ATF4 Cancer Research Results

ATF4, Activating Transcription Factor 4: Click to Expand ⟱
Source:
Type: protein
ATF4 (Activating Transcription Factor 4) is a protein that plays a crucial role in various cellular processes, including stress response, cell growth, and differentiation.
ATF4 is overexpressed in several types of cancer, including breast, lung, colon, and pancreatic cancer. The overexpression of ATF4 can contribute to cancer cell growth, survival, and resistance to chemotherapy.
ATF4 promotes cancer cell growth by regulating the expression of genes involved in cell proliferation, angiogenesis, and metastasis. It also inhibits apoptosis (programmed cell death) by regulating the expression of anti-apoptotic genes.


AML, Acute Myeloid Leukemia: Click to Expand ⟱
Acute Myeloid Leukemia

Scientific Papers found: Click to Expand⟱
5107- SSE,    Involvement of p38 in signal switching from autophagy to apoptosis via the PERK/eIF2α/ATF4 axis in selenite-treated NB4 cells
- vitro+vivo, AML, APL NB4
PERK↑, eIF2α↑, ATF4↑, Apoptosis↑, AntiTum↑, ER Stress↑, p38↑,

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:


Cell Death

Apoptosis↑, 1,   p38↑, 1,  

Protein Folding & ER Stress

eIF2α↑, 1,   ER Stress↑, 1,   PERK↑, 1,  

Angiogenesis & Vasculature

ATF4↑, 1,  

Functional Outcomes

AntiTum↑, 1,  
Total Targets: 7

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ATF4, Activating Transcription Factor 4
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:2  Cells:%  prod#:%  Target#:730  State#:%  Dir#:2
wNotes=0 sortOrder:rid,rpid

 

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