CDK5 Cancer Research Results
CDK5, Cyclin-dependent kinase 5: Click to Expand ⟱
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CDK5 is primarily expressed in neurons and is important for normal brain development, synaptic function, and neuronal signaling. However, CDK5 becomes dysregulated in AD, contributing to neurodegeneration.
-CDK5 is generally upregulated or hyperactivated in both cancer and Alzheimer's disease (AD)
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Scientific Papers found: Click to Expand⟱
*GSK‐3β↓, Firstly, curcumin can inhibit kinases, such as GSK-3β and Cyclin-Dependent Kinase 5 (Cdk5), that excessively phosphorylate Tau protein
*CDK5↓,
*p‑tau↓,
*IronCh↑, curcumin's metal ion chelating capability contributes to the reduction of free radicals
*ROS↓,
*HO-1↑, upregulating antioxidant enzymes including heme oxygenase 1 (HO-1), superoxide dismutase (SOD), catalase, and enzymes involved in the synthesis of endogenous antioxidants, specifically glutathione (GSH)
*SOD↑,
*Catalase↑,
*GSH↑,
*TNF-α↓, inhibiting the expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-12,
*IL6↓,
*IL12↓,
*NRF2↑, inducing the production of anti-inflammatory mediators including HO-1/NRF-2, PPARα-γ, and IL-4
*PPARγ↑,
*IL4↑,
*AChE↓, researchers have observed that curcumin can suppress AChE mRNA expression levels, effectively preventing the Cd-induced rise in AChE activity
*Dose↝, While curcumin directly interacts with AChE, its inhibitory activity remains weak (IC50 = 67.69 μM)
*GutMicro↑, curcumin's interaction with gut microbiota exhibits potential anti-AD properties.
*Aβ↓, We found that curcumin-treated AD rats markedly reduced the levels of Aβ40 and Aβ42 in the brain and in the plasma in comparison to untreated AD rats
*p‑tau↓, Moreover, the levels of phosphorylated tau at Ser396 (PHF13), Ser202/Thr205 (AT8), and Aβ40/42 (MOAB2) were decreased significantly in AD rats treated with curcumin.
*GSK‐3β↓, Phospho-GSK3β (Tyr216), the active form of GSK3β, and total GSK3β were significantly decreased in AD rats treated with curcumin.
*CDK5↓, Cdk5 and its activators p35 and p25 were significantly decreased in curcumin-treated AD rats.
*memory↑, Impaired spatial memory and locomotor activity in AD rats were partially reversed by curcumin.
*antiOx↑, Curcumin, a natural compound with potent antioxidant and anti-inflammatory properties
*Inflam↓,
*AntiAge↑, Its potential anti-aging properties are due to its power to alter the levels of proteins associated with senescence, such as adenosine 5′-monophosphate-activated protein kinase (AMPK) and sirtuins
*AMPK↑,
*SIRT1↑,
*NF-kB↓, preventing pro-aging proteins, such as nuclear factor-kappa-B (NF-κB) and mammalian target of rapamycin (mTOR)
*mTOR↓,
*NLRP3↓, Moreover, curcumin, by inhibiting the NF-κB pathway, can directly restrain the assembly or even inhibit the activation of the NOD-like receptor pyrin domain-containing 3 (NLRP3) inflammasome
*NADPH↓, by inhibiting nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and elevating the activity of antioxidant enzymes and consequently lowering reactive oxygen species (ROS)
*ROS↓,
*COX2↓, (COX-2), granulocyte colony-stimulating factor (G-CSF), and monocyte chemotactic protein-1 (MCP-1) can be decreased by curcumin
*MCP1↓,
*IL1β↓, by decreasing IL-1β, IL-17, IL-23, TNF-α, and myeloperoxidase, enhancing levels of IL-10, and downregulating activation of NF-κB
*IL17↓,
*IL23↓,
*TNF-α↓,
*MPO↓,
*IL10↑,
*lipid-P↓, curcumin showed a significant decline in lipid peroxidation and increased superoxide dismutase levels, in addition to a reduction in Aβ aggregation and tau hyperphosphorylation through the regulation of GSK3β, Cdk5, p35, and p25
*SOD↑,
*Aβ↓,
*p‑tau↓,
*GSK‐3β↓,
*CDK5↓,
*TXNIP↓, Curcumin also has an inhibitory role on the thioredoxin-interacting protein (TXNIP)/NLRP3 inflammasome pathway
*NRF2↑, well as upregulation of Nrf2, NAD(P)H quinine oxidoreductase 1 (NQO1), HO-1, and γ-glutamyl cysteine synthetase (γ-GCS) in brain cells.
*NQO1↑,
*HO-1↑,
*OS↑, significant improvement in OS, and a positive evolution in memory and spatial learning
*memory↑,
*BDNF↑, Besides that, it promoted neurogenesis through increasing brain-derived neurotrophic factor (BDNF) levels
*neuroP↑, Curcumin can promote neuroprotection
*BACE↓, Figure 7
*AChE↓, figure 7
*LDL↓, and reduced total cholesterol and LDL levels.
*cognitive↑, ELF-MF exposure ameliorated cognitive deficits and increased synaptic proteins in 3xTg mice.
*neuroP↑, protective effects of ELF-MF exposure may have also been caused by the inhibition of apoptosis and/or decreased oxidative stress levels that were observed in the hippocampus tissues of treated mice.
*Apoptosis↓,
*ROS↓,
*p‑tau↓, tau hyperphosphorylation was decreased in vivo because of ELF-MF exposure, and this decrease was induced by the inhibition of GSK3β and CDK5 activities and activation of PP2Ac.
*GSK‐3β↓,
*CDK5↓,
*CDK5↓, BAD, CDK5, FN1, ITGA4, and MAPK9 were identified. Quercetin and Berberine have shown significant binding affinities to these biomarkers
*CDK5↓, Two potential compounds, andrographolide, and rosmarinic acid, produced the best binding affinities following the molecular docking of the active compounds against the GSK-3β and CDK5 targets.
*GSK‐3β↓,
*AChE↓, Daily administration of CP (150 mg/kg) for 3 months along with aluminium chloride (50 mg/kg) decreased the elevated enzymatic activity of acetylcholine esterase and also inhibited the decline in Na(+)/K(+)ATPase activity which resulted from aluminium
*ChAT↑, Oral administration of CP preserved the mRNA levels of muscarinic receptor 1 (M1 receptor), choline acetyl transferase (ChAT) and Nerve Growth Factor-Tyrosine kinase A receptor (NGF-TrkA).
*NGF↑,
*CDK5↓, It also ameliorated the upregulated protein expression of cyclin dependent kinase5 (Cdk5) induced by aluminium.
*neuroP↑, , indicative of its neuroprotective effects.
*MDA↓, Data showed co-treatment of CP to alu-
minium treated rats led to a significant reduction in MDA by
â¼23% and protein carbonyl by â¼71% as compared to group II.
Showing Research Papers: 1 to 7 of 7
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 7
Pathway results for Effect on Cancer / Diseased Cells:
Total Targets: 0
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, Catalase↑, 1, GSH↑, 1, HO-1↑, 2, lipid-P↓, 1, MDA↓, 1, MPO↓, 1, NQO1↑, 1, NRF2↑, 2, ROS↓, 3, SOD↑, 2,
Metal & Cofactor Biology ⓘ
IronCh↑, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 1, LDL↓, 1, NADPH↓, 1, PPARγ↑, 1, SIRT1↑, 1,
Cell Death ⓘ
Apoptosis↓, 1,
Proliferation, Differentiation & Cell State ⓘ
GSK‐3β↓, 5, mTOR↓, 1,
Migration ⓘ
CDK5↓, 7, TXNIP↓, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL10↑, 1, IL12↓, 1, IL17↓, 1, IL1β↓, 1, IL23↓, 1, IL4↑, 1, IL6↓, 1, Inflam↓, 1, MCP1↓, 1, NF-kB↓, 1, TNF-α↓, 2,
Synaptic & Neurotransmission ⓘ
AChE↓, 3, BDNF↑, 1, ChAT↑, 1, NGF↑, 1, p‑tau↓, 4,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 1, NLRP3↓, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1, IL6↓, 1,
Functional Outcomes ⓘ
AntiAge↑, 1, cognitive↑, 1, memory↑, 2, neuroP↑, 3, OS↑, 1,
Total Targets: 50
Scientific Paper Hit Count for: CDK5, Cyclin-dependent kinase 5
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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