what is akt pathway?

Question

signaling

Answer 1

Try this link:

http://www.biocarta.com/pathfiles/aktpathway.asp

It is a pathway related to apoptosis and cell survival, parts of the pathway are potential sources of cancer and have been targeted by drug discovery companies.

Hope this helps! (I really like that link by the way)

Answer 2

Akt1, also known as "Akt" or protein kinase B (PKB) is an important molecule in mammalian cellular signaling.

In humans, there are three genes in the "Akt family": Akt1, Akt2, and Akt3. These enzymes are members of the serine/threonine-specific protein kinase family (EC 2.7.11.1).

Akt1 is involved in cellular survival pathways, by inhibiting apoptotic processes. Akt1 is also able to induce protein synthesis pathways, and is therefore a key signaling protein in the cellular pathways that lead to skeletal muscle hypertrophy, and general tissue growth. Since it can block apoptosis, and thereby promote cell survival, Akt1 has been implicated as a major factor in many types of cancer. Akt (now also called Akt1) was originally identified as the oncogene in the transforming retrovirus, AKT8.

Akt2 is an important signaling molecule in the Insulin signaling pathway. It's required to induce glucose transport.

These separate roles for Akt1 and Akt2 were demonstrated by studying mice in which either the Akt1 or the Akt2 gene was deleted, or "knocked out". In a mouse which is null for Akt1 but normal for Akt2, glucose homeostasis is unperturbed, but the animals are smaller, consistent with a role for Akt1 in growth. In contrast, mice which do not have Akt2, but have normal Akt1, have mild growth deficiency and display a diabetic phenotype (insulin resistance), again consistent with the idea that Akt2 is more specific for the insulin receptor signaling pathway [1].

The role of Akt3 is less clear, though it appears to be predominantly expressed in brain. It has been reported that mice lacking Akt3 have small brains [2].

Answer 3

well that's exciting... theres nothing left ot be said, but i do work on the akt pathway and beta-catenin for Hepatitis C research

Answer 4

What Is Akt

Answer 5

Akt (protein kinase B), a serine/threonine kinase, has emerged as a critical enzyme in signal transduction pathways involved in cell proliferation, apoptosis, angiogenesis, and diabetes. In mammals three isoforms of Akt (a, b, g or Akt 1, 2, 3) are reported that exhibit a high degree of homology, but differ slightly in the localization of their regulatory phosphorylation sites. Akta is the predominant isoform in most tissues, whereas the highest expression of Aktb is observed in the insulin-responsive tissues, and Aktg is abundant in brain tissue. Each Akt isoform is composed of three functionally distinct regions: an N-terminal pleckstrin homology (PH) domain that provides a lipid-binding module to direct Akt to PIP2 and PIP3, a central catalytic domain, and a C-terminal hydrophobic motif.

The principal role of Akt is to facilitate growth factor-mediated cell survival and to block apoptotic cell death. This is achieved by phosphorylating and deactivating pro-apoptotic factors such as Bad, caspase-9, and Forkhead transcription factors (AFX, Daf-16, FKHR). The phosphorylation of Bad at Ser136 promotes its association with 14-3-3 proteins in the cytosol, which prevents Bad from localizing at the mitochondria to induce apoptosis. Akt is also known to promote cell survival by inactivating caspase-9 through phosphorylating it at Ser196. Likewise, activated Akt phosphorylates Forkhead family members, resulting in their sequestration in the cytoplasm. In the absence of survival factors and Akt activity, Forkhead family members translocate to the nucleus, where they initiate a program of gene expression (e.g., FasL) that promotes cell death. Akt is also reported to phosphorylate IKKa at Thr23 and activate it. The activated IKKa, in turn, phosphorylates IkB, targeting it for ubiquitination and proteasomal degradation. This leads to the activation and nuclear translocation of NF-kB, and transcription of NF-kB-dependent pro-survival genes, including Bcl-xL and caspase inhibitors. Akt also phosphorylates and inactivates GSK-3, allowing the activation of glycogen synthase to proceed. An important point to note is that phosphorylation of cyclin D by GSK-3 targets it for proteolysis; hence the inactivation of GSK-3 may promote the up-regulation of cyclin D and enhance cell cycling. Recently it has been shown that when Chk1, a DNA damage effector kinase, is phosphorylated by Akt at Ser280 it can no longer be phosphorylated by ATM/ATR at Ser345 to undergo activation. This may be of therapeutic significance as Chk1 inhibition is shown to enhance sensitization of tumors to chemotherapeutic agents. Akt also phosphorylates Cdc25B on Ser353, resulting in its cytoplasmic accumulation. Cdc25B undergoes activation during S-phase and plays a role in activating the mitotic kinase Cdk1/cyclinB in the cytoplasm. In relocating Cdc25B to the cytoplasm, Akt regulates its function and participates in controlling the entry of cells into mitosis.

A number of oncogenes and tumor suppressor genes that function upstream of Akt influence cancer progression by regulating Akt. Akta is expressed to various degrees in breast cancer cell lines and is important in estrogen-stimulated growth. Treatment of multiple myeloma cell lines with the Akt inhibitor, 1L-6-Hydroxymethyl-chiro-inositol 2-(R)-2-O-methyl-3-O-octadecylcarbonate (Cat. No. 124005), results in reduced survival of both drug resistant and drug sensitive cells. Akt plays a critical role in tumorigenesis, becoming activated when tumor suppressors such as p27 and PTEN lose their functions. Phosphorylation of p27 at Thr157 by Akt impairsits nuclear import. Cytoplasmic mislocalization of p27 has been strongly linked to loss of differentiation and poor outcome in breast cancer. Akt is also reported to physically associate with endogenous p21, a cell cycle inhibitor, and phosphorylate it at Thr145, causing its localization to the cytoplasm and subsequent degradation.

The link below has a great interactive model that you may find helpful!

Answer 6

suppression vs induction of androgen receptor function by the phosphatidinositoln in prostrate cancer