Completing the Immunological Fingerprint by Refractory Proteins: Autoantibody Screening via an Improved Immunoblotting Technique

2019 ◽  
Vol 13 (4) ◽  
pp. 1800157 ◽  
Author(s):  
Christian P. Moritz ◽  
Yannick Tholance ◽  
Carole Rosier ◽  
Evelyne Reynaud‐Federspiel ◽  
Juliette Svahn ◽  
...  
1984 ◽  
Vol 29 (4) ◽  
pp. 415-419 ◽  
Author(s):  
Katsushi Tokunaga ◽  
Noriko Yamamura ◽  
Keiichi Omoto

1989 ◽  
Vol 5 (1) ◽  
pp. 22-30 ◽  
Author(s):  
G. Dettori ◽  
R. Grillo ◽  
G. Mora ◽  
A. Cavalli ◽  
A. Alinovi ◽  
...  

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4005-4005
Author(s):  
Byung-Su Kim ◽  
Chansu Lee ◽  
Juwon Park ◽  
Kwang-Sung Ahn ◽  
Byoung Kook Kim ◽  
...  

Abstract Activation of the JAK/STAT pathway appears common in AML, occurring in up to 70% of AML patients. Therefore, JAK/STAT signal inhibitors are promising as candidate anti-cancer agents in AML. Recently, we reported that SK-7041, an HDAC inhibitor, inhibited the growth of AML cells via activation of caspase-3 and down-regulation of cyclin D1. These findings lead us to further examine whether SK-7041 inhibits the growth of KG1 AML cells via inactivation of JAK/STAT signals. Multi-immunoblotting technique (Kinetworks™ analysis) showed that expression of p-STAT-3, p-STAT-5, and p-Erk was down-regulated in KG1 cells treated with SK-7041. These results were confirmed by individual western blot analysis. In addition, IL-6-induced activation of STAT-3 and Erk was inhibited by treatment of SK-7041. Combined treatment of SK-7041 and JAK inhibitor (AG490) showed additive anti-leukemic effect as evidenced by caspase-3 activation, down-regulation of cyclin D1 (cMYC), and inhibition of phosphorylation of STATs (−1, −3). These results suggest that HDAC inhibitor, SK-7041, inhibited AML cell growth via inactivation of JAK/STATs pathway.


Cytometry ◽  
1992 ◽  
Vol 13 (8) ◽  
pp. 863-871 ◽  
Author(s):  
E. P. C. T. de Rijk ◽  
M. Terlou ◽  
P. M. J. M. Cruijsen ◽  
B. G. Jenks ◽  
E. W. Roubos

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Ewa Pniewska ◽  
Milena Sokolowska ◽  
Izabela Kupryś-Lipińska ◽  
Monika Przybek ◽  
Piotr Kuna ◽  
...  

Allergens, viral, and bacterial infections are responsible for asthma exacerbations that occur with progression of airway inflammation. cPLA2α and sPLA2X are responsible for delivery of arachidonic acid for production of eicosanoids—one of the key mediators of airway inflammation. However, cPLA2α and sPLA2X role in allergic inflammation has not been fully elucidated. The aim of this study was to analyze the influence of rDer p1 and rFel d1 and lipopolysaccharide (LPS) on cPLA2α expression and sPLA2X secretion in PBMC of asthmatics and in A549 cell line. PBMC isolated from 14 subjects, as well as A549 cells, were stimulated with rDer p1, rFel d1, and LPS. Immunoblotting technique was used to study the changes in cPLA2α protein expression and ELISA was used to analyze the release of sPLA2X. PBMC of asthmatics released more sPLA2X than those from healthy controls in the steady state. rDer p1 induced more sPLA2X secretion than cPLA2α protein expression. rFel d1 caused decrease in cPLA2α relative expression in PBMC of asthmatics and in A549 cells. Summarizing, Der p1 and Fel d1 involve phospholipase A2enzymes in their action. sPLA2X seems to be one of important PLA2isoform in allergic inflammation, especially caused by house dust mite allergens.


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