PKCδ Cancer Research Results

PKCδ, Protein Kinase C delta: Click to Expand ⟱
Source:
Type:
PKCδ is one of the novel isoforms of the Protein Kinase C (PKC) family, involved in regulating various cellular processes.
It participates in diverse signaling pathways influencing cell proliferation, differentiation, survival, apoptosis, and migration.

In some cancers, PKCδ is upregulated and associated with higher tumor aggressiveness, particularly when it contributes to pathways that promote cell survival and invasion.
Conversely, in other contexts, PKCδ has been reported to act as a tumor suppressor where its activation can promote apoptosis or inhibit cell proliferation.
Scientific Papers found: Click to Expand⟱
5344- Ajoene,    Ajoene, a Stable Garlic By-Product, Has an Antioxidant Effect through Nrf2-Mediated Glutamate-Cysteine Ligase Induction in HepG2 Cells and Primary Hepatocytes
- in-vitro, Nor, HepG2
*Nrf1↑, Ajoene treatment activated Nrf2, as indicated by increased phosphorylation and nuclear accumulation of Nrf2
*PKCδ↑, Ajoene activated protein kinase C-δ (PKCδ).
*GSH↑, Our results demonstrate that ajoene increases PKCd-dependent Nrf2 activation, GCL induction, and the cellular GSH concentration, which may contribute to protecting cells from oxidative stress.
*antiOx↑,

2661- AL,    Allicin alleviates traumatic brain injury-induced neuroinflammation by enhancing PKC-δ-mediated mitophagy
- in-vivo, Nor, NA
*TNF-α↓, Allicin treatment reduced TNF-α, IL-1β, IL-6, ROS levels, and the expression of NLRP3 and TLR4 proteins in mice with CCI, while IL-4 and IL-10 levels remained unchanged.
*IL1β↓,
*IL6↓,
*ROS↓,
*NLRP3↓,
*TLR4↓,
*PKCδ↑, allicin increased PKC-δ expression and PLS3 phosphorylation in the CL-related mitophagy process in both the CCI and Bv2 cell stretch models.
neuroP↑, allicin reduces mitophagy-related neuroinflammation and further prevents neuronal injury in vitro.

3272- ALA,    Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential
- Review, AD, NA
*antiOx↑, LA has long been touted as an antioxidant,
*glucose↑, improve glucose and ascorbate handling,
*eNOS↑, increase eNOS activity, activate Phase II detoxification via the transcription factor Nrf2, and lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*NRF2↑,
*MMP9↓,
*VCAM-1↓,
*NF-kB↓,
*cardioP↑, used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits,
*cognitive↑,
*eff↓, The efficiency of LA uptake was also lowered by its administration in food,
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies;
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑, LA markedly increases intracellular glutathione (GSH),
*PKCδ↑, PKCδ, LA activates Erk1/2 [92,93], p38 MAPK [94], PI3 kinase [94], and Akt
*ERK↑,
*p38↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN [95],
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, stimulate GLUT4 translocation
*GLUT1↑, LA-stimulated translocation of GLUT1 and GLUT4.
*Inflam↓, LA as an anti-inflammatory agent

3539- ALA,    Alpha-lipoic acid as a dietary supplement: Molecular mechanisms and therapeutic potential
- Review, AD, NA
*ROS↓, scavenges free radicals, chelates metals, and restores intracellular glutathione levels which otherwise decline with age.
*IronCh↑, LA preferentially binds to Cu2+, Zn2+ and Pb2+, but cannot chelate Fe3+, while DHLA forms complexes with Cu2+, Zn2+, Pb2+, Hg2+ and Fe3+
*GSH↑,
*antiOx↑, LA has long been touted as an antioxidant
*NRF2↑, activate Phase II detoxification via the transcription factor Nrf2
*MMP9↓, lower expression of MMP-9 and VCAM-1 through repression of NF-kappa-B.
*VCAM-1↓,
*NF-kB↓,
*cognitive↑, it has been used to improve age-associated cardiovascular, cognitive, and neuromuscular deficits, and has been implicated as a modulator of various inflammatory signaling pathways
*Inflam↓,
*BioAv↝, LA bioavailability may be dependent on multiple carrier proteins.
*BioAv↝, observed that approximately 20-40% was absorbed [
*BBB↑, LA has been shown to cross the blood-brain barrier in a limited number of studies
*H2O2∅, Neither species is active against hydrogen peroxide
*neuroP↑, chelation of iron and copper in the brain had a positive effect in the pathobiology of Alzheimer’s Disease by lowering free radical damage
*PKCδ↑, In addition to PKCδ, LA activates Erk1/2 [92, 93], p38 MAPK [94], PI3 kinase [94], and Akt [94-97].
*ERK↑,
*MAPK↑,
*PI3K↑,
*Akt↑,
*PTEN↓, LA decreases the activities of Protein Tyrosine Phosphatase 1B [99], Protein Phosphatase 2A [95], and the phosphatase and tensin homolog PTEN
*AMPK↑, LA activates peripheral AMPK
*GLUT4↑, In skeletal muscle, LA is proposed to recruit GLUT4 from its storage site in the Golgi to the sarcolemma, so that glucose uptake is stimulated by the local increase in transporter abundance.
*GlucoseCon↑,
*BP↝, Feeding LA to hypertensive rats normalized systolic blood pressure and cytosolic free Ca2+
*eff↑, Clinically, LA administration (in combination with acetyl-L-carnitine) showed some promise as an antihypertensive therapy by decreasing systolic pressure in high blood pressure patients and subjects with the metabolic syndrome
*ICAM-1↓, decreased demyelination and spinal cord expression of adhesion molecules (ICAM-1 and VCAM-1)
*VCAM-1↓,
*Dose↝, Considering the transient cellular accumulation of LA following an oral dose, which does not exceed low micromolar levels, it is entirely possible that some of the cellular effects of LA when given at supraphysiological concentrations may be not be c

5925- CAR,    Neuroprotective effects of carvacrol against Alzheimer’s disease and other neurodegenerative diseases: A review
- Review, AD, NA - Review, Park, NA - Review, Stroke, NA
*Inflam↓, anti-inflammatory, antioxidant, and AChEI properties
*antiOx↑,
*AChE↓,
*BBB↑, Carvacrol is able to cross the blood brain barrier easily, notably improving its therapeutic efficacy in neurodegenerative disorders
*cardioP↑, prevention of many chronic diseases, such as cancer as well as infectious, cardiovascular and neurodegenerative diseases
*neuroP↑, Extensive researches have revealed carvacrol neuroprotective properties
*memory↑, memory-enhancing activities
*TAC↑, Carvacrol has antioxidant activity and was shown to act as a dietary phyto-additive to boost animal antioxidant status (sharifi-Rad et al., 2018
*ROS↓, carvacrol could protect neuronal injuries against Aluminum-induced oxidative stress leading to lipid peroxidation
*lipid-P↓,
*MDA↓, carvacrol has been indicated to reduce malondialdehyde (MDA) and neuronal cell necrosis, and increase superoxide dismutase (SOD) and catalase (CAT) activity levels in the hippocampus (
*SOD↑,
*Catalase↑,
*NRF2↑, carvacrol activated nuclear factor-erythroid 2-related factor 2 (Nrf2) as an endogenous antioxidant
*cognitive↑, Carvacrol administration (25, 50, and 100 mg/kg) during 21 days attenuated memory impairments and enhanced cognition compared to the control group.
*IL1β↓, Carvacrol administration diminished the expression of interleukin-1β (IL-1β), cyclooxygenase-2 (COX-2), and tumor necrosis factor-α (TNF-α).
*COX2↓,
*TNF-α↓,
*TLR4↓, carvacrol could significantly decrease Toll-like receptor 4 (TLR4) and increase brain-derived neurotrophic factor (BDNF) expression.
*BDNF↑,
*PKCδ↑, carvacrol and thymol might have protective ability on cognitive function in AD by activation of PKC pathway
*5LO↓, Carvacrol inhibited AChE and lipoxygenase activity that supports its anti-inflammation and anti-Alzheimer effects
*TRPM7↓, Reduced caspase-3 levels, and TRPM7 channels inhibitor
*GSH↑, Antioxidant activity, Increased glutathione
*other↑, revealed a remarkable neuroprotective action of carvacrol in cerebral ischemia in animal models
*Ferroptosis↓, via ferroptosis inhibition by elevating GPx4 expression
*GPx4↑,

6816- EMD,    Emodin attenuates Alzheimer's disease by activating the protein kinase C signaling pathway
- in-vivo, AD, NA
*cognitive↑, escape latency was significantly shortened given a emodin prognosis.
*Aβ↓, emodin to Aβ- overexpression induced the protective effect of hippocampus cells in HT22 mice.
*p‑PKCδ↑, phosphorylation level of PKC in mice increased significantly after emodin administration.
*ROS↓, Emodin can attenuate oxidative stress and inflammatory response in Alzheimer's model mice by activating PKC pathway, thereby improving cognitive function.

6820- EMD,    The Health Benefits of Emodin, a Natural Anthraquinone Derived from Rhubarb—A Summary Update
- Review, Nor, NA - Review, Arthritis, NA - Review, AD, NA
*diuretic↑, Emodin has a wide range of biological activities, including diuretic, antibacterial, antiulcer, anti-inflammatory, anticancer and antinociceptive.
*Bacteria↓,
*Inflam↓,
AntiCan↑,
TumCP↓, emodin inhibits processes of neoplasia at the stages of proliferation, invasion and angiogenesis.
TumCI↓,
angioG↓,
*toxicity↓, The results showed that administration of emodin at the doses of 20, 40, and 80 mg/kg for 12 weeks is safe and did not cause any pathophysiological disorders in major organs in mammals.
IFN-γ↑, more interferon gamma (IFN-γ), interleukin (IL)-12 and reactive oxygen species (ROS) and less IL-6, tumor necrosis factor alpha (TNF-α) and transforming growth factor beta1 (TGF-β1) in he alveolar cavity in the emodin group than those in the control
IL12↑,
ROS↑, In vitro, emodin at the dose of 20 μM had no effect on cell viability in HL-60N1, but increased ROS and decreased autophagy, and thus induced apoptosis in HL-60N2
TNF-α↓,
TNF-α↓,
TGF-β↓,
MAPK↓, Antitumor properties of emodin are associated with inhibiting the activity of tyrosine kinases, such as mitogen-activated protein kinase (MAPK), protein kinase C (PKC), factor kappa-light-chain-enhancer of activated B cells (NF-κB)
PKCδ↓,
NF-kB↓,
HER2/EBBR2↓, emodin suppresses the activity of HER-2/neu tyrosine kinase [55]; whereas, in colon cancer cells, emodin inhibits phosphorylation of vascular endothelial growth factor (VEGF)
VEGF↓,
DNAdam↑, Another antiproliferative mechanism of emodin activity involves induction of DNA damage by the ROS, whose concentration is considerably increased in the cells treated with this anthraquinone.
Necroptosis↑, emodin induces necroptosis in the cells of renal cancer (RCC), which is resistant to conventional cancer therapy, such as chemotherapy or radiotherapy.
Glycolysis↓, and also inhibits glycolysis by downregulation of GLUT1 through ROS-mediated inactivation of the phosphoinositide 3-kinases (PI3K)/AKT signaling pathway.
GLUT1↓,
PI3K↓,
Akt↓,
Casp9↑, increasing active caspase-9, active caspase-3, and bcl-2-like protein 4 (Bax) levels and downregulating Bcl-2.
Casp3↑,
BAX↑,
Bcl-2↓,
eff↑, Li et al. [61] revealed that a bifunctional molecule of β-dihydro-artemisinin-emodin has high antiproliferative activity (suppressing Ki-67 expression),
MMP2↓, Emodin effectively inhibits the expression of the angiogenic-related NF-kB factor, as well as its regulatory factors, including VEGF, MMP-2, MMP-9.
MMP9↓,
eff↑, Combinatorial therapy with emodin and thymoquinone was also efficient in attenuating migration of MCF-7 breast cancer cells, inducing apoptosis, inhibiting cell proliferation, while enhancing cytotoxicity
ChemoSen↑, For example, combination therapy using emodin and doxorubicin sensitize breast cancer cells to doxorubicin by inhibition of proliferation in the DNA damage pathway
P-gp↓, It was demonstrated that emodin downregulated Pgp expression, and enhanced cisplatin-induced apoptosis and DNA damage in the cancer cells
SREBP2↓, suppressing the cholesterol biosynthesis (inhibition the activity of SREBP-2 protein) and inhibiting the expression of the AKT.
eff↑, emodin combined with berberine significantly inhibited the activity of salt-inducible kinases 3 (SIK3), belonging to the AMPK-related kinases, which elevated expressions in breast cancer cells contributing to tumorigenesis.
*other↝, emodin has therapeutic potential for the treatment of various kinds of inflammation, such as pancreatitis, asthma, arthritis, atherosclerosis, myocarditis, glomerulonephritis and Alzheimer’s disease.
*COX2↓, Therapeutic properties of emodin in the treatment of joint inflammation are also associated with inhibition of expression of VEGF, cyclooxygenase 2 (COX-2), hypoxia-inducible factor 1 (HIF-1)α and histone deacetylase (HDAC).
*Hif1a↓,
*HDAC↓,
*tau↓, Emodin effectively prevents abnormal aggregation of tau proteins in PHFs
*PKCδ↑, emodin improved cognitive functions by activating the protein kinase C signaling pathway (PKC), attenuating oxidative stress and inflammatory response in mice with Alzheimer’s disease.
*ROS↓,
*Inflam↓,
AntiAg?,

6824- EMD,    Neuroprotective, Anti-Inflammatory and Antifibrillogenic Offerings by Emodin against Alzheimer’s Dementia: A Systematic Review
- Review, AD, NA
*Inflam?, Emodin is a bioactive phytochemical with potent multimodal anti-inflammatory, antioxidant, and antifibrillogenic properties.
*antiOx↑,
*tau↓, While emodin effectively prevents tau and amyloid-beta (Aβ) oligomerization, it also mitigates their neurotoxicity by attenuating neuroinflammatory, oxidative, and bioenergetic defects.
*Aβ↓,
*neuroP↑, In recent years, several studies have advocated for a robust neuroprotective function of emodin
*ROS↓,
*memory↑, Evidences for emodin-mediated enhancements in memory, learning, and cognition were also found in the literature
*cognitive↑,
*other↝, Well-known sources of emodin include Rheum palmatum,10Polygonum cuspidatum,11Aloe vera,12Polygonum multifarum,13 and Casia obtusofolia.
*AChE↓, potent in vitro inhibition of AChE (IC50 of 21.8 μM), in addition to amelioration of H2O2-induced oxidative damage in PC12 cells
*BACE↓, potent inhibition of the activities of BACE-1 (IC50 of 4.5 μM) and AChE (IC50 of 9.7 μM); and strong and mixed-type inhibition for BACE-1 (Ki of 20 μM) in kinetic studies
*LC3II↓, Inhibition of autophagic (LC3-II and beclin-1)
*Beclin-1↓,
*p‑tau↓, 80 mg/kg/day for 2 weeks (intragastric administration) repression of the levels of BACE-1, Aβ species and phosphorylated-tau, stimulation of CREB signaling
*CREB↑,
*HNE↓, downregulation of Aβ and phosphorylated-tau levels, reduced oxidative damage and 4-HNE levels
*BioAv↓, Bioavailability of exogenously administered emodin suffers from some issues, including its weak intestinal absorption, high rate of elimination, and first-pass metabolism
*BioAv↝, bioavailability of orally supplemented emodin may show appreciable dependence on gender, given that there are four times higher plasma levels of emodin in male rats, compared to females after a single oral dosing of emodin at 8 mg/kg body weight.
*BioAv↑, pretreatment with stilbene glucosides from Radix Polygoni Multiflori prevents glucuronidation of emodin, and increases its plasma concentration upon oral administration
*BioAv↑, cotreatment with piperine was also found to inhibit glucuronide formation of orally administered emodin, while increasing the bioavailability of its free form
*BioAv↑, Nanoemulsification may also decreses the clearance of orally administered emodin, while increasing its brain distribution and bioavailability.
*BioAv↑, Lastly, treatment of emodin with sodium hydroxide to form its sodium salt may represent another strategy for improving the solubility and bioavailability of emodin
BioAv↑, ultrasound-sensitive emodin-containing lecithin-based nanoformulations squamous cell carcinoma FaDu and CAL-27 cells neck squamous cell carcinoma sonodynamic therapy-based beneficial actions
*HO-1↑, figure 3, neuroproctive
*PKCδ↑,
*Akt↑,
*NLRP3↓,
*NF-kB↓,
*TLR3↓,

2848- FIS,    Fisetin alleviates cellular senescence through PTEN mediated inhibition of PKCδ-NOX1 pathway in vascular smooth muscle cells
- in-vitro, Nor, NA
*ROS↓, Therefore, we hypothesized that the anti-aging effect of fisetin might involve regulation of the PKCδ-ROS production signaling pathway via PTEN activation in VSMC.
*PTEN↑,
*PKCδ↑, Fisetin-mediated PKCδ activation suppressed the inflammatory signaling pathway in human airway epithelial cells (Lee et al., 2018) and protected human umbilical vein endothelial cells from oxidative stress
*Inflam↓,

4941- PEITC,    PEITC: A resounding molecule averts metastasis in breast cancer cells in vitro by regulating PKCδ/Aurora A interplay
- in-vitro, BC, MCF7 - in-vitro, BC, MDA-MB-231
PKCδ↑, PEITC was found to increase the expression of PKCδ with subsequent nuclear translocation
Apoptosis↓, PEITC was chaperoned with inhibition of the aggressiveness of breast cancer cells and ultimately induction of apoptosis.
selectivity↑, However, PEITC did not elicit any cytotoxic effect in normal breast epithelial cell line MCF-10A.
tumCV↓, The percentage of viable MDA-MB-231 cells was not significantly reduced at a lower concentration (1 μM) of PEITC but at highest concentration (5 μM), used
p‑NRF2↑, PEITC-mediated upregulation of PKCδ escalated Nrf2 phosphorylation at Ser 40 residue as well as nuclear accumulation of phospho-Nrf2. Total Nrf2 expression was found to be increased alongside the cytoplasmic fraction, but not in the nuclear one.
cl‑PARP1↑, PARP1 cleavage was observed in PEITC-treated MCF-7 and MDA-MB-231 cells.
TumCMig↓, PEITC restrained the migratory ability of breast cancer cells by regulating serine/threonine kinase signaling
ROS↓, Our team previously demonstrated facilitation of nuclear translocation of Nrf2 to nucleus from cytosol upon PEITC treatment which by activating diverse antioxidant enzymes reduced intracellular burden of reactive oxygen species (ROS) in breast cancer
Hif1a↓, PEITC in breast cancer cells as observed earlier in our laboratory evidenced downregulation of HIF1α due to potential activation of Nrf2 and subsequent induction of cellular antioxidant system [

2565- RES,    https://onlinelibrary.wiley.com/doi/10.1111/j.1365-2141.2007.06788.x
- in-vitro, NA, NA - in-vivo, NA, NA
AntiAg↑, Resveratrol (0·15 and 0·25 μmol/l) inhibited collagen-induced platelet activation accompanied by [Ca+2]i mobilization, thromboxane A2 (TxA2) formation, phosphoinositide breakdown, and protein kinase C (PKC) activation.
TXA2↑,
PKCδ↑,
Dose↝, In an in vivo study, resveratrol (5 mg/kg) significantly prolonged platelet plug formation of mice

4996- Sal,    The Molecular Basis for Inhibition of Stemlike Cancer Cells by Salinomycin
CSCs↓, The natural product salinomycin, a K+ -selective ionophore, was recently found to exert selectivity against such cancer stem cells.
selectivity↑,
Wnt↓, This selective effect is thought to be due to inhibition of the Wnt signaling pathway, but the mechanistic basis remains unclear.
ERStress↑, accumulation in the endoplasmic reticulum (ER).
Ca+2↓, This localization is connected to induction of Ca2+ release from the ER into the cytosol.
UPR↑, Depletion of Ca 2+ from the ER induces the unfolded protein response a
CHOP↑, salinomycin-induced ER Ca2+ depletion up-regulates C/EBP homologous protein (CHOP), which inhibits Wnt signaling by down-regulating β-catenin.
β-catenin/ZEB1↓,
CD44↓, alinomycin efficiently and selectively reduced the proportion of breast cancer CD44 + /CD24− cells, a phenotype associated with enhanced tumorigenic capacity.
CD24↓,
PKCδ↑, Salinomycin Induces ER Ca2+ Release, ER Stress, and PKC Activation


Showing Research Papers: 1 to 12 of 12

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 12

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

p‑NRF2↑, 1,   ROS↓, 1,   ROS↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Glycolysis↓, 1,   SREBP2↓, 1,  

Cell Death(tgid=5) ⓘ

Akt↓, 1,   Apoptosis↓, 1,   BAX↑, 1,   Bcl-2↓, 1,   Casp3↑, 1,   Casp9↑, 1,   MAPK↓, 1,   Necroptosis↑, 1,  

Kinase & Signal Transduction(tgid=6) ⓘ

HER2/EBBR2↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

Protein Folding & ER Stress(tgid=8) ⓘ

CHOP↑, 1,   ERStress↑, 1,   UPR↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

DNAdam↑, 1,   cl‑PARP1↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD24↓, 1,   CD44↓, 1,   CSCs↓, 1,   PI3K↓, 1,   Wnt↓, 1,  

Migration(tgid=13) ⓘ

AntiAg?, 1,   AntiAg↑, 1,   Ca+2↓, 1,   MMP2↓, 1,   MMP9↓, 1,   PKCδ↓, 1,   PKCδ↑, 3,   TGF-β↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   TumCP↓, 1,   β-catenin/ZEB1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   TXA2↑, 1,   VEGF↓, 1,  

Barriers & Transport(tgid=15) ⓘ

GLUT1↓, 1,   P-gp↓, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

IFN-γ↑, 1,   IL12↑, 1,   NF-kB↓, 1,   TNF-α↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   ChemoSen↑, 1,   Dose↝, 1,   eff↑, 3,   selectivity↑, 2,  

Clinical Biomarkers(tgid=22) ⓘ

HER2/EBBR2↓, 1,  

Functional Outcomes(tgid=23) ⓘ

AntiCan↑, 1,   neuroP↑, 1,  
Total Targets: 55

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

diuretic↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 5,   Catalase↑, 1,   Ferroptosis↓, 1,   GPx4↑, 1,   GSH↑, 4,   H2O2∅, 1,   HNE↓, 1,   HO-1↑, 1,   lipid-P↓, 1,   MDA↓, 1,   Nrf1↑, 1,   NRF2↑, 3,   ROS↓, 7,   SOD↑, 1,   TAC↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 2,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

AMPK↑, 2,   CREB↑, 1,   glucose↑, 1,   GlucoseCon↑, 1,  

Cell Death(tgid=5) ⓘ

Akt↑, 3,   Ferroptosis↓, 1,   MAPK↑, 2,   p38↑, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

other↑, 1,   other↝, 2,  

Autophagy & Lysosomes(tgid=9) ⓘ

Beclin-1↓, 1,   LC3II↓, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

ERK↑, 2,   HDAC↓, 1,   PI3K↑, 2,   PTEN↓, 2,   PTEN↑, 1,   TRPM7↓, 1,  

Migration(tgid=13) ⓘ

5LO↓, 1,   MMP9↓, 2,   PKCδ↑, 8,   p‑PKCδ↑, 1,   VCAM-1↓, 3,  

Angiogenesis & Vasculature(tgid=14) ⓘ

eNOS↑, 1,   Hif1a↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 3,   GLUT1↑, 1,   GLUT4↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2↓, 2,   ICAM-1↓, 1,   IL1β↓, 2,   IL6↓, 1,   Inflam?, 1,   Inflam↓, 6,   NF-kB↓, 3,   TLR3↓, 1,   TLR4↓, 2,   TNF-α↓, 2,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 2,   BDNF↑, 1,   tau↓, 2,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 2,   BACE↓, 1,   NLRP3↓, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,   BioAv↑, 4,   BioAv↝, 3,   Dose↝, 1,   eff↓, 1,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BP↝, 1,   IL6↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cardioP↑, 2,   cognitive↑, 5,   memory↑, 2,   neuroP↑, 3,   toxicity↓, 1,  

Infection & Microbiome(tgid=24) ⓘ

Bacteria↓, 1,  
Total Targets: 76

Scientific Paper Hit Count for: PKCδ, Protein Kinase C delta
3 Emodin
2 Alpha-Lipoic-Acid
1 Ajoene (compound of Garlic)
1 Allicin (mainly Garlic)
1 Carvacrol
1 Fisetin
1 Phenethyl isothiocyanate
1 Resveratrol
1 salinomycin
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

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