Search results for: Anti AKT phospho specific pS473
#29507689 2018/01/04 To Up
Single cell profiling of phospho-protein levels in chronic lymphocytic leukemia.
Chronic lymphocytic leukemia (CLL) has a high incidence and a steeply growing prevalence in the Western world. The heterogeneity of the disease necessitates individual mapping of biology and predicted drug response in each patient as basis for administration of tailored treatments. Cell signaling aberrations may serve as biological indicators for suitable therapy. By applying phospho-specific flow cytometry, we mapped basal and induced phosphorylation levels of 20 phospho-epitopes on proteins relevant to B-cell signaling in B cells from 22 CLL patients and 25 normal controls. The signaling response of the cytostatic drugs fludarabine, doxorubicin and vincristine was also investigated. CLL cells exerted similar or lower basal phosphorylation levels compared to normal B cells, with the exception of STAT3 (pY705) which was increased. Interestingly, STAT3 inhibitors normalized the STAT3 (pY705) level and reduced cell viability. Vincristine treatment significantly modulated phosphorylation levels in CLL cells, while no effect was observed in controls or after fludarabine or doxorubicin treatment. After BCR stimulation, CLL cells showed a tendency towards impaired phosphorylation levels, significant for several of the analyzed proteins. However, the level of Akt (pS473) was more potently induced in unmutated CLL (UM-CLL) patient samples and was significantly higher than in M-CLL samples. Importantly, the PI3Kδ inhibitor idelalisib potently reversed the effect of anti-IgM on Akt (pS473). Thus, signaling aberrations could be identified by phosphoflow cytometry and aberrant signaling could be normalized by small molecule drugs. This approach can identify relevant drug targets as well as drug effects in the individual patient.Ida K Myhrvold, Andrea Cremaschi, Johanne U Hermansen, Geir E Tjønnfjord, Ludvig A Munthe, Kjetil Taskén, Sigrid S Skånland
1436 related Products with: Single cell profiling of phospho-protein levels in chronic lymphocytic leukemia.
100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized2 Pieces/Box100ug Lyophilized2 Pieces/Box2 Pieces/Box100ug Lyophilized100ug Lyophilized2 Pieces/Box100ug LyophilizedRelated Pathways
#16604263 // To Up
Neuroprotection of insulin against oxidative stress-induced apoptosis in cultured retinal neurons: involvement of phosphoinositide 3-kinase/Akt signal pathway.
In order to investigate the neuroprotection of insulin in retinal neurons, we used retinal neuronal culture as a model system to study the protective effects of insulin against H2O2-induced cytotoxicity and apoptotic death. Primary retinal neuronal cultures were grown from retinas of 0-2-day old Sprague-Dawley rats. Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl-tetrazolium bromide assay. Apoptotic cell death was evaluated by the TdT-mediated digoxigenin-dUTP nick-end labeling assay, and by DNA laddering analysis. Phosphoinositide 3-kinase (PI3K) activity was measured using phosphoinositide 4,5-bisphophate and [gamma-32P]ATP as substrate. Western blot analysis with anti-phospho-Akt (pS473) antibody was performed to examine the level of phosphorylated Akt. We observed that treatment with 100 microM H2O2 for 24 h significantly decreased cell viability and induced apoptotic death of retinal neurons, and that pretreatment with 10 nM insulin significantly inhibited or attenuated H2O2-induced cytotoxicity and apoptosis. Pretreatment with LY294002, a specific PI3K inhibitor, abolished the cytoprotective effect of insulin. Insulin also strongly activated both PI3K and the downstream effector Akt. These results suggest that insulin protects retinal neurons from oxidative stress-induced apoptosis and that the PI3K/Akt signal pathway is involved in insulin-mediated retinal neuroprotection.Xiao-Rui Yu, Guo-Rong Jia, Guang-Dao Gao, Shu-Hong Wang, Yan Han, Wei Cao
2821 related Products with: Neuroprotection of insulin against oxidative stress-induced apoptosis in cultured retinal neurons: involvement of phosphoinositide 3-kinase/Akt signal pathway.
2 Pieces/BoxInhibitors2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/Box7 inhibitors2 Pieces/Box2 Pieces/Box2 Pieces/Box2 Pieces/BoxRelated Pathways
Contact Us:
Belgium
Voortstraat 49, 1910 Kampenhout BELGIUM
Tel 0032 16 58 90 45 Fax 0032 16 50 90 45
[email protected]
France
9, rue Lagrange, 75005 Paris
Tel 01 43 25 01 50 Fax 01 43 25 01 60
[email protected]
Germany
GENTAUR GmbH
Marienbongard 20
52062 Aachen Deutschland
Tel 0241 40 08 90 86 Fax 0241 55 91 05 36
[email protected]
United Kingdom
GENTAUR Ltd.
Howard Frank Turnberry House
1404-1410 High Road
Whetstone London N20 9BH
Tel 020 3393 8531 Fax 020 8445 9411
[email protected]
Also in
Luxembourg +35220880274
Schweiz Züri +41435006251
Danmark +4569918806
Österreich +43720880899
Česká republika Praha +420246019719
Ireland Dublin +35316526556
Norge Oslo +4721031366
Finland Helsset +358942419041
Sverige Stockholm +46852503438
Ελλάς Αθήνα +302111768494
Magyarország Budapest +3619980547
Poland
GENTAUR Poland Sp. z o.o.
ul. Grunwaldzka 88/A m.2
81-771 Sopot, Poland
Tel 058 710 33 44
Fax 058 710 33 48
[email protected]
skype gentaurpoland
Nederland
GENTAUR Nederland BV
Kuiper 1
5521 DG Eersel Nederland
Tel 0208-080893 Fax 0497-517897
[email protected]
Italy
GENTAUR SRL
IVA IT03841300167
Piazza Giacomo Matteotti, 6, 24122 Bergamo
Tel 02 36 00 65 93 Fax 02 36 00 65 94
[email protected]
Spain
GENTAUR Spain
Tel 0911876558
[email protected]
Bulgaria
GENTAUR Bulgaria
53 Iskar Str. 1191 Kokalyane, Sofia
Sofia 1000
Tel 0035924682280
Fax 0035929830072
[email protected]