AKT1 Cancer Research Results

AKT1, v-akt murine thymoma viral oncogene homolog 1: Click to Expand ⟱
Source: CGL-Driver Genes
Type: Oncogene
RAC‑α serine/threonine‑protein kinase (commonly referred to as AKT1)
It is known as the “survival kinase”. Akt mediates cell survival proliferation mainly by inhibiting the Bcl2 and MDM2 pathways, which otherwise promotes apoptosis.
Mechanisms of Akt1 in Cancer
Cell Survival: Akt1 promotes cell survival by inhibiting apoptotic pathways, allowing cancer cells to evade programmed cell death.
Cell Proliferation: It enhances cell cycle progression and proliferation through various signaling pathways.
Metabolism: Akt1 regulates glucose metabolism and lipid synthesis, supporting the metabolic demands of rapidly dividing cancer cells.
Angiogenesis: It promotes the formation of new blood vessels, facilitating tumor growth and metastasis.

Akt1 is frequently activated, with its expression levels often correlating with prognosis across various cancer types.
Scientific Papers found: Click to Expand⟱
4252- EA,    Effect of ellagic acid on BDNF/PI3K/AKT-mediated signaling pathways in mouse models of depression
- in-vivo, NA, NA
*BDNF↑, *p‑AKT1↑,

Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


Core Metabolism/Glycolysis ⓘ

p‑AKT1↑, 1,  

Synaptic & Neurotransmission ⓘ

BDNF↑, 1,  
Total Targets: 2

Scientific Paper Hit Count for: AKT1, v-akt murine thymoma viral oncogene homolog 1
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:5  State#:1  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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