GSR Cancer Research Results

GSR, Glutathione Reductase: Click to Expand ⟱

Source:

Type:

Glutathione reductase is an enzyme that plays a crucial role in maintaining the balance of glutathione, a powerful antioxidant found in cells. Glutathione is involved in various cellular processes, including detoxification, cell signaling, and protection against oxidative stress. Glutathione reductase helps maintain the levels of reduced glutathione (GSH) in cells. Cancer cells often have elevated levels of glutathione reductase, which allows them to maintain high levels of GSH and resist oxidative stress.
Glutathione reductase has been shown to promote cell proliferation and survival in cancer cells. Elevated levels of glutathione reductase have been found in various types of cancer, including breast, lung, and colon cancer.
Several studies have shown that inhibiting glutathione reductase can increase the sensitivity of cancer cells to chemotherapy and radiation therapy, and may also induce apoptosis in cancer cells.

Scientific Papers found: Click to Expand⟱

1902-

AgNPs,

Modulation of the mechanism of action of antibacterial silver N-heterocyclic carbene complexes by variation of the halide ligand

in-vitro,

NA,

0.03–0.12 μM

bacterial

TrxR↓, antibacterial silver NHC complexes with halide ligands of the general type (NHC)AgX (X = Cl, Br or I) that showed potent inhibition of purified bacterial thioredoxin reductase (TrxR) and glutathione reductase (GR
GSR↓,
GSH↓, glutathione (GSH) depletion

2818-

CUR,

Novel Insight to Neuroprotective Potential of Curcumin: A Mechanistic Review of Possible Involvement of Mitochondrial Biogenesis and PI3/Akt/ GSK3 or PI3/Akt/CREB/BDNF Signaling Pathways

Review,

AD,

*neuroP↑, Curcumin's protective functions against neural cell degeneration due to mitochondrial dysfunction and consequent events such as oxidative stress, inflammation, and apoptosis in neural cells have been documented
*ROS↓, studies show that curcumin exerts neuroprotective effects on oxidative stress.
*Inflam↓,
*Apoptosis↓,
*cognitive↑, cognitive performance to receive the title of neuroprotective
*cardioP↑, Studies have shown that curcumin can induce cell regeneration and defense in multiple organs such as the brain, cardiovascular system,
other↑, It has been shown that chronic use of curcumin in patients with neurodegenerative disorder can cause gray matter volume increase
*COX2↓, Curcumin also decreased the brain protein levels and activity of cyclooxygenase 2 (COX-2)
*IL1β↓, inhibition of IL-1β and TNF-α production, and enhancement of Nf-Kβ inhibition
*TNF-α↓,
NF-kB↓,
*PGE2↓, hronic curcumin therapy has shown a significant decrease in lipopolysaccharide (LPS)-induced elevation of brain prostaglandin E2 (PGE2) synthesis in rats
*iNOS↓, curcumin pretreatment decreased NOS activity in the ischemic rat model
*NO↓, curcumin has been shown to decrease NOS expression and NO production in rat brain tissue
*IL2↓, IL-2 is a cytokine that is anti-inflammatory. Numerous studies have shown that curcumin increases the secretion of IL-2
*IL4↓, curcumin reduced levels of IL-4
*IL6↓, Numerous studies have shown that curcumin in neurodegenerative events attenuates IL-6 production
*INF-γ↓, curcumin reduced the production of INF-γ, as pro-inflammatory cytokine
*GSK‐3β↓, Furthermore, previous findings have confirmed that inhibition of GSK-3β or CREB activation by curcumin has reduced the production of pro-inflammatory mediators under different conditions
*STAT↓, Inhibition of GSK-3β by curcumin has been found to result in reduced STAT activation
*GSH↑, chronic curcumin therapy increased glutathione levels in primary cultivated rat cerebral cortical cells
*MDA↓, multiple doses of 5, 10, 40 and 60 mg/kg) in rodents will inhibit neurodegenerative agent malicious effects, and reduce the amount of MDA and lipid peroxidation in brain tissue
*lipid-P↓,
*SOD↑, Curcumin induces increased production of SOD, glutathione peroxidase (GPx), CAT, and glutathione reductase (GR) activating antioxidant defenses
*GPx↑,
*Catalase↑,
*GSR↓,
*LDH↓, Curcumin decreased lactate dehydrogenase, lipoid peroxidation, ROS, H2O2 and inhibited Caspase 3 and 9
*H2O2↓,
*Casp3↓,
*Casp9↓,
*NRF2↑, ncreased mitochondrial uncoupling protein 2 and increased mitochondrial biogenesis. Nuclear factor-erythroid 2-related factor 2 (Nrf2)
*AIF↓, Curcumin treatment decreased the number of AIF positive nuclei 24 h after treatment in the hippocampus,
*ATP↑, curcumin in hippocampal cells induced an increase in mitochondrial mass leading to increased production of ATP with major improvements in mitochondrial efficiency

5012-

DSF,

Cu,

Advancing Cancer Therapy with Copper/Disulfiram Nanomedicines and Drug Delivery Systems

ROS↑, DSF’s anticancer mechanism is primarily due to its generating reactive oxygen species, inhibiting aldehyde dehydrogenase (ALDH) activity inhibition, and decreasing the levels of transcriptional proteins
ALDH↓,
TumCP↓, DSF also shows inhibitory effects in cancer cell proliferation, the self-renewal of cancer stem cells (CSCs), angiogenesis, drug resistance, and suppresses cancer cell metastasis.
CSCs↓,
angioG↓,
TumMeta↓,
DNAdam↑, anti-cancer mechanism of DSF/Cu (II) may be mediated by the regulation of reactive oxygen species (ROS), enzyme activity regulation, induction of DNA damage, proteasome inhibition, and transcription factors
Proteasome↓,
SOD1↓, The complex of DSF and Cu (II)has been reported to inhibit the enzyme superoxide dismutase 1 (SOD1), one of the major enzymesthat mitigates oxidative damage in melanoma cells
GSR↓, The inhibition of Glutathione reductase (GSR) inhibition by DSF disrupts glutathione GSH redox cycling, producing an accumulation of oxidized glutathione (GSSG) and a lower GSH/GSSG ratio, producing an increase in ROS level
ox-GSSG↑,
GSH/GSSG↓,
MMP↓, DSF induces the disruption of the mitochondrial membrane potential and cause apoptosis in human melanoma cell lines
Akt↓, induced the apoptosis of erbB2-positive breast cancer cells by inhibiting AKT, cyclin D1, and NFκB signaling
cycD1/CCND1↓,
NF-kB↓,
CSCs↓, In hepatocellular carcinoma, DSF decreases CSCs by inhibiting the p38 mitogen-activated protein kinase (MAPK) pathway [118].
MAPK↓,
angioG↓, Thus, the inhibition of DSF/Cu (II) in CSCs decrease angiogenesis.
DrugR↓, DSF/Cu (II) overcomes drug resistance via targeting the proteasome, epithelial–mesenchymal transition (EMT), P-gp, CSC activity
EMT↓,
Vim↓, By downregulating associated proteins such as Vimentin, DSF/Cu (II) inhibits the EMT, which consequently overcomes the paclitaxel resistance of prostate and lung cancer
BioAv↑, The use of these nanoparticle-based formulations can increase the accumulation of DSF at the target site, thereby reducing the toxic effects on healthy tissues and improving the therapeutic index.
eff↑, In clinical trials, DSF is provided orally, but Cu (II) is critical for the efficacy of DSF

2919-

LT,

Luteolin as a potential therapeutic candidate for lung cancer: Emerging preclinical evidence

Review,

Var,

RadioS↑, it can be used as an adjuvant to radio-chemotherapy and helps to ameliorate cancer complications
ChemoSen↑,
chemoP↑,
*lipid-P↓, ↓LPO, ↑CAT, ↑SOD, ↑GPx, ↑GST, ↑GSH, ↓TNF-α, ↓IL-1β, ↓Caspase-3, ↑IL-10
*Catalase↑,
*SOD↑,
*GPx↑,
*GSTs↑,
*GSH↑,
*TNF-α↓,
*IL1β↓,
*Casp3↓,
*IL10↑,
NRF2↓, Lung cancer model ↓Nrf2, ↓HO-1, ↓NQO1, ↓GSH
HO-1↓,
NQO1↓,
GSH↓,
MET↓, Lung cancer model ↓MET, ↓p-MET, ↓p-Akt, ↓HGF
p‑MET↓,
p‑Akt↓,
HGF/c-Met↓,
NF-kB↓, Lung cancer model ↓NF-κB, ↓Bcl-XL, ↓MnSOD, ↑Caspase-8, ↑Caspase-3, ↑PARP
Bcl-2↓,
SOD2↓,
Casp8↑,
Casp3↑,
PARP↑,
MAPK↓, LLC-induced BCP mouse model ↓p38 MAPK, ↓GFAP, ↓IBA1, ↓NLRP3, ↓ASC, ↓Caspase1, ↓IL-1β
NLRP3↓,
ASC↓,
Casp1↓,
IL6↓, Lung cancer model ↓TNF‑α, ↓IL‑6, ↓MuRF1, ↓Atrogin-1, ↓IKKβ, ↓p‑p65, ↓p-p38
IKKα↓,
p‑p65↓,
p‑p38↑,
MMP2↓, Lung cancer model ↓MMP-2, ↓ICAM-1, ↓EGFR, ↓p-PI3K, ↓p-Akt
ICAM-1↓,
EGFR↑,
p‑PI3K↓,
E-cadherin↓, Lung cancer model ↑E-cadherin, ↑ZO-1, ↓N-cadherin, ↓Claudin-1, ↓β-Catenin, ↓Snail, ↓Vimentin, ↓Integrin β1, ↓FAK
ZO-1↑,
N-cadherin↓,
CLDN1↓,
β-catenin/ZEB1↓,
Snail↓,
Vim↑,
ITGB1↓,
FAK↓,
p‑Src↓, Lung cancer model ↓p-FAK, ↓p-Src, ↓Rac1, ↓Cdc42, ↓RhoA
Rac1↓,
Cdc42↓,
Rho↓,
PCNA↓, Lung cancer model ↓Cyclin B1, ↑p21, ↑p-Cdc2, ↓Vimentin, ↓MMP9, ↑E-cadherin, ↓AIM2, ↓Pro-caspase-1, ↓Caspase-1 p10, ↓Pro-IL-1β, ↓IL-1β, ↓PCNA
Tyro3↓, Lung cancer model ↓TAM RTKs, ↓Tyro3, ↓Axl, ↓MerTK, ↑p21
AXL↓,
CEA↓, B(a)P induced lung carcinogenesis ↓CEA, ↓NSE, ↑SOD, ↑CAT, ↑GPx, ↑GR, ↑GST, ↑GSH, ↑Vitamin E, ↑Vitamin C, ↓PCNA, ↓CYP1A1, ↓NF-kB
NSE↓,
SOD↓,
Catalase↓,
GPx↓,
GSR↓,
GSTs↓,
GSH↓,
VitE↓,
VitC↓,
CYP1A1↓,
cFos↑, Lung cancer model ↓Claudin-2, ↑p-ERK1/2, ↑c-Fos
AR↓, ↓Androgen receptor
AIF↑, Lung cancer model ↑Apoptosis-inducing factor protein
p‑STAT6↓, ↓p-STAT6, ↓Arginase-1, ↓MRC1, ↓CCL2
p‑MDM2↓, Lung cancer model ↓p-PI3K, ↓p-Akt, ↓p-MDM2, ↑p-P53, ↓Bcl-2, ↑Bax
NOTCH1↓, Lung cancer model ↑Bax, ↑Cleaved-caspase 3, ↓Bcl2, ↑circ_0000190, ↓miR-130a-3p, ↓Notch-1, ↓Hes-1, ↓VEGF
VEGF↓,
H3↓, Lung cancer model ↑Caspase 3, ↑Caspase 7, ↓H3 and H4 HDAC activities
H4↓,
HDAC↓,
SIRT1↓, Lung cancer model ↑Bax/Bcl-2, ↓Sirt1
ROS↑, Lung cancer model ↓NF-kB, ↑JNK, ↑Caspase 3, ↑PARP, ↑ROS, ↓SOD
DR5↑, Lung cancer model ↑Caspase-8, ↑Caspase-3, ↑Caspase-9, ↑DR5, ↑p-Drp1, ↑Cytochrome c, ↑p-JNK
Cyt‑c↑,
p‑JNK↑,
PTEN↓, Lung cancer model 1/5/10/30/50/80/100 μmol/L ↑Cleaved caspase-3, ↑PARP, ↑Bax, ↓Bcl-2, ↓EGFR, ↓PI3K/Akt/PTEN/mTOR, ↓CD34, ↓PCNA
mTOR↓,
CD34↓,
FasL↑, Lung cancer model ↑DR 4, ↑FasL, ↑Fas receptor, ↑Bax, ↑Bad, ↓Bcl-2, ↑Cytochrome c, ↓XIAP, ↑p-eIF2α, ↑CHOP, ↑p-JNK, ↑LC3II
Fas↑,
XIAP↓,
p‑eIF2α↑,
CHOP↑,
LC3II↑,
PD-1↓, Lung cancer model ↓PD-L1, ↓STAT3, ↑IL-2
STAT3↓,
IL2↑,
EMT↓, Luteolin exerts anticancer activity by inhibiting EMT, and the possible mechanisms include the inhibition of the EGFR-PI3K-AKT and integrin β1-FAK/Src signaling pathways
cachexia↓, luteolin could be a potential safe and efficient alternative therapy for the treatment of cancer cachexi
BioAv↑, A low-energy blend of castor oil, kolliphor and polyethylene glycol 200 increases the solubility of luteolin by a factor of approximately 83
*Half-Life↝, ats administered an intraperitoneal injection of luteolin (60 mg/kg) absorbed it rapidly as well, with peak levels reached at 0.083 h (71.99 ± 11.04 μg/mL) and a prolonged half-life (3.2 ± 0.7 h)
*eff↑, Luteolin chitosan-encapsulated nano-emulsions increase trans-nasal mucosal permeation nearly 6-fold, drug half-life 10-fold, and biodistribution of luteolin in brain tissue 4.4-fold after nasal administration

2544-

M-Blu,

Methylene blue and its importance in medicine

Review,

NA,

*ROS↓, Methylene blue was recognized as an antimalarial agent when it was observed that it reduced reactive oxygen species (ROS) by inhibiting Plasmodium falciparum glutathione reductase and by selectively inducing oxidative stress.
antiOx↑, Methylene blue has been used in Alzheimer's treatment, considering its features of tau protein inhibition, anti-ROS antioxidant properties
BBB↑, Methylene blue (MB, methylthioninium chloride), a phenothiazine known for its ability to cross the blood-brain barrier and exert neuroprotective effects
neuroP↑,
GSR↓, MB can be both a substrate and an inhibitor of glutathione reductase, which is an important enzyme of glutathione metabolism
tau↓, Methylene blue has been proven to inhibit the accumulation of tau proteins, which is considered among the causes of AD,

3249-

PBG,

Can Propolis Be a Useful Adjuvant in Brain and Neurological Disorders and Injuries? A Systematic Scoping Review of the Latest Experimental Evidence

Review,

Var,

*Inflam↓, ropolis was consistently demonstrated to reduce the expression of inflammatory and oxidative markers such as malonaldehyde (MDA), tumor necrosis factor-α (TNF-α), nitric oxide (NO), and inducible nitric oxide synthase (iNOS)
*ROS↓,
*MDA↓,
*TNF-α↓,
*NO↓,
*iNOS↓,
*SOD↑, while increasing and maintaining antioxidant parameters, namely superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR), and glutathione (GSH)
*GPx↑,
*GSR↓,
*GSH↑,
*neuroP↑, neuroprotective effect of propolis was also demonstrated in terms of alleviating symptoms associated with aneurysm, ischemia, ischemia-reperfusion and traumatic brain injuries.
*IL6↓, Propolis reduced the expression of interleukin-6 (IL-6), TNF-α, matrix metalloproteinase-2 (MMP-2), MMP-9, monocyte chemotactic protein-1 (MCP-1), and iNOS
*MMP2↓,
*MMP9↓,
*MCP1↓,
*HSP70/HSPA5↑, while increasing the expression of protective proteins such as heat shock protein-70 (hsp70)
*motorD↑, significantly ameliorate the impairment of sensory–motor and other physical indices in animals subjected to these injuries
*Pain↓, Unsurprisingly, propolis was shown to be effective in attenuating symptoms of neuroinflammation, pain, and oxidative stress.
*VCAM-1↓, consistently shown to reduce inflammation markers such as vascular cell adhesion molecule-1 (VCAM-1), nuclear factor kappa B (NF-kB), mitogen-activated protein kinase (MAPK), and c-Jun N-terminal kinase (JNK)-
*NF-kB↓,
*MAPK↓,
*JNK↓,
*IL1β↓, It also reduced the expression of reactive oxygen species (ROS) and pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α
*AChE↓, propolis inhibited the activity of both acetylcholinesterase and butyrylcholinesterase in a dose-dependent manner
*toxicity∅, Kalia et al. (2014) observed no cytotoxicity in organs, including the brain of normal mice fed up to 1000 mg propolis extract/ kg body weight.
cognitive↑, figure 4

2651-

PLB,

Oxidative Stress Inducers in Cancer Therapy: Preclinical and Clinical Evidence

Review,

Var,

ROS↑, Various studies have shown that plumbagin is a potent inducer of ROS
TrxR↓, The mechanism underlying ROS induction by plumbagin has predominantly been attributed to inhibition of the antioxidant enzymes TrxR
GSR↓, and glutathione reductase
ER Stress↓, mediates its anticancer effect by inducing ER stress-mediated apoptosis
TumCCA↑, S/G2 and G2/M cell cycle arrest
MMP↓, and mitochondrial membrane depolarization in an ROS-dependent manner
NF-kB↓, plumbagin was found to inhibit the NF-κB [57], PI3K/AKT/mTOR [58] and MKP1/2 [59] pathways in non-small cell lung cancer, bladder cancer, and lymphoma,
PI3K↓,
Akt↓,
mTOR↓,
MKP1↓,
MKP2↓,
ChemoSen↑, improve the efficacy of existing chemotherapeutic strategies

4911-

Sal,

MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells

in-vitro,

Var,

DU145

IC50 = 0.45 μM

MUC1-C↓, Our results show that SAL-induced MUC1-C suppression downregulates a MUC1-C→MYC pathway
Ferroptosis↑, SAL as a unique small molecule inhibitor of MUC1-C signaling and demonstrate that MUC1-C is an important effector of resistance to ferroptosis.
CSCs↓, SAL is an effective inhibitor of CSCs
NF-kB↓, SAL suppressed MUC1-C and NF-κB expression in DU-145 and H660 cells
GSR↓, MUC1-C induces GSR expression and GSH production. We found that SAL treatment decreases GSR mRNA and protein levels
GSH↑,
Iron↑, SAL kills CSCs by sequestering iron in lysosomes and inducing ferroptosis

1477-

SFN,

Sulforaphane Induces Oxidative Stress and Death by p53-Independent Mechanism: Implication of Impaired Glutathione Recycling

in-vitro,

OS,

MG63

>10 μM

tumCV↓,
Apoptosis↑,
Casp3↑,
ROS↑, >=10 μM, At these higher doses, SFN increased ROS levels
GSR↓, inhibition of glutathione reductase
GPx↓,

3313-

SIL,

Silymarin attenuates post-weaning bisphenol A-induced renal injury by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 signaling modulation in male Wistar rats

in-vivo,

NA,

50-100 mg/kg/day

Twenty-four male Wistar rats

*NRF2↑, silymarin activates the Nrf2/HO-1 pathway, thus providing cellular defense
*HO-1↑,
*creat↓, Silymarin diminished BPA-induced rise in serum urea, creatinine, BUN, and plasma kim-1 levels.
*BUN↓,
*RenoP↑, improved renal histoarchitecture in BPA-exposed rats.
*MDA↓, suppression of BPA-induced rise in renal iron, MDA, TNF-α, IL-1β, and cytochrome c levels, and myeloperoxidase and caspase 3 activities by silymarin therapy.
*TNF-α↓,
*IL1β↓,
*Cyt‑c↓,
*Casp3↓,
*GSTs↓, silymarin attenuated BPA-induced downregulation of Nrf2 and GSH levels, and HO-1, GPX4, SOD, catalase, GST, and GR activities.
*GSH↑,
*GPx4↑,
*SOD↑,
*GSR↓,
*Ferroptosis↓, silymarin mitigated post-weaning BPA-induced renal toxicity by suppressing ferroptosis and amyloidosis through Kim-1/Nrf2/HO-1 modulation.

114-

VitC,

QC,

Chemoprevention of prostate cancer cells by vitamin C plus quercetin: role of Nrf2 in inducing oxidative stress

in-vitro,

Pca,

PC3

 0.1-1000 uM

in-vitro,

Pca,

DU145

GPx↓, significant reduction of GPx, GR and NQO1 enzymatic activity
GSR↓,
NQO1↓,
NRF2↓, Our study revealed the significant effects of sequential treatment with VC + Q on Nrf2 suppression in prostate cancer cells
ROS↑, The level of ROS had significant reduction up to 18% (P ¼ 0.046) when DU145 cells treated with dose no.1 of VC þ Q to compare with the control

Showing Research Papers: 1 to 11 of 11

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 11

Pathway results for Effect on Cancer / Diseased Cells:

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Catalase↑, 2, Ferroptosis↓, 1, GPx↑, 3, GPx4↑, 1, GSH↑, 4, GSR↓, 3, GSTs↓, 1, GSTs↑, 1, H2O2↓, 1, HO-1↑, 1, lipid-P↓, 2, MDA↓, 3, NRF2↑, 2, ROS↓, 3, SOD↑, 4,

Mitochondria & Bioenergetics ⓘ

AIF↓, 1, ATP↑, 1,

Core Metabolism/Glycolysis ⓘ

BUN↓, 1, LDH↓, 1,

Cell Death ⓘ

Apoptosis↓, 1, Casp3↓, 3, Casp9↓, 1, Cyt‑c↓, 1, Ferroptosis↓, 1, iNOS↓, 2, JNK↓, 1, MAPK↓, 1,

Protein Folding & ER Stress ⓘ

HSP70/HSPA5↑, 1,

Proliferation, Differentiation & Cell State ⓘ

GSK‐3β↓, 1, STAT↓, 1,

Migration ⓘ

MMP2↓, 1, MMP9↓, 1, VCAM-1↓, 1,

Angiogenesis & Vasculature ⓘ

NO↓, 2,

Immune & Inflammatory Signaling ⓘ

COX2↓, 1, IL10↑, 1, IL1β↓, 4, IL2↓, 1, IL4↓, 1, IL6↓, 2, INF-γ↓, 1, Inflam↓, 2, MCP1↓, 1, NF-kB↓, 1, PGE2↓, 1, TNF-α↓, 4,

Synaptic & Neurotransmission ⓘ

AChE↓, 1,

Drug Metabolism & Resistance ⓘ

eff↑, 1, Half-Life↝, 1,

Clinical Biomarkers ⓘ

creat↓, 1, IL6↓, 2, LDH↓, 1,

Functional Outcomes ⓘ

cardioP↑, 1, cognitive↑, 1, motorD↑, 1, neuroP↑, 2, Pain↓, 1, RenoP↑, 1, toxicity∅, 1,
Total Targets: 59

Scientific Paper Hit Count for: GSR, Glutathione Reductase

1 Silver-NanoParticles
1 Curcumin
1 Disulfiram
1 Copper and Cu NanoParticles
1 Luteolin
1 Methylene blue
1 Propolis -bee glue
1 Plumbagin
1 salinomycin
1 Sulforaphane (mainly Broccoli)
1 Silymarin (Milk Thistle) silibinin
1 Vitamin C (Ascorbic Acid)
1 Quercetin

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#:633  State#:%  Dir#:1
  wNotes=on  sortOrder:rid,rpid

GSR Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Transcription & Epigenetics ⓘ

Protein Folding & ER Stress ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Cell Cycle & Senescence ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Protein Aggregation ⓘ

Hormonal & Nuclear Receptors ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Protein Folding & ER Stress ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Immune & Inflammatory Signaling ⓘ

Synaptic & Neurotransmission ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

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