Immunofluorescent analysis of 14.3.3 pan (green) showing staining in the cytoplasm of NIH-3T3 cells. Formalin-fixed cells were permeabilized with 0.1% Triton X-100 in TBS for 5-10 minutes and blocked with 3% BSA-PBS for 30 minutes at room temperature. Cells were probed with a 14.3.3 pan monoclonal antibody (Product # MA5-12242) in 3% BSA-PBS at a dilution of 1:100 and incubated overnight at 4 °C in a humidified chamber. Cells were washed with PBST and incubated with a DyLight-conjugated secondary antibody in PBS at room temperature in the dark. F-actin (red) was stained with a flourescent red phalloidin and nuclei (blue) were stained with Hoechst or DAPI. Images were taken at a magnification of 60x.
|Tested species reactivity||Human, Mouse|
|Published species reactivity||Mouse, Human|
|Host / Isotype||Mouse / IgG1, kappa|
|Immunogen||14-3-3 gamma recombinant human protein|
|Storage buffer||PBS, pH 7.4, with 0.2% BSA|
|Contains||0.09% sodium azide|
|Storage Conditions||4° C|
|Tested Applications||Dilution *|
|Immunohistochemistry (Paraffin) (IHC (P))||1:10-1:100|
|Immunoprecipitation (IP)||2 µg/ml|
|Western Blot (WB)||1-2 µg/ml|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
MA5-12242 targets 14.3.3 pan in IP, ICC/IF, IHC (P) and WB applications and shows reactivity with Human and Mouse samples.
The MA5-12242 immunogen is 14-3-3 gamma recombinant human protein.
14.3.3 proteins are a family of small, widely expressed, highly conserved cytosolic proteins. 14.3.3 proteins bind to and influence the activities of a diverse group of molecules involved in signal transduction, cell cycle regulation and apoptosis, including Raf, PKC, Bad, Cbl, and c-Bcr. Interactions between 14.3.3 and target proteins are strongly influenced by the phosphorylation state of 14.3.3 and the target protein.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
p53/TAp63 and AKT regulate mammalian target of rapamycin complex 1 (mTORC1) signaling through two independent parallel pathways in the presence of DNA damage.
MA5-12242 was used in western blot to study the regulation of mTORC1 signaling in response to DNA damage and the role of p53/TAp63 and AKT pathways
|Cam M,Bid HK,Xiao L,Zambetti GP,Houghton PJ,Cam H||The Journal of biological chemistry (289:4083)||2014|
Rescue of atypical protein kinase C in epithelia by the cytoskeleton and Hsp70 family chaperones.
MA5-12242 was used in western blot to examine the role of atypical protein kinase C in epithelial cell asymmetry
|Mashukova A,Oriolo AS,Wald FA,Casanova ML,Kröger C,Magin TM,Omary MB,Salas PJ||Journal of cell science (122:2491)||2009|
The central proline rich region of POB1/REPS2 plays a regulatory role in epidermal growth factor receptor endocytosis by binding to 14-3-3 and SH3 domain-containing proteins.
MA5-12242 was used in western blot to investigate the role of the central proline rich region of POBI/REPS2 in epidermal growth factor receptor endocytosis
|Tomassi L,Costantini A,Corallino S,Santonico E,Carducci M,Cesareni G,Castagnoli L||BMC biochemistry (9:null)||2008|
|Mouse||1 ug/mg protein||
mTOR activity under hypoxia.
MA5-12242 was used in immunoprecipitation and western blot to study the effects of hypoxia on the activity of mTOR
|Vadysirisack DD,Ellisen LW||Methods in molecular biology (Clifton, N.J.) (821:45)||2011|
Hypoxia regulates TSC1/2-mTOR signaling and tumor suppression through REDD1-mediated 14-3-3 shuttling.
MA5-12242 was used in immunoprecipitation to study the mechanism by which hypoxia regulates TSC1/2-mTOR signaling and tumor suppression
|DeYoung MP,Horak P,Sofer A,Sgroi D,Ellisen LW||Genes and development (22:239)||2008|
Mechanism of Akt1 inhibition of breast cancer cell invasion reveals a protumorigenic role for TSC2.
MA5-12242 was used in immunoprecipitation and western blot to study the roles of Akt1 and TSC2 in breast cancer cell invasion
|Liu H,Radisky DC,Nelson CM,Zhang H,Fata JE,Roth RA,Bissell MJ||Proceedings of the National Academy of Sciences of the United States of America (103:4134)||2006|