Trusted by 10,000+ Scientists Since 2002. View Our Customer Testimonials and 2,000+ Cited Publications at Google Scholar.

Phospho-Akt (Thr308) Antibody, Cat#CAF11033

$279.00

Cat#

CAF11033

Size: 100ug

Quantity:

Request Information

Species Reactivity

Human, Mouse, Rat

Host

Rabbit

Clonality

Polyclonal

Application

WB, IHC, IF/ICC, ELISA

Estimated Turnaround Time

4-7 business days

Isotype

IgG

Immunogen

A synthesized peptide derived from human Akt around the phosphorylation site of Threonine 308

Conjugation

Unconjugated

Specificity

Phospho-Akt (Thr308) Antibody detects endogenous levels of Akt only when phosphorylated at Threonine 308

Gene ID

207

Gene Name

AKT1

Swiss-Prot

P31749/P31751/Q9Y243

Purification

The antibody is from purified rabbit serum by affinity purification via sequential chromatography on phospho- and non-phospho-peptide affinity columns.

Concentration

1mg/ml

Storage

-20°C

Expiry Date

1 year

Shipping Condition

Ice packs

Comments

AKT1 is one of 3 closely related serine/threonine-protein kinases (AKT1, AKT2 and AKT3) called the AKT kinase, and which regulate many processes including metabolism, proliferation, cell survival, growth and angiogenesis. This is mediated through serine and/or threonine phosphorylation of a range of downstream substrates. Over 100 substrate candidates have been reported so far, but for most of them, no isoform specificity has been reported. AKT is responsible of the regulation of glucose uptake by mediating insulin-induced translocation of the SLC2A4/GLUT4 glucose transporter to the cell surface. Phosphorylation of PTPN1 at 'Ser-50' negatively modulates its phosphatase activity preventing dephosphorylation of the insulin receptor and the attenuation of insulin signaling. Phosphorylation of TBC1D4 triggers the binding of this effector to inhibitory 14-3-3 proteins, which is required for insulin-stimulated glucose transport. AKT regulates also the storage of glucose in the form of glycogen by phosphorylating GSK3A at 'Ser-21' and GSK3B at 'Ser-9', resulting in inhibition of its kinase activity. Phosphorylation of GSK3 isoforms by AKT is also thought to be one mechanism by which cell proliferation is driven. AKT regulates also cell survival via the phosphorylation of MAP3K5 (apoptosis signal-related kinase). Phosphorylation of 'Ser-83' decreases MAP3K5 kinase activity stimulated by oxidative stress and thereby prevents apoptosis. AKT mediates insulin-stimulated protein synthesis by phosphorylating TSC2 at 'Ser-939' and 'Thr-1462', thereby activating mTORC1 signaling and leading to both phosphorylation of 4E-BP1 and in activation of RPS6KB1. AKT is involved in the phosphorylation of members of the FOXO factors (Forkhead family of transcription factors), leading to binding of 14-3-3 proteins and cytoplasmic localization. In particular, FOXO1 is phosphorylated at 'Thr-24', 'Ser-256' and 'Ser-319'. FOXO3 and FOXO4 are phosphorylated on equivalent sites. AKT has an important role in the regulation of NF-kappa-B-dependent gene transcription and positively regulates the activity of CREB1 (cyclic AMP (cAMP)-response element binding protein). The phosphorylation of CREB1 induces the binding of accessory proteins that are necessary for the transcription of pro-survival genes such as BCL2 and MCL1. AKT phosphorylates 'Ser-454' on ATP citrate lyase (ACLY), thereby potentially regulating ACLY activity and fatty acid synthesis. Activates the 3B isoform of cyclic nucleotide phosphodiesterase (PDE3B) via phosphorylation of 'Ser-273', resulting in reduced cyclic AMP levels and inhibition of lipolysis. Phosphorylates PIKFYVE on 'Ser-318', which results in increased PI3P-5 activity. The Rho GTPase-activating protein DLC1 is another substrate and its phosphorylation is implicated in the regulation cell proliferation and cell growth. AKT plays a role as key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation. Signals downstream of phosphatidylinositol 3-kinase (PI3K) to mediate the effects of various growth factors such as platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin and insulin-like growth factor I (IGF-I). AKT mediates the antiapoptotic effects of IGF-I. Essential for the SPATA13-mediated regulation of cell migration and adhesion assembly and disassembly. May be involved in the regulation of the placental development. Phosphorylates STK4/MST1 at 'Thr-120' and 'Thr-387' leading to inhibition of its: kinase activity, nuclear translocation, autophosphorylation and ability to phosphorylate FOXO3. Phosphorylates STK3/MST2 at 'Thr-117' and 'Thr-384' leading to inhibition of its: cleavage, kinase activity, autophosphorylation at Thr-180, binding to RASSF1 and nuclear translocation. Phosphorylates SRPK2 and enhances its kinase activity towards SRSF2 and ACIN1 and promotes its nuclear translocation. Phosphorylates RAF1 at 'Ser-259' and negatively regulates its activity. Phosphorylation of BAD stimulates its pro-apoptotic activity. Phosphorylates KAT6A at 'Thr-369' and this phosphorylation inhibits the interaction of KAT6A with PML and negatively regulates its acetylation activity towards p53/TP53.

Technical Notes

WB: 1:500-1:2000, IHC: 1:50-1:200, IF/ICC: 1:100-1:500

Restriction

For Research Use Only. Not for use in vitro diagnostic procedures, drug use, or for administration to humans or animals.

To edit this page simply login to the control panel, click the Website Content tab and choose the View Web Pages option. Click Edit next to the Shipping & Returns page and you can change this text. A sample returns policy is shown below which you can edit as needed.

Returns Policy

You may return most new, unopened items within 30 days of delivery for a full refund. We'll also pay the return shipping costs if the return is a result of our error (you received an incorrect or defective item, etc.).

You should expect to receive your refund within four weeks of giving your package to the return shipper, however, in many cases you will receive a refund more quickly. This time period includes the transit time for us to receive your return from the shipper (5 to 10 business days), the time it takes us to process your return once we receive it (3 to 5 business days), and the time it takes your bank to process our refund request (5 to 10 business days).

If you need to return an item, simply login to your account, view the order using the "Complete Orders" link under the My Account menu and click the Return Item(s) button. We'll notify you via e-mail of your refund once we've received and processed the returned item.

Shipping

We can ship to virtually any address in the world. Note that there are restrictions on some products, and some products cannot be shipped to international destinations.

When you place an order, we will estimate shipping and delivery dates for you based on the availability of your items and the shipping options you choose. Depending on the shipping provider you choose, shipping date estimates may appear on the shipping quotes page.

Please also note that the shipping rates for many items we sell are weight-based. The weight of any such item can be found on its detail page. To reflect the policies of the shipping companies we use, all weights will be rounded up to the next full pound.

Integer et est tellus non bibendum est. Namcos tempus turpis at metus scelerisque placerat nulla eu sollicitudin felis. Pellentesque diam dolor elementum et lobortis at mollis ut risus. Sed faucibus ullamcorper mattis. Fusce molestie elit a loremos tempus scelerisque blandit tortor cursus. Quisque dolutpat orci ut metus malesuada lorem in interdum lectus scelerisque. Praesent eu odio ut nisi ullamcorper ultricies. Cum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus.

Praesent at justo congue leo adipiscing
  • Integer et est tellusInteger et est tellus non bibendum est.
  • Namcos tempusNamcos tempus turpis at metus scelerisque placerat nulla eu sollicitudin felis.
  • Pellentesque diam dolorPellentesque diam dolor elementum et lobortis at mollis ut risus.
  • Sed faucibusSed faucibus ullamcorper mattis.
  • Fusce molestie elitosFusce molestie elit a loremos tempus scelerisque blandit tortor cursus.
  • Quisque dolutpat orcisQuisque dolutpat orci ut metus malesuada lorem in interdum lectus scelerisque.
  • Praesent an modioPraesent eu odio ut nisi ullamcorper ultricies.
  • Cum sociis natoque penatibusCum sociis natoque penatibus et magnis dis parturient montes, nascetur ridiculus mus.
Top