Akt signaling - @ a glance


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Akt (PKB) is a major intracellular signaling kinase, regulating a number of cellular processes including cell cycle progression, survival, migration, proliferation, metabolism and apoptosis. It is primarily thought of as pro-proliferative and is commonly up-regulated in many cancers1,2,3. Akt activation mediates signaling initiated from various pathways including growth factors (including IGF, EFG and VEGF), cytokines (including IL-1, IL-6 and TNF-α) as well as GPCRs (including chemokines and prostaglandins).  


Akt, a serine/threonine kinase, consists of three isoforms referred to as Akt1, 2 and 34 which are differentially expressed in a tissue specific manner. It functions to promote cell survival through phosphorylation of various downstream kinases, transcription factors and signaling intermediates. Akt phosphorylation targets include glycogen synthase kinase 3 (GSK-3)5, bcl-2-associated agonist of cell death (BAD)6, caspase 97, forkhead proteins8, endothelial nitric oxide synthase (eNOS)9, mammalian target of rapamycin (mTOR)10, p2111, p2712 and p5313. It is clear therefore that Akt is a key mediator in these vital cellular processes.


Akt isoforms - genetic and protein information

IsoformEnsemblEntrez geneChromosomal locationLength (bp)Length (aa)
Akt1 ENSG00000142208 207 14q32.32 2866 480
Akt2 ENSG00000105221 208 19q13.1-q13.2 5300 481
Akt3 ENSG00000117020 10000 1q44 5127 479


Protein modifications including phosphorylation and ubiquitination regulate Akt functioning and cellular location. Phosphorylation at Ser-308 (via PDL1), Thr-478 (via mTOR & DNA-PK), Tyr-474 and Tyr-178 (viaTNK2) activate Akt's kinase activity. Ubiquitination (Ly-48 and -63) is crucial for activation and allows Akt translocation to the plasma membrane for phosphorylation and activation. Polyubiquitination in the nucleus causes proteosomal degradation following signaling14.   

Akt signaling pathway

Download the Akt signaling pathway card


Available products


ProductBiological descriptionPurityReference
SC-66 Allosteric Akt inhibitor >99% Jo et al, 2011
Luteolin Antioxidant, anti-inflammatory, anti-cancer flavonoid >99% Kim et al, 2011
LY 294002 PI-3 kinase inhibitor >99% Gharbi et al, 2007
Wortmannin PI-3 kinase inhibitor >98% Ui et al, 1995
Ro 31-8220 mesylate Protein kinase inhibitor >98% Dieter et al, 1991
Rottlerin Kinase inhibitor >95% Gschwendt et al, 1994
Okadaic acid PP1 and PP2A inhibitor >98% Fernandez et al, 2002
Pifithrin-α-HBr p53 inhibitor >98% Sohn et al, 2009
Z-D(OMe)E(OMe)VD(OMe)-FMK Cell permeable caspase-3 inhibitor >90% Stepanichev et al, 2005
Z-LE(OMe)VD(OMe)-FMK Cell permeable derivative of caspase-4 inhibitor Z-LEVD-FMK >90% Bian et al, 2009
Z-VAD-FMK Irreversible general caspase inhibitor >98% Vandenabeele et al, 2006
Nitrogen oxide      
L-Arginine Precursor to nitric oxide synthesis >99% Bode-Boger et al, 1998
(S)-Nitrosoglutathione NO donor   Hogg et al, 2002
SNAP NO donor   Ignarro et al, 2002
Spermidine hydrochloride Endogenous polyamine. nNOS inhibitor. >99% Hu et al, 1994
1400W  Selective iNOS inhibitor >99% Garvey et al, 1997
Calcium signaling      
K252a Highly potent inhibitor of protein and CAM kinases >99% Kase et al, 1987
KN-62 CaM kinase II inhibitor. P2X7 antagonist. >98% Tokumitsu et al, 1990
Cyclin-dependent kinase      
Purvalanol A Potent CDK inhibitor >98% Villerbu et al, 2002
Purvalanol B CDK2 inhibitor >98% Gray et al, 1999
Phospho-Glycogen Synthase Peptide-2 GSK substrate >99% Davies et al, 2000
SB 216763 Potent selective GSK-3 inhibitor >98% Zhu et al, 2007
Lithium chloride - coming soon! GSK-3β inhibitor   Makoukji et al, 2012
Ku-0063794 - coming soon! Potent and selective inhibitor of mammalian target of rapamycin (mTOR) >99% Garcia-Martinez JM, et al, 2009
ZM 336372 Potent, selective c-Raf inhibitor >99% Deming et al, 2010

Recommended resources from our technical team


Poster Library


1 Carnero A. The PKB/AKT pathway in cancer. Curr Pharm De, 16:34-44 (2010). Read more (PubMed: 20214616) »
2 Testa J R & Tsichlis P N. AKT signaling in normal and malignant cells. Oncogene 24:7391-3 (2005). Read more (PubMed: 16288285) » 
3 Paez J & Sellers W R.  PI3K/PTEN/AKT pathway. A critical mediator of oncogenic signaling. Cancer Treat Res 115:145-67 (2003). Read more (PubMed: 12613196) »
4 Le Page C et al. Expression and localisation of Akt-1, Akt-2 and Akt-3 correlate with clinical outcome of prostate cancer patients. Br J Cancer 94:1906-12 (2006). Read more (PubMed: 16721361) »
5 Doble B W & Woodgett J R. GSK-3: tricks of the trade for a multi-tasking kinase. J Cell Sci 116:1175-86 (2003). Read more (PubMed: 12615961) »
6 Datta S R et al. Akt phosphorylation of BAD couples survival signals to the cell-intrinsic death machinery. Cell 91:231-41 (1997). Read more (PubMed: 9346240) »
7 Cardone M H et al. Regulation of cell death protease caspase-9 by phosphorylation. Science 282:1318-21 (1998). Read more (PubMed: 9812896) »
8 Brunet A et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 96:857-68 (1999). Read more (PubMed: 10102273) »
9 Montagnani M et al. Insulin-stimulated activation of eNOS is independent of Ca2+ but requires phosphorylation by Akt at Ser(1179). J Biol Chem 276:30392-8 (2001). Read more (PubMed: 11402048) »
10 Schmelzle T & Hall M N. TOR, a central controller of cell growth. Cell 103:253-62 (2000). Read more (PubMed: 11057898) »
11 Zhou B P et al. Cytoplasmic localization of p21Cip1/WAF1 by Akt-induced phosphorylation in HER-2/neu-overexpressing cells. Nat Cell Biol 3:245-52 (2001). Read more (PubMed: 11231573) »
12 Shin I et al. PKB/Akt mediates cell-cycle progression by phosphorylation of p27(Kip1) at threonine 157 and modulation of its cellular localization. Nat Med 8:1145-52 (2002). Read more (PubMed: 12244301) »
13 Zhou B P et al. HER-2/neu induces p53 ubiquitination via Akt-mediated MDM2 phosphorylation. Nat Cell Biol 3:973-82 (2001b). Read more (PubMed: 11715018) »
14 Yang W L et al. Regulation of Akt signaling activation by ubiquitination. Cell Cycle 9(3):487-97 (2012). Read more (PubMed: 20081374)»

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