Necroptosis Cancer Research Results

Necroptosis, Necroptosis: Click to Expand ⟱
Source:
Type: type of cell death
Necroptosis, is a form of programmed cell death that is regulated by the cell's own mechanisms. It is a form of cell death that is mediated by specific signaling pathways, including the RIP1-RIP3-MLKL pathway. Necroptosis is characterized by the activation of specific enzymes, such as RIP1 and RIP3, which lead to the formation of a necroptotic complex that ultimately causes cell death.

Necroptosis expression can be elevated in certain types of cancer, it can also be reduced in other types of cancer.
Bladder, Bladder Cancer: Click to Expand ⟱
Bladder Cancer
Scientific Papers found: Click to Expand⟱
2009- SK,    Necroptosis inhibits autophagy by regulating the formation of RIP3/p62/Keap1 complex in shikonin-induced ROS dependent cell death of human bladder cancer
- in-vitro, Bladder, NA
TumCG↓, selectivity↑, *toxicity∅, Necroptosis↑, ROS↑, p62↑, Keap1↑, *NRF2↑, eff↑,

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 ⓘ

Keap1↑, 1,   ROS↑, 1,  

Cell Death ⓘ

Necroptosis↑, 1,  

Autophagy & Lysosomes ⓘ

p62↑, 1,  

Proliferation, Differentiation & Cell State ⓘ

TumCG↓, 1,  

Drug Metabolism & Resistance ⓘ

eff↑, 1,   selectivity↑, 1,  
Total Targets: 7

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

NRF2↑, 1,  

Functional Outcomes ⓘ

toxicity∅, 1,  
Total Targets: 2

Scientific Paper Hit Count for: Necroptosis, Necroptosis
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:32  Cells:%  prod#:%  Target#:944  State#:%  Dir#:2
  wNotes=0  sortOrder:rid,rpid

 

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