BAD Cancer Research Results
BAD, BCL2 associated agonist of cell death: Click to Expand ⟱
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BCL2 associated agonist of cell death (BAD) protein is a pro-apoptotic member of the Bcl-2 gene family.
Expression of the BAD is associated with the development and progression of cancer.
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Scientific Papers found: Click to Expand⟱
*AntiCan↑, antibacterial, antiviral, anticancer, anticonvulsant, anti-oxidant, hepatoprotective, and neuroprotective effects.
*antiOx↑,
*hepatoP↑,
*neuroP↑,
*ROS↓, pharmacological properties of baicalin and baicalein are due to their abilities to scavenge reactive oxygen species (ROS)
Ca+2↑, Baicalein mainly induced apoptosis through Ca+2 influx via Ca2+ release from the reticulum to cytosol dependent on phospholipase C protein
ROS↑, ROS production is associated with baicalein-induced apoptosis via Ca2+-dependent apoptosis in tongue and breast cancer cells (78, 79)
BAX↑, The level of Bax/Bcl-2 increased and caspase-3 and -9 were activated following the release of cytochrome C (80).
Casp3↑,
Casp9↑,
Cyt‑c↑,
MMP↓, In gastric cancer cells, baicalein mediated apoptosis in a dose-dependent manner through disruption of mitochondrial membrane potential
Mcl-1↓, In pancreatic cancer cells, baicalein induced apoptosis via suppression of the Mcl-1 protein.
PI3K↓, In HepG2 cells, baicalin-copper induced apoptosis through down-regulation of phosphoinositide-3 kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway
Akt↓,
mTOR↓,
BAD↓, Studies demonstrated that baicalein treatment suppressed Bad, ERK1/2 phosphorylation, and MEK1 expression both in vitro and in vivo.
ERK↓,
MEK↓,
DR5↑, Baicalein enhanced the activity of death receptor-5 (DR5) in prostate cancer PC3 cells.
Fas↑, baicalin is the active ingredient that acts as Fas ligand and caused up-regulation of Fas protein (89).
TumMeta↓, Baicalin/baicalein not only induced apoptosis in cancer cells but also suppressed metastasis.
EMT↓, both baicalin and baicalein inhibited epithelial-mesenchymal transition (EMT) through the suppression of TGF-β in breast epithelial cells through the NF-κB pathway (92).
SMAD4↓, baicalein suppressed metastasis in gastric cancer through inactivation of the Smad4/TGF-β pathway (93).
TGF-β↓,
MMP9↓, baicalin and baicalein inhibition of the expression level of matrix metalloproteinases (MMP) such as MMP-9 and MMP-2 in liver, breast, lung, ovarian, gastric, and colorectal cancers and glioma
MMP2↓,
HIF-1↓, Baicalin attenuated lung metastasis through inhibition of hypoxia-inducible factor (HIF)
12LOX↓, Baicalein acts as an anticancer agent via inhibiting 12-lipooxygenase (12-LOX),
tumCV↓,
BAX↑,
BID↑,
BOK↑,
APAF1↑,
TNF-α↑,
FasL↑,
Fas↑,
FADD↑,
Casp3↑,
Casp7↑,
Casp8↑,
Casp9↑,
Mcl-1↓,
NAIP↓,
Bcl-2↓,
CDK4↓,
CycB/CCNB1↓,
cycD1/CCND1↓,
cycE1↓,
TRAIL↑,
p‑Akt↓,
Akt↓,
mTOR↓,
PDK1↓,
BAD↓,
GSK‐3β↑,
AMPK↑, AMPKa
p27↑,
P53↑,
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in-vitro, |
AD, |
HT22 |
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in-vivo, |
AD, |
NA |
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*ROS↓, suppressed intracellular reactive oxygen species (ROS) accumulation and Ca2+ overload compared with untreated cells.
*Ca+2↓, crocin strongly inhibited the overload of Ca2+ compared with the l-Glu-damaged HT22 cells,
*BAX↓, crocin significantly decreased the expression levels of Bax, Bad and cleaved caspase-3
*BAD↓,
*Casp3↓,
*cognitive↑, crocin substantially improved the cognition and memory abilities of the mice as measured by their coordination of movement in an open field test,
*memory↑,
*Aβ↓, Crocin improved cognitive abilities of AD mice, and reduced Aβ deposition in their brains
*GPx↑, crocin was able to reduce the Aβ1-42 content in the mouse brains, increase the levels of glutathione peroxidase, superoxide dismutase, acetylcholine and choline acetyltransferase,
*SOD↑,
*ChAT↑,
*Ach↑,
*AChE↓, and reduce the levels of ROS and acetylcholinesterase in the serum, cerebral cortex and hypothalamus compared with untreated mice.
*ROS↓,
*p‑Akt↑, crocin upregulated the phosphorylation levels of Akt and mTOR in 24-h l-Glu-exposed cells.
*p‑mTOR↑,
*neuroP↑, crocin-mediated neuroprotection of l-Glu-damaged HT22 cells.
14-3-3 proteins↓,
p‑BAD↓, p-Bad
p‑Akt↓,
Akt↓,
cl‑Casp9↑, cleaved
cl‑PARP↑, cleaved
Apoptosis↑,
TumCCA↑, G2/M cell cycle arrest
p‑Akt↓,
Akt↓,
Bcl-2↓,
p‑BAD↓,
BAD↑,
cl‑PARP↑,
ROS↑,
HSP27↑,
Beclin-1↑,
p62↑,
GPx1↓,
GPx4↓,
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in-vitro, |
Pca, |
PC3 |
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in-vitro, |
Pca, |
LNCaP |
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in-vivo, |
NA, |
NA |
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SDC1↑,
p‑PCK1↓,
Akt↓,
BAD↓,
BAD↓,
cl‑PARP↑,
Casp7↑,
IκB↓,
Ki-67↓,
VEGF↓,
EGFR↓,
FGF↓,
TGF-β↓,
TNF-α↓,
SCF↓,
Bax:Bcl2↑,
NF-kB↓,
chemoP↑, This study provides a novel regimen to enhance the therapeutic effect of Doc in a less-toxic manner and reduce its risk of side effects in treatment of CRPC.
ChemoSen↑, GT and Q with LD Doc significantly enhanced the potency of Doc 2-fold and reduced tumor growth by 62 % compared to LD Doc in 7-weeks intervention.
TumVol↓,
TumCP↓, 80 μM eugenol could significantly inhibit the proliferation of HER-2 positive MCF-10AT cells and the inhibition rate was up to 32.8%,
TumCCA↑, Eugenol also significantly induced human breast precancerous lesion MCF-10AT cell apoptosis and cell cycle S-phase arrest
HER2/EBBR2↓, In MCF-10AT cells treated by 180 μM eugenol, the protein expressions of HER2, AKT, PDK1, p85, Bcl2, NF-κB, Bad and Cyclin D1 were decreased
Akt↓,
PDK1↓,
Bcl-2↓,
NF-kB↓,
BAD↓,
cycD1/CCND1↓,
Dose↝, Eugenol, a significant bioactive compound, is found in cloves and other traditional Indian medicinal plants, such as cinnamon, tulsi, ginger, turmeric, and Japanese star anise, which have been reported to have significant anticancer properties.
AntiCan↑,
*Inflam↓, also exhibits different pharmacological effects (anti-inflammatory, cardio-protection, and neuroprotection).
*cardioP↑,
*neuroP↑,
angioG↓, eugenol exhibits anti-apoptotic, anti-angiogenic, and anti-metastatic properties in cancer cell lines and in vivo animal models, which we discuss in this review.
TumMeta↓,
*BioAv↑, Oral administration of eugenol promoted rapid absorption by different organs and metabolism in the liver. encapsulation is required to address the issues of early absorption, increased water solubility, and improved efficiency
*eff↑, Eugenol encapsulation as an inclusion with β-cyclodextrin, chitosan, and 2-hydroxypropyl-β-cyclodextrin nanoparticles improves its thermal stability
*toxicity↝, Eugenol at lower doses displayed minimal adverse effects, including contact dermatitis, local irritation, and rare allergic responses. However, at its higher doses, it can lead to liver and kidney damage, tissue injury, sudden onset of seizures, and
antiNeop↑, exhibit antineoplastic properties against different cancers by triggering cell cycle arrest and apoptosis in cancer cells
TumCCA↑,
Apoptosis↑,
*antiOx↑, Eugenol exhibits its antioxidant property due to its unique structural configuration, specifically the presence of an allyl group, as revealed by electron spin resonance
*lipid-P↓, Eugenol prevents lipid peroxidation (Nagababu and Lakshmaiah 1994), hexanal oxidation (Lee and Shibamoto 2001), copper-dependent LDL oxidation, and nonenzymatic peroxidation in liver mitochondria
*ROS↓, Eugenol exhibited 58–81 % DPPH radical scavenging potential in its 0.25–1.0 µM/ml concentration
*SOD↑, Eugenol protects against oxidative damage by increasing the levels of certain antioxidant enzymes, such as SOD, CAT, GST, and GPx (Huang et al. 2015).
*Catalase↑,
*GSTs↑,
*GPx↑,
*iNOS↓, Eugenol pre-treatment increased the levels of antioxidant enzymes and decreased the expression of iNOS, COX2, IL-6, and tumor necrosis factor-α (TNF-α) (Kaur et al. 2010).
*COX2↓,
*IL6↓,
*TNF-α↓,
*AntiArt↑, Administration of eugenol at 33 mg/kg dose in arthritis-induced male Sprague-Dawley rats decreased the swelling of paws and joints (
*Bacteria↓, Along with cinnamaldehyde and thymol, Li et al. determined eugenol's antibacterial activity against E. coli and S. aureus.
TumAuto↑, eugenol activated apoptosis and autophagy through the PI3K/AKT/FOXO3a pathway in cancer cells(breast cancer cells).
PI3K↓, PI3K/Akt/mTOR pathway inhibition
Akt↓,
FOXO3↝,
BAX↑,
mTOR↓, PI3K/Akt/mTOR pathway inhibition
NF-kB↓, NF-κB signaling pathway inhibition
P53↑, In some cancers, eugenol has been shown to upregulate p53, thereby inhibiting cancer growth.
TumCG↓,
CSCs↓, eugenol downregulated certain signaling cascades of the Wnt signaling pathway and specific cancer stem cell markers, including CD44, EpCAM, Notch1, and Oct4, in breast cancer cell lines treated with eugenol.
CD44↓,
EpCAM↓,
NOTCH1↓,
OCT4↓,
Bcl-2↓, Eugenol also downregulates the protein expressions of p85, BCL-2, PDK1, HER2, AKT, BAD, Cyclin D1, and NF-KB.
PDK1↓,
HER2/EBBR2↓,
BAD↓,
cycD1/CCND1↓,
ROS↑, EUG-medium chain triglyceride nanoemulsions Liver cancer HB8065 cells Increased the levels of ROS generation to initiated the apoptotic cell death
Casp3↑, apoptosis initiated by Caspase-3
protein upregulation
selectivity↑, Eugenol was not cytotoxic to MCF10A cells; however, it displayed cytotoxic activity in the transformed MCF10A cells (MCF10A-ras).
MMP2↓, A significant decline in matrix metalloproteinase (MMP-2, MMP-9) levels and an increase in tissue inhibitor of metalloproteinase-1 (TIMP-1) expression were also observed.
MMP9↓,
TIMP1↑,
VEGF↓, Eugenol also inhibits metastatic invasion and angiogenesis, as evident from the downregulation of MMP-2, MMP-9, VEGF, and VEGFR1, along with the upregulation of RECK and TIMP-2
VEGFR1↓,
RECK↑,
TIMP2↑,
DNAdam↑, Eugenol demonstrated an apoptosis-inducing effect in HL-60 cells, as evidenced by DNA fragmentation and a DNA ladder assay.
MMP↓, It is accompanied by a decline in mitochondrial membrane potential and thiol levels, early disruption of the lipid layer, DNA fragmentation, and activation of proapoptotic markers (Caspase-3, PARP, p53)
Thiols↓,
PARP↑,
*Pain↓, eugenol nanoemulsion may significantly reduce pain-associated arteriovenous fistula (AVF)
E2Fs↓, t interferes with several critical cancer signaling pathways, including the Wnt/b-Catenin pathway, PI3K/AKT pathway, MAPK/ERK pathway, E2F1/survivin pathway, JNK/STAT3 pathway, and NF-κB signaling pathway, among others.
survivin↓, cause E2F1/survivin downregulation, which activates apoptosis in breast cancer cells
AntiCan↑, In this review, we document distinct biological characteristics of GA as a novel anti-cancer agent.
angioG↓, anti-angiogenesis, and chemo-/radiation sensitizer activities
ChemoSen↑, Moreover, GA has shown chemotherapy/radiation sensitization properties in different types of cancers
RadioS↑,
VEGF↓, Figure 2
MMP2↓,
MMP9↓,
Telomerase↓,
TrxR↓,
ERK↓,
HSP90↓,
ROS↑,
SIRT1↑,
survivin↓,
cFLIP↓,
Casp3↑,
Casp8↑,
Casp9↑,
BAD↓,
BID↓,
Bcl-2↓,
BAX↑,
STAT3↓,
hTERT/TERT↓,
NF-kB↓,
Myc↓,
Hif1a↓,
FOXD3↑,
BioAv↓, Unfortunately, the aqueous solubility of GA (0.013 mg/mL) is very low, thus limiting its clinical application.
BioAv↑, For example, GA can be coupled with alkanolamines to improve aqueous solubility and achieve equivalent anti-proliferation effects
P53↑, This inhibition was co-related with increase of p53 levels and reduced bcl-2 levels
eff↓, Such effect was received for GA due to production of ROS which can be removed by N-acetyl-L-cysteine (NAC, a ROS inhibitor)
OCR↓, GA exhibited a dose-dependent generation of intracellular ROS levels and lowered the oxygen consumption rate and the mitochondrial membrane potential.
MMP↓,
PI3K↓, GA happens to promote antimetastasis properties in melanoma cells by active inhibition of PI3K/Akt and ERK signaling pathways
Akt↓,
BBB↑, This study demonstrated successful uptake of GA through blood-brain barrier (BBB)
TumCG↓, GA-based nanomedicine is efficient in targeting tumors, capable to inhibit tumor growth, metastasis, angiogenesis, and reverse drug resistance
TumMeta↓,
BioAv↑, deliver GA using nanoparticles for enhanced solubility, bioavailability, adsorption and tumor imaging and targeting
TumCP↓,
p‑CHK1↓, reducing the increased expression of total IĸB and phosphorylated-CHK1 induced by doxorubicin
Ca+2↑, caused by PEMF alone
Casp3↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
Casp7↓, PEMF stimulation significantly reduced the enhancement of caspase 3/7 activity by doxorubicin at 24 h
p‑BAD↓,
ChemoSen↑, Our results indicate that combination of PEMF and doxorubicin could be a novel chemotherapeutic strategy.
*BAD↓,
*BAX↓,
*Casp3↓,
*Bcl-xL↑,
*p‑Akt↑,
*MMP9↓, EMF significantly decreased levels of IL-1β and MMP9 in the peri-infarct area at 24 h and 3rd day of the experiment
*p‑ERK↑, ERK1/2
*HIF-1↓,
*ROS↓, n a similar experiment, ELF-MF (50 Hz/1 mT) increased cell viability and decreased intracellular ROS/RNS in mesenchymal stem cells submitted to OGD conditions and 3 h ELF-MF exposure
*VEGF↑,
*Ca+2↓,
*SOD↑,
*IL2↑,
*p38↑,
*HSP70/HSPA5↑,
*Apoptosis↓, PEMF decreased apoptosis
*ROS↓, Nevertheless, in the presence of ischemia, EMF decreased NO and ROS concentrations.
*NO↓,
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in-vitro, |
Pca, |
LNCaP |
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in-vitro, |
Pca, |
PrEC |
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in-vitro, |
Pca, |
YPEN-1 |
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in-vitro, |
Pca, |
HCT116 |
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Casp8↑, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Casp9↑,
PARP↑,
BAD↓,
BAX↑,
PI3K/Akt↓, quercetin inhibits the PI3K/Akt pathway, suppresses phosphorylation of Bad, and subsequently alters interaction between Bcl-xL and Bax in human prostate carcinoma LNCaP cells
Cyt‑c↑, accompanied by cytochrome c release, and procaspases-3, -8 and -9 cleavage and increased poly (ADP-ribose) polymerase (PARP) cleavage.
selectivity↑, quercetin treatment did not affect the viability or rate of apoptosis in normal human prostate epithelial cell line (PrEC)
AR↓,
PI3K/Akt↓, The combination treatment significantly inhibited both AR and PI3K/Akt pathways compared to control.
miR-21↓,
STAT3↓,
BAD↓,
PRAS40↓,
GSK‐3β↓,
PSA↓,
NKX3.1↑,
Bax:Bcl2↑, a significantly increased ratio of Bax to Bcl-2 protein expression was observed in LAPC-4 cells by the combination treatment compared to Q alone, and a trend to increase in LNCaP cells
miR-19b↓,
miR-148a↓,
AMPKα↓,
TumCP↓, The anti-proliferative activity of arctigenin was 10-20 fold stronger than quercetin in both cell lines.
chemoPv↑, combination of arctigenin and quercetin, that target similar pathways, at low physiological doses, provides a novel regimen with enhanced chemoprevention in prostate cancer.
TumCMig↓, Enhanced inhibition of cell migration
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in-vitro, |
GC, |
HGC27 |
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in-vitro, |
GC, |
NCI-N87 |
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AntiTum↑, The in vivo antitumor effect of sodium selenite on gastric carcinoma has been demonstrated.
HOXB-AS1↓, Na2SeO3 downregulated the expression of HOXB-AS1 in the human gastric cancer (HGC) cell lines, HGC-27, NCI-N87, and KATO III cells, while inhibiting their proliferation and invasion and inducing apoptosis.
TumCP↓,
TumCI↓,
Apoptosis↑,
BAD↓, the expression of apoptosis-related (Bad, Bcl-2, and cleaved-caspase-3) and invasion-related (MMP2, E-cadherin, and N-cadherin) proteins, indicating increased apoptosis and decreased invasion.
Bcl-2↓, f Bcl-2, MMP2, and N-cadherin proteins was significantly downregulated
cl‑Casp3↑,
MMP2↓,
E-cadherin↑,
N-cadherin↓,
ROS↑, Na2SeO3 can increase ROS levels and inhibit the NF-κB signaling pathway, effectively inhibiting the growth, metastasis, and inducing apoptosis of renal cell carcinoma both in vitro and in vivo [41]
NF-kB↓,
Showing Research Papers: 1 to 15 of 15
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 15
Pathway results for Effect on Cancer / Diseased Cells:
Redox & Oxidative Stress ⓘ
GPx1↓, 1, GPx4↓, 1, ROS↑, 5, Thiols↓, 1, TrxR↓, 1,
Mitochondria & Bioenergetics ⓘ
BOK↑, 1, MEK↓, 1, MMP↓, 3, OCR↓, 1,
Core Metabolism/Glycolysis ⓘ
12LOX↓, 1, AMPK↑, 1, p‑PCK1↓, 1, PDK1↓, 3, PI3K/Akt↓, 2, SIRT1↑, 1,
Cell Death ⓘ
14-3-3 proteins↓, 1, Akt↓, 8, p‑Akt↓, 3, APAF1↑, 1, Apoptosis↑, 3, BAD↓, 10, BAD↑, 1, p‑BAD↓, 3, BAX↑, 5, Bax:Bcl2↑, 2, Bcl-2↓, 6, BID↓, 1, BID↑, 1, Casp3↓, 1, Casp3↑, 4, cl‑Casp3↑, 1, Casp7↓, 1, Casp7↑, 2, Casp8↑, 3, Casp9↑, 4, cl‑Casp9↑, 1, cFLIP↓, 1, Cyt‑c↑, 2, DR5↑, 1, FADD↑, 1, Fas↑, 2, FasL↑, 1, hTERT/TERT↓, 1, Mcl-1↓, 2, Myc↓, 1, NAIP↓, 1, p27↑, 1, survivin↓, 2, Telomerase↓, 1, TRAIL↑, 1,
Kinase & Signal Transduction ⓘ
AMPKα↓, 1, FOXD3↑, 1, HER2/EBBR2↓, 2,
Transcription & Epigenetics ⓘ
miR-21↓, 1, tumCV↓, 1,
Protein Folding & ER Stress ⓘ
HSP27↑, 1, HSP90↓, 1,
Autophagy & Lysosomes ⓘ
Beclin-1↑, 1, p62↑, 1, TumAuto↑, 1,
DNA Damage & Repair ⓘ
p‑CHK1↓, 1, DNAdam↑, 1, NKX3.1↑, 1, P53↑, 3, PARP↑, 2, cl‑PARP↑, 3,
Cell Cycle & Senescence ⓘ
CDK4↓, 1, CycB/CCNB1↓, 1, cycD1/CCND1↓, 3, cycE1↓, 1, E2Fs↓, 1, TumCCA↑, 3,
Proliferation, Differentiation & Cell State ⓘ
CD44↓, 1, CSCs↓, 1, EMT↓, 1, EpCAM↓, 1, ERK↓, 2, FGF↓, 1, FOXO3↝, 1, GSK‐3β↓, 1, GSK‐3β↑, 1, HOXB-AS1↓, 1, mTOR↓, 3, NOTCH1↓, 1, OCT4↓, 1, PI3K↓, 3, SCF↓, 1, STAT3↓, 2, TumCG↓, 2,
Migration ⓘ
Ca+2↑, 2, E-cadherin↑, 1, Ki-67↓, 1, miR-148a↓, 1, miR-19b↓, 1, MMP2↓, 4, MMP9↓, 3, N-cadherin↓, 1, RECK↑, 1, SDC1↑, 1, SMAD4↓, 1, TGF-β↓, 2, TIMP1↑, 1, TIMP2↑, 1, TumCI↓, 1, TumCMig↓, 1, TumCP↓, 4, TumMeta↓, 3, VEGFR1↓, 1,
Angiogenesis & Vasculature ⓘ
angioG↓, 2, EGFR↓, 1, HIF-1↓, 1, Hif1a↓, 1, VEGF↓, 3,
Barriers & Transport ⓘ
BBB↑, 1,
Immune & Inflammatory Signaling ⓘ
IκB↓, 1, NF-kB↓, 5, PSA↓, 1, TNF-α↓, 1, TNF-α↑, 1,
Hormonal & Nuclear Receptors ⓘ
AR↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↓, 1, BioAv↑, 2, ChemoSen↑, 3, Dose↝, 1, eff↓, 1, RadioS↑, 1, selectivity↑, 2,
Clinical Biomarkers ⓘ
AR↓, 1, EGFR↓, 1, HER2/EBBR2↓, 2, hTERT/TERT↓, 1, Ki-67↓, 1, Myc↓, 1, PSA↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 2, antiNeop↑, 1, AntiTum↑, 1, chemoP↑, 1, chemoPv↑, 1, PRAS40↓, 1, TumVol↓, 1,
Total Targets: 141
Pathway results for Effect on Normal Cells:
NA, unassigned ⓘ
AntiArt↑, 1,
Redox & Oxidative Stress ⓘ
antiOx↑, 2, Catalase↑, 1, GPx↑, 2, GSTs↑, 1, lipid-P↓, 1, ROS↓, 6, SOD↑, 3,
Cell Death ⓘ
p‑Akt↑, 2, Apoptosis↓, 1, BAD↓, 2, BAX↓, 2, Bcl-xL↑, 1, Casp3↓, 2, iNOS↓, 1, p38↑, 1,
Transcription & Epigenetics ⓘ
Ach↑, 1,
Protein Folding & ER Stress ⓘ
HSP70/HSPA5↑, 1,
Proliferation, Differentiation & Cell State ⓘ
p‑ERK↑, 1, p‑mTOR↑, 1,
Migration ⓘ
Ca+2↓, 2, MMP9↓, 1,
Angiogenesis & Vasculature ⓘ
HIF-1↓, 1, NO↓, 1, VEGF↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL2↑, 1, IL6↓, 1, Inflam↓, 1, TNF-α↓, 1,
Synaptic & Neurotransmission ⓘ
AChE↓, 1, ChAT↑, 1,
Protein Aggregation ⓘ
Aβ↓, 1,
Drug Metabolism & Resistance ⓘ
BioAv↑, 1, eff↑, 1,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
AntiCan↑, 1, cardioP↑, 1, cognitive↑, 1, hepatoP↑, 1, memory↑, 1, neuroP↑, 3, Pain↓, 1, toxicity↝, 1,
Infection & Microbiome ⓘ
Bacteria↓, 1,
Total Targets: 45
Scientific Paper Hit Count for: BAD, BCL2 associated agonist of cell death
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#:426 State#:% Dir#:1
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