ATR Cancer Research Results

ATR, Ataxia-Telangiectasia and Rad3-related: Click to Expand ⟱
Source:
Type:
ATR (Ataxia-Telangiectasia and Rad3-related) is a serine/threonine kinase that plays a crucial role in maintaining genome stability and preventing cancer.

ATR is a protein kinase that is activated in response to DNA damage, particularly replication stress and single-strand breaks. When DNA damage occurs, ATR is activated and phosphorylates a variety of downstream targets, including Chk1, p53, and BRCA1. This activation of ATR triggers a signaling cascade that leads to cell cycle arrest, DNA repair, and apoptosis (programmed cell death) if the damage is too severe to be repaired.
ATR is frequently overexpressed in cancers, and its expression is associated with a more aggressive disease and poorer outcomes.
Pca, Prostate Cancer: Click to Expand ⟱
Prostate Cancer: Alterations in genes such as ERG, SPOP, MYC, androgen receptor (AR), and CHD1, drive PCa progression.
TP53 is the most commonly mutated gene in human cancer.
HH↑, GLI-1↑, SHH↑ P53↓
The loss of p53 and/or other tumor suppressor genes, reduced capacity for DNA repair, the dysfunction of telomerase activity, and changes in the pathways that govern the growth of cells also mediate the progression of Pca.
It has been well documented that Ca2+ influx and MDR1 upregulation are highly associated with GEM metabolism in human pancreatic carcinoma.
Increased Growth factor IGF-1/IGF-1R axis activation mediated by both PI3K/Akt or RAF/MEK/ERK system and AR expression remains important in the development and progression of prostate cancer.
It has been demonstrated that prostate cancer cells are relatively sensitive to heat stress.
Long non-coding RNA MALAT1 has been reported as an oncogenic target in multiple types of cancers, including PC.
Scientific Papers found: Click to Expand⟱
7507- FA,    Assessment of the anticancer mechanism of ferulic acid via cell cycle and apoptotic pathways in human prostate cancer cell lines
- in-vitro, Pca, LNCaP - in-vitro, Pca, PC3
Dose↝, ATR↑, ATM↑, P21↑, p27/CDKN1B↑, E2F4↑, RB1↑, TP53↑, cycD1/CCND1↓, CDK2↓, CDK4↓, CDK6↓, TumCP↓, Casp1↑, Casp2↑, Casp8↑, Fas↑, TRADD↑, Bcl-2↓, XIAP↓, TumCCA↑,

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:


NA, unassigned(tgid=0) ⓘ

E2F4↑, 1,   TRADD↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

XIAP↓, 1,  

Cell Death(tgid=5) ⓘ

Bcl-2↓, 1,   Casp1↑, 1,   Casp2↑, 1,   Casp8↑, 1,   Fas↑, 1,   p27/CDKN1B↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,   ATR↑, 1,   TP53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

CDK2↓, 1,   CDK4↓, 1,   cycD1/CCND1↓, 1,   P21↑, 1,   RB1↑, 1,   TumCCA↑, 1,  

Migration(tgid=13) ⓘ

TumCP↓, 1,  

Hormonal & Nuclear Receptors(tgid=20) ⓘ

CDK6↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

Dose↝, 1,  

Clinical Biomarkers(tgid=22) ⓘ

TP53↑, 1,  
Total Targets: 22

Pathway results for Effect on Normal Cells:


Total Targets: 0

Scientific Paper Hit Count for: ATR, Ataxia-Telangiectasia and Rad3-related
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:22  Cells:%  prod#:%  Target#:717  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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