ATG5 Cancer Research Results

ATG5, Autophagy-related 5: Click to Expand ⟱
Source:
Type:
ATG5 (Autophagy-related 5) is a protein that plays a crucial role in the process of autophagy, a cellular mechanism that involves the degradation and recycling of damaged or dysfunctional cellular components. ATG5 is a key component of the autophagy machinery and is involved in the formation of autophagosomes, which are double-membraned vesicles that engulf and digest cellular components.
Increased expression in: breast, GBM (poor prognosis).
Decreased in: Colon, Prostate (associated with improved prognosis).


Cerv, Cervical Cancer: Click to Expand ⟱
Cervical Cancer

Scientific Papers found: Click to Expand⟱
1993- PTL,    Parthenolide induces apoptosis and autophagy through the suppression of PI3K/Akt signaling pathway in cervical cancer
- in-vitro, Cerv, HeLa
tumCV↓, TumAuto↑, Casp3↑, BAX↑, Beclin-1↑, ATG3↑, ATG5↑, Bcl-2↓, mTOR↓, PI3K↓, Akt↓, PTEN↑, ROS↑, MMP↓,

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:


Redox & Oxidative Stress

ROS↑, 1,  

Mitochondria & Bioenergetics

MMP↓, 1,  

Cell Death

Akt↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,  

Transcription & Epigenetics

tumCV↓, 1,  

Autophagy & Lysosomes

ATG3↑, 1,   ATG5↑, 1,   Beclin-1↑, 1,   TumAuto↑, 1,  

Proliferation, Differentiation & Cell State

mTOR↓, 1,   PI3K↓, 1,   PTEN↑, 1,  
Total Targets: 14

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ATG5, Autophagy-related 5
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:29  Cells:%  prod#:%  Target#:723  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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