Database Query Results : Allicin (mainly Garlic), , ER Stress

AL, Allicin (mainly Garlic): Click to Expand ⟱
Features:
Garlic (Allium sativum L.) (active ingredient- Allicin, an active sulfer compound).

Allicin — a reactive organosulfur thiosulfinate generated in situ when garlic (Allium sativum) tissue is crushed (alliin → allicin via alliinase). Functionally, it behaves as a short-lived electrophilic “reactive sulfur species” that rapidly modifies cellular thiols (e.g., glutathione and cysteine residues on proteins), producing broad redox and stress-signaling effects. Classification: small-molecule phytochemical (organosulfur thiosulfinate). Standard abbreviation(s): AL (common in Nestronics), “allicin”. Source/origin: freshly crushed raw garlic; allicin is not present in intact cloves and is chemically unstable, converting to other organosulfur metabolites after formation.

Primary mechanisms (ranked):

  1. Thiol reactivity and redox disruption: rapid GSH/protein-thiol modification (S-thioallylation), shifting redox buffering and triggering oxidative/electrophilic stress signaling.
  2. Mitochondrial stress and intrinsic apoptosis (context-dependent): ΔΨm disruption, cytochrome-c release, caspase activation, ER stress/UPR engagement (often downstream of redox stress).
  3. Inflammatory transcriptional suppression (context-dependent): inhibition of NF-κB–linked programs and, in some models, STAT3 signaling.
  4. Acetate metabolism constraint (model-dependent): reversible inhibition of acetyl-CoA synthetase activity (ACS/ACSS), potentially impacting acetate→acetyl-CoA flux under metabolic stress.
  5. Growth and invasion signaling attenuation (model-dependent): PI3K/AKT and MAPK network modulation with downstream effects on EMT/MMPs and angiogenic programs (e.g., HIF-1α/VEGF).

Bioavailability / PK relevance: “Allicin exposure” is dominated by formation conditions and rapid chemical/biologic turnover. Many oral preparations deliver alliin/alliinase that may generate allicin after ingestion; measured systemic allicin is typically transient, while downstream allyl-sulfur metabolites (e.g., allyl methyl sulfide–related products) are more detectable. Cooking/processing and GI conditions substantially change allicin bioequivalence versus crushed raw garlic.

In-vitro vs systemic exposure relevance: Many anticancer cell studies use ~50–300 µM allicin; whether such free allicin concentrations are achievable at tumor sites after dietary/supplement intake is uncertain because of rapid thiol quenching and conversion to other sulfur species. Reported biological effects at lower concentrations may still occur locally (GI lumen/mucosa) or via metabolites, but direct extrapolation from high-µM in-vitro dosing is high-risk.

Clinical evidence status: Predominantly preclinical (cell/animal) for anticancer mechanisms; human data are mixed and often evaluate garlic preparations rather than purified allicin, with outcomes confounded by formulation-dependent “allicin bioequivalence” and co-occurring organosulfur compounds (e.g., DADS/DATS/SAMC). Cancer-therapeutic evidence remains inconclusive.

DADS (diallyl disulfide is a sulfur-based anticancer drug generated from garlic)
Summary:
- Four main organic sulfides in garlic, diallyl disulfide (DADS), diallyl trisulfide (DATS), S-allylmercaptocysteine (SAMC) and allicin.
- Reversible inhibitor of ACSS2.
- may inhibit NF-κB signaling
- induce oxidative stress in cancer cells by generating ROS
- might downregulate STAT3 activation
- Inconclusive evidence for cancer treatment.
- may inhibit platelet aggregation
Allicin is a reactive sulfur species (RSS) [23] with oxidizing properties, and it is able to oxidize thiols in cells, e.g., glutathione and cysteine residues in proteins.
-Allicin is not present in intact garlic; rather, it is formed when garlic is chopped or crushed. -Using crushed or chopped raw garlic or adding garlic at the end of the cooking process (after the heat is reduced) can help preserve its potential allicin content.
"Consumption of alliinase-inhibited cooked garlic was found to give higher than expected allicin bioequivalence, with AMS formation being about 30% (roasted garlic) or 16% (boiled garlic) that of crushed raw garlic."

-Allicin is not present in intact garlic.
-It's formed enzymatically when alliin (a sulfur-containing amino acid) is converted by alliinase when garlic is chopped or crushed.Best consumed raw immediately after crushing (wait 5–10 min before consuming for full conversion)
-Allicin is unstable, degrading within hours into other sulfur compounds (like diallyl disulfide).

-Note half-life reports vary 2.5-90hrs?.
-moderately water-soluble but rapidly degrades/quenched (especially with thiols), so aqueous solutions have limited practical stability : BioAv


Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, Ca+2↑, Cyt‑c↑, Caspases↑, DNA damage↑, UPR↑, cl-PARP↑, HSP↓
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, GSH↓
- Raises AntiOxidant defense in Normal Cells: NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, p38↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- PI3K/AKT(Inhibition), JAK/STATs, Wnt/β-catenin, AMPK, MAPK/ERK, and JNK.
- inhibit Growth/Metastases : EMT↓, MMP2↓, MMP9↓, VEGF↓, ERK↓
- reactivate genes thereby inhibiting cancer cell growth : HDAC↓(not commonly listed as inhibitor), DNMT1↓, P53↑, HSP↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓, cyclin E↓, CDK2↓, CDK4↓, CDK6↓,
- inhibits Migration/Invasion : TumCMig↓, FAK↓, ERK↓,
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓,
- inhibits Cancer Stem Cells : CSC↓,
- Others: PI3K↓, AKT↓, STAT3, Wnt↓, β-catenin↓, AMPK↓, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,
- Selectivity: Cancer Cells vs Normal Cells

Allicin has been reported to exhibit a range of effects, including:
Antimicrobial activity: 10-50 μM
Antioxidant activity: 10-100 μM
Anti-inflammatory activity: 20-50 μM
Anticancer activity: 50-100 μM or (50–300uM) (2–5 mg allicin per kilogram of body weight per day)
Cardiovascular health: 20-50 μM

Approximate μM concentrations of allicin that can be achieved:
1 clove of garlic (3g): approximately 10-50 μM of allicin
single clove of garlic may yield about 5–9 mg of allicin,
1 tablespoon of minced garlic (15g): approximately 50-150 μM of allicin
1 cup of chopped garlic (100g): approximately 200-500 μM of allicin
1 tablespoon of chopped garlic chives (15g): approximately 5-20 μM of allicin
1 cup of chopped garlic chives (100g): approximately 20-50 μM of allicin
1 ounce (28g) of garlic microgreens: approximately 50-200 μM of allicin
1 cup of garlic microgreens (100g): approximately 200-500 μM of allicin
1 ounce (28g) of garlic chive microgreens: approximately 20-50 μM of allicin
1 cup of garlic chive microgreens (100g): approximately 50-100 μM of allicin

Allicin is a bioactive compound derived from garlic that has garnered significant interest for its potential anticancer properties through multiple mechanisms, including antioxidant activity, induction of apoptosis, cell cycle arrest, and modulation of key signaling pathways. While regular dietary intake of garlic is associated with cancer prevention benefits, allicin is also being explored as an adjunct to conventional cancer treatments.

Available in supplement tablet/capsule form for example at 2000mg (fresh bulb equilvalent)
IC50 of normal cells it >160mg/mL (large selectivity).
IC50 might be about 12-30ug/ml (approximately 62-185 µM) (which is about 30-90 grams of garlic consumption).
This makes it difficult to consume enough supplements to achieve that level.

Pathways:

ROS Generation and Oxidative Stress (inducing)
• ROS generation is often considered a primary trigger that feeds into downstream pathways (e.g., MAPK activation, mitochondrial membrane permeabilization).
Mitochondrial (Intrinsic) Apoptotic Pathway
• ROS-induced mitochondrial damage can lead to the release of cytochrome c and subsequent activation of caspases (e.g., caspase-9 and caspase-3).
NF-κB Signaling Inhibition (block)
Modulation of MAPK Pathways (e.g., p38 MAPK and JNK)
• ROS generation by allicin can activate stress-responsive kinases such as p38 MAPK and c-Jun N-terminal kinase (JNK).
Inhibition of PI3K/Akt Pathway
ROS levels and PI3K/Akt signaling, with increased oxidative stress often correlating with reduced Akt phosphorylation and activity.

At lower doses, allicin may lead to a modest increase in ROS levels that the cell’s antioxidant defenses (e.g., glutathione, superoxide dismutase) can manage

Allicin (Garlic) — mechanistic axes relevant to oncology

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Thiol chemistry and redox buffering GSH↓, protein thiols modified; ROS↑ (dose-dependent) Adaptive buffering often stronger; ROS↔/↑ (context-dependent) P Electrophilic/thiol stress that re-wires signaling Central “first-contact” mechanism: allicin rapidly reacts with cysteine/GSH, so many downstream pathway changes are secondary to thiol stress.
2 Mitochondria and intrinsic apoptosis ΔΨm↓, Cyt-c↑, Caspase↑, cl-PARP↑ Typically less apoptosis at matched doses (selectivity varies) R Pro-apoptotic stress execution Frequently downstream of rank #1; selectivity can reflect baseline redox fragility and metabolic state.
3 ER stress and UPR ER stress↑, UPR↑ (model-dependent) UPR↔/↑ (context-dependent) R Proteostasis stress amplification Can couple to Ca²⁺ release, apoptosis, and inflammatory signaling changes.
4 Ca²⁺ signaling Ca²⁺↑ (model-dependent) Ca²⁺↔/↑ (context-dependent) R Stress coupling to mitochondria/ER Often reported as part of the ER–mitochondria stress axis rather than a primary target.
5 NF-κB inflammatory axis NF-κB↓; cytokine programs↓ (context-dependent) Inflammatory tone↓ (context-dependent) G Anti-inflammatory transcriptional suppression May be beneficial in tumor-promoting inflammation contexts; also relevant to platelet/vascular biology.
6 STAT3 signaling STAT3↓ (model-dependent) STAT3↔ (context-dependent) G Reduced survival/proliferation programs Evidence is model-specific; frequently downstream of redox/inflammation modulation.
7 NRF2 antioxidant response NRF2↓ or maladaptive NRF2 response (context-dependent) NRF2↑ (context-dependent) G Differential stress adaptation Reported “cancer vs normal” divergence is plausible but not universal; strongly dose/model dependent.
8 Acetate to acetyl-CoA metabolism ACS/ACSS activity↓ (model-dependent) ACS/ACSS activity↓ (context-dependent) R Limits acetate utilization under stress Primary biochemical evidence exists for acetyl-CoA synthetase inhibition by allicin; translation to tumor-selective ACSS2 targeting is uncertain without exposure confirmation.
9 PI3K/AKT and MAPK network PI3K/AKT↓, ERK/JNK↔/↓ (model-dependent) ↔ (context-dependent) G Reduced growth/survival signaling Commonly reported but typically secondary to upstream stress/redox effects.
10 HIF-1α and angiogenesis HIF-1α↓, VEGF↓ (model-dependent) ↔ (context-dependent) G Anti-angiogenic signaling shift Most supportive data are preclinical; dependent on hypoxia models and dosing.
11 EMT, migration, invasion EMT↓, MMPs↓ (model-dependent) ↔ (context-dependent) G Reduced invasive phenotype Usually downstream of PI3K/MAPK/inflammation rewiring and/or oxidative stress–driven cytostasis.
12 Radiosensitization and chemosensitization Sensitization↑ (context-dependent) Protection↔/↑ (context-dependent) G Stress-based therapeutic interaction Potential bidirectionality: pro-oxidant sensitization in tumors vs antioxidant adaptation in normal tissues depends on schedule and formulation.
13 Clinical Translation Constraint Chemical instability; rapid thiol quenching; formulation-dependent “allicin bioequivalence”; uncertain tumor-site free-allicin exposure; many in-vitro studies use high µM levels; human cancer outcomes largely from heterogeneous garlic preparations rather than purified allicin. Primary constraint is exposure control, not target plausibility.


ER Stress, endoplasmic reticulum (ER) stress signaling pathway: Click to Expand ⟱
Source:
Type:
Protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress.
The endoplasmic reticulum (ER) stress signaling pathway plays a crucial role in maintaining cellular homeostasis and responding to various stressors, including those encountered in cancer. When cells experience stress, such as the accumulation of misfolded proteins, they activate a series of signaling pathways collectively known as the unfolded protein response (UPR). The UPR aims to restore normal function by enhancing the protein-folding capacity of the ER, degrading misfolded proteins, and, if the stress is unresolved, triggering apoptosis.
The activation of ER stress pathways can contribute to resistance against chemotherapy and targeted therapies. Cancer cells may utilize the UPR to survive treatment-induced stress, making it challenging to achieve effective therapeutic outcomes.

-ER stress-associated proteins include: phosphorylation of PERK, eIF2α, ATF4, CHOP and cleaved-caspase 12
Scientific Papers found: Click to Expand⟱
2647- AL,    The Mechanism in Gastric Cancer Chemoprevention by Allicin
- Review, GC, NA
ChemoSen↓, Experiments have shown that allicin can be chemopreventive to gastric cancer
TumCG↓, by inhibiting the growth of cancer cells, arresting cell cycle at G2/M phase, endoplasmic reticulum (ER) stress, and mitochondria-mediated apoptosis, which includes the caspase-dependent/-independent pathways and death receptor pathway.
TumCCA↑,
ER Stress↑,
Apoptosis↑,
Casp↑,
DR5↑, DR5 (death receptor 5) was found to be upregulated following allicin treatment

2657- AL,    Allicin pharmacology: Common molecular mechanisms against neuroinflammation and cardiovascular diseases
- Review, CardioV, NA - Review, AD, NA
*Inflam↓, allicin integrate a broad spectrum of properties (e.g., anti-inflammatory, immunomodulatory, antibiotic, antifungal, antiparasitic, antioxidant, nephroprotective, neuroprotective, cardioprotective, and anti-tumoral activities, among others).
*antiOx↑, improving the antioxidant system
*neuroP↑,
*cardioP↑,
*AntiTum↑,
*mtDam↑, Indeed, the current evidence suggests that allicin improves mitochondrial function by enhancing the expression of HSP70 and NRF2, decreasing RAAS activation, and promoting mitochondrial fusion processes.
*HSP70/HSPA5↑, llicin improves mitochondrial function by enhancing the expression of HSP70 and decreasing RAAS activation
*NRF2↑,
*RAAS↓,
*cognitive↑, Allicin enhances the cognitive function of APP (amyloid precursor protein)/PS1 (presenilin 1) double transgenic mice by decreasing the expression levels of Aβ, oxidative stress, and improving mitochondrial function.
*SOD↑, positive effects on cognition in an AD mouse model by administrating a preventive dose of allicin. These effects might be mediated by an increase of SOD and reduction of ROS
*ROS↓,
*NRF2↑, Chronic treatment with allicin increased the expression of NRF2 and targeted downstream of NRF2, such as NADPH, quinone oxidoreductase 1 (NQO1), and γ-glutamyl cysteine synthetase (γ-GCS), in the hippocampus of aged mice
*ER Stress↓, protective effects of 16 weeks of allicin treatment in a rat model of endoplasmic reticulum stress-related cognitive deficits.
*neuroP↑, allicin was able to ameliorate depressive-like behaviors by decreasing neuroinflammation, oxidative stress iron aberrant accumulation,
*memory↑, allicin improved lead acetate-caused learning and memory deficits and decreased the ROS level
*TBARS↓, Oral administration of allicin was able to reduce thiobarbituric reactive substances (TBARS) and myeloperoxidase (MPO) levels, and concurrently increased (SOD) activity, glutathione S-transferase (GST) and glutathione (GSH) levels in a rat model of
*MPO↓,
*SOD↑,
*GSH↑,
*iNOS↓, decreasing the expression of iNOS and increased the phosphorylation of endothelial NOS (eNOS)
*p‑eNOS↑,
*HO-1↑, OSCs upregulate the endogenous antioxidant NRF2 and heme oxygenase-1 (HO-1)

2655- AL,    Allicin and Digestive System Cancers: From Chemical Structure to Its Therapeutic Opportunities
- Review, GC, NA
TGF-β↓, Allicin can reduce the expression of TGF-2 and its receptor after entering directly into gastric cancer cell
cycD1/CCND1↓, followed by not only downexpression of cyclinD1, cyclinE, and cyclin-dependent kinase (CDK),
cycE/CCNE↓,
CDK1↓, cyclin-dependent kinase (CDK)
DNAdam↑, but also causing DNA damage and generating ROS
ROS↑,
BAX↑, Allicin increases the levels of Bax (proapoptotic protein), Bcl-2 (antiapoptotic protein), and JNK
JNK↑,
MMP↓, through reduction in outer mitochondrial membrane potential
p38↑, allicin induces p38 mitogen that could induce the protein kinase (MAPK) and then increase the expression of Fas binding to Fas ligand (Fas L) and finally activate death pathway through activation of cyt C and caspase-8.
MAPK↑,
Fas↑,
Cyt‑c↑,
Casp8↑,
PARP↑, allicin makes caspase-dependent apoptosis through elevating PARP, caspase-3 and caspase-9, which are mediated by enhanced discharging of mitochondria cyt C to the cytosol.
Casp3↑,
Casp9↑,
Ca+2↑, allicin induces apoptosis via increasing the amounts of free Ca2+, ER stress.
ER Stress↑,
P21↑, generating ROS to produce p21 and phospho-p53 (Ser15).
CDK2↓, Then p21 suppressed the CDK-4/6/cyclinD complex, P21-PCNA, P21-CDK2, and subsequently reduced cdk1/cyclinB1 complex for G2/M phase cell cycle arrest
CDK6↑,
TumCCA↑,
CDK4↓, Then p21 suppressed the CDK-4/6/cyclinD complex

2646- AL,    Anti-Cancer Potential of Homemade Fresh Garlic Extract Is Related to Increased Endoplasmic Reticulum Stress
- in-vitro, Pca, DU145 - in-vitro, Melanoma, RPMI-8226
AntiCan↑, simple homemade ethanol-based garlic extract (GE). We show that GE inhibits growth of several different cancer cells in vitro
eff↓, These activities were lost during freeze or vacuum drying, suggesting that the main anti-cancer compounds in GE are volatile.
ChemoSen↑, We found that GE enhanced the activities of chemotherapeutics
ER Stress↑, Our data indicate that the reduced proliferation of the cancer cells treated by GE is at least partly mediated by increased endoplasmic reticulum (ER) stress.
tumCV↓, homemade GE was found to reduce the viability of the two multiple myeloma (MM) cell lines, RPMI-8226 and JJN3, as well as the prostate cancer cell line DU145 in a dose-dependent manner,
DNAdam↑, GE alone slightly increased the percentage of tail DNA (% Tail) (representing cumulative levels of abasic sites, as well as single- and double-strand DNA breaks) measured at day one, compared to untreated cells
GSH∅, We could not detect any changes in cellular GSH levels after treatments with GE
HSP70/HSPA5↓, ; however, in support of increased ER stress after GE treatment, we detected an increased pulldown of HSPA5 (BIP), a member of the Hsp70 family
UPR↑, s leading to the accumulation of unfolded proteins in the ER (also known as GRP78)
β-catenin/ZEB1↓, we also found a reduction in the β-catenin leve
ROS↑, In further support for increased ER stress induced by GE, which will lead to elevated ROS-levels and oxidative stress
HO-2↑, we found a significant increase in proteins activated by and important for regulating cellular ROS levels, e.g., OXR1, Txnl1, Hmox2, and Sirt1
SIRT1↑,
GlucoseCon∅, glucose consumption, as well as lactate secretion, were not changed.
lactateProd∅,
chemoP↑, Garlic is reported to reduce cisplatin-induced nephrotoxicity and oxidative stress

5356- AL,    Therapeutic role of allicin in gastrointestinal cancers: mechanisms and safety aspects
- Review, GC, NA
Apoptosis↑, induction of apoptosis, inhibition of proliferation, and disruption of cancer cell signaling pathways, including the MAPK, PI3K/AKT, and NF-κB pathways.
TumCP↓,
MAPK↓,
PI3K↓,
Akt↓,
NF-kB↓,
AntiCan↑, Allicin and its other derivatives, such as diallyl disulfide (DADS) and ajoene, have been found to have strong anticancer potential both in vitro and in vivo.
ChemoSen↑, effectiveness of allicin in augmenting conventional chemotherapy and retarding tumor growth proves that allicin is one of the most efficient complementary therapies.
TumCCA↑, In liver cancer, allicin has been shown to mediate cell cycle arrest and apoptosis
Apoptosis↑,
BioAv↑, Allicin (diallyl thiosulfinate) is a compound that is generated when a garlic clove is crushed
selectivity↑, Furthermore, it has no influence on the growth of healthy intestinal cells when it causes stomach cancer cells to undergo apoptosis
TGF-β↓, Allicin can reduce the production of TGF-β2 and its receptor after directly entering gastric cancer cells.
ROS↑, It induces oxidative stress by generating reactive oxygen species (ROS), leading to DNA damage and activation of key apoptotic mediators such as phospho-p53 and p21 [81].
DNAdam↑,
p‑P53↑,
P21↑,
cycD1/CCND1↓, Additionally, cyclin D1, cyclin E, and cyclin-dependent kinases (CDKs) can all be inhibited by allicin.
cycE/CCNE↓,
CDK4↓, suppressing the CDK-4/6/cyclin D complex
CDK6↓,
MMP↓, By lowering the outer mitochondrial membrane potential (MMP), allicin raises levels of nuclear factor kappa B (NF-κB), the proapoptotic protein Bax, while decreasing the antiapoptotic protein Bcl-2, which leads to apoptosis.
NF-kB↑,
BAX↑,
Bcl-2↓,
ER Stress↑, cellular effects of allicin, including its role in inducing ER stress
Casp↑, enhancing caspase activation and apoptosis-inducing factor (AIF)-mediated cell death.
AIF↑,
Fas↑, increasing Fas receptor expression and its binding to Fas ligand (FasL), leading to apoptosis through caspase-8 and cytochrome c activation.
Casp8↑,
Cyt‑c↑,
cl‑PARP↑, leading to poly (ADP-ribose) polymerase (PARP) cleavage and DNA fragmentation.
Ca+2↑, allicin elevates intracellular free Ca2⁺ levels, causing endoplasmic reticulum (ER) stress, which plays a critical role in apoptosis induction
*NRF2↑, by activating the Nrf2 pathway via KLF9, allicin protects against arsenic trioxide-induced liver damage,
*chemoP↑, Additionally, allicin has shown promise in reducing hepatotoxicity caused by tamoxifen (TAM), a commonly used treatment for hormone-dependent breast cancer
*GutMicro↑, Shi et al. [85] found that allicin can ameliorate high-fat diet-induced obesity in mice by altering their gut microbiome.
CycB/CCNB1↑, DATS impaired cell survival in the G2 phase by significantly upregulating cyclins A2 and B1.
H2S↑, DATS can also react with the cellular thiol glutathione to create H2S gas, which can control several other cellular functions [79].
HIF-1↓, allicin treatment (40 µg/ml) for NSCLC lowers the expression of HIF-1 and HIF-2 in hypoxic cells [73]
RadioS↑, Allicin has been shown to increase the sensitivity of X-ray radiation therapy in colorectal cancer, presumably by suppressing the levels of NF-κB, IKKβ mRNA, p-NF-κB, and p-IKKβ protein expression in vitro and in vivo


* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 5

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

GSH∅, 1,   HO-2↑, 1,   ROS↑, 3,  

Mitochondria & Bioenergetics ⓘ

AIF↑, 1,   MMP↓, 2,  

Core Metabolism/Glycolysis ⓘ

GlucoseCon∅, 1,   H2S↑, 1,   lactateProd∅, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Akt↓, 1,   Apoptosis↑, 3,   BAX↑, 2,   Bcl-2↓, 1,   Casp↑, 2,   Casp3↑, 1,   Casp8↑, 2,   Casp9↑, 1,   Cyt‑c↑, 2,   DR5↑, 1,   Fas↑, 2,   JNK↑, 1,   MAPK↓, 1,   MAPK↑, 1,   p38↑, 1,  

Transcription & Epigenetics ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↑, 4,   HSP70/HSPA5↓, 1,   UPR↑, 1,  

DNA Damage & Repair ⓘ

DNAdam↑, 3,   p‑P53↑, 1,   PARP↑, 1,   cl‑PARP↑, 1,  

Cell Cycle & Senescence ⓘ

CDK1↓, 1,   CDK2↓, 1,   CDK4↓, 2,   CycB/CCNB1↑, 1,   cycD1/CCND1↓, 2,   cycE/CCNE↓, 2,   P21↑, 2,   TumCCA↑, 3,  

Proliferation, Differentiation & Cell State ⓘ

PI3K↓, 1,   TumCG↓, 1,  

Migration ⓘ

Ca+2↑, 2,   TGF-β↓, 2,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature ⓘ

HIF-1↓, 1,  

Immune & Inflammatory Signaling ⓘ

NF-kB↓, 1,   NF-kB↑, 1,  

Hormonal & Nuclear Receptors ⓘ

CDK6↓, 1,   CDK6↑, 1,  

Drug Metabolism & Resistance ⓘ

BioAv↑, 1,   ChemoSen↓, 1,   ChemoSen↑, 2,   eff↓, 1,   RadioS↑, 1,   selectivity↑, 1,  

Functional Outcomes ⓘ

AntiCan↑, 2,   chemoP↑, 1,  
Total Targets: 59

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress ⓘ

antiOx↑, 1,   GSH↑, 1,   HO-1↑, 1,   MPO↓, 1,   NRF2↑, 3,   ROS↓, 1,   SOD↑, 2,   TBARS↓, 1,  

Mitochondria & Bioenergetics ⓘ

mtDam↑, 1,  

Cell Death ⓘ

iNOS↓, 1,  

Protein Folding & ER Stress ⓘ

ER Stress↓, 1,   HSP70/HSPA5↑, 1,  

Angiogenesis & Vasculature ⓘ

p‑eNOS↑, 1,  

Immune & Inflammatory Signaling ⓘ

Inflam↓, 1,  

Hormonal & Nuclear Receptors ⓘ

RAAS↓, 1,  

Clinical Biomarkers ⓘ

GutMicro↑, 1,  

Functional Outcomes ⓘ

AntiTum↑, 1,   cardioP↑, 1,   chemoP↑, 1,   cognitive↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 22

Scientific Paper Hit Count for: ER Stress, endoplasmic reticulum (ER) stress signaling pathway
5 Allicin (mainly Garlic)
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#:27  Target#:103  State#:%  Dir#:%
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