later, inflammation proteins (SAA1, SAA2, PON1, C4B) increased early and continued to increase. Interestingly, platelet adhesion proteins (DSG1, JUP, ITGB1, ITGA2, TUBB, DNAH3, PF4) were abundantly present in only later samples. Conclusion: 1) patients who maintain or improve HDL CEC post stroke exhibit better recovery scores, 2) post stroke HDL proteome remodeling is dynamic with distinct time-dependent protein signatures that may associate with stroke recovery.


2011 ◽  
Vol 6 (2) ◽  
pp. 93-97 ◽  
Author(s):  
Hui Wei ◽  
Zidong Wang ◽  
Jiong Zhang ◽  
Stephen House ◽  
Yi-Gui Gao ◽  
...  

1989 ◽  
Vol 260 (1) ◽  
pp. 27-36 ◽  
Author(s):  
E Kilgour ◽  
N G Anderson ◽  
M D Houslay

Incubation of a hepatocyte particulate fraction with ATP and the isolated catalytic unit of cyclic AMP-dependent protein kinase (A-kinase) selectively activated the high-affinity ‘dense-vesicle’ cycle AMP phosphodiesterase. Such activation only occurred if the membranes had been pre-treated with Mg2+. Mg2+ pre-treatment appeared to function by stimulating endogenous phosphatases and did not affect phosphodiesterase activity. Using the antiserum DV4, which specifically immunoprecipitated the 51 and 57 kDa components of the ‘dense-vesicle’ phosphodiesterase from a detergent-solubilized membrane extract, we isolated a 32P-labelled phosphoprotein from 32P-labelled hepatocytes. MgCl2 treatment of such labelled membranes removed 32P from the immunoprecipitated protein. Incubation of the Mg2+-pre-treated membranes with [32P]ATP and A-kinase led to the time-dependent incorporation of label into the ‘dense-vesicle’ phosphodiesterase, as detected by specific immunoprecipitation with the antiserum DV4. The time-dependences of phosphodiesterase activation and incorporation of label were similar. It is suggested (i) that phosphorylation of the ‘dense-vesicle’ phosphodiesterase by A-kinase leads to its activation, and that such a process accounts for the ability of glucagon and other hormones, which increase intracellular cyclic AMP concentrations, to activate this enzyme, and (ii) that an as yet unidentified kinase can phosphorylate this enzyme without causing any significant change in enzyme activity but which prevents activation and phosphorylation of the phosphodiesterase by A-kinase.


Development ◽  
1973 ◽  
Vol 29 (2) ◽  
pp. 363-382
Author(s):  
Richard B. Crawford ◽  
Charles E. Wilde ◽  
Murk H. Heinemann ◽  
F. J. Hendler

The reversible inhibition of protein synthesis at the 75–95% level in the early zygote of Fundulus results in a specific series of developmental failures dependent upon the times of inhibitor pulse initiation. The severity of the morphogenetic failure is inversely related to the time of initiation and directly to the length of the pulse. The defects reflect the time dependent serial order of events in morphogenesis. The defects range from failure of cleavage through disorders of blastulation, failure of axiation, anencephaly to microcephaly and are entirely predictable. With the exception of cleavage failure the pattern is identical with that found using pulses of actinomycin D in a similar manner. The agent used was pactamycin, an antibiotic which reversibly inhibits amino acid incorporation into protein by disturbing the assembly of the functional ribosomal complex. The significance of time dependent protein synthesis as an active expression in morphogenesis of similarly time dependent information flow via RNA synthesis is discussed.


2014 ◽  
pp. 171-176
Author(s):  
G. Buron-Moles ◽  
I. Viñas ◽  
N. Teixidó ◽  
J. Usall ◽  
R. Torres ◽  
...  

2019 ◽  
Vol 295 ◽  
pp. 456-465 ◽  
Author(s):  
Juan J. Izquierdo-González ◽  
Francisco Amil-Ruiz ◽  
Sabina Zazzu ◽  
Rosa Sánchez-Lucas ◽  
Carlos A. Fuentes-Almagro ◽  
...  

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