PKA Cancer Research Results
PKA, protein kinase A: Click to Expand ⟱
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Protein kinase A (PKA)
• PKA is composed of regulatory (R) and catalytic (C) subunits. Binding of cAMP to the regulatory subunits releases the catalytic subunits, which then phosphorylate target proteins.
– Increased PKA activity has been associated with the activation of downstream signaling pathways that promote cell growth and survival.
– Thus, the level of PKA activation (often indirectly inferred by phosphorylation status of downstream targets) can serve as a marker for tumor progression and treatment resistance.
– PKA does not act in isolation—it interacts with other signaling pathways (e.g., MAPK, PI3K/AKT).
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Scientific Papers found: Click to Expand⟱
Warburg↓, Capsaicin inhibits the Warburg effect by binding directly to Cys424 residue and LDHA of pyruvate kinase isoenzyme type M2 (PKM2).
*PKM2↓,
*COX2↓, capsaicin targets COX-2 and down-regulates its expression, which results in the further inhibition of inflammation
*Inflam↓,
*Sepsis↓, capsaicin may be used as a new active ingredient to treat sepsis and inflammation
*AMPK↑, capsaicin activates adenylate-activated protein kinase (AMPK) and protein kinase A (PKA), in turn enhancing the activity of the mitochondrial respiratory chain and promoting fatty acid oxidation
*PKA↑,
*mitResp↑,
*FAO↑,
*FASN↓, capsaicin can inhibit the activity of fatty acid synthetase
*PGM1?,
*ATP↑, treatment resulted in increased intracellular ATP levels (the end product of glycolysis)
*ROS↓, Capsaicin can mitigate the negative effects of oxidative stress on human health by scavenging these free radicals and reducing the oxidative stress response.
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in-vitro, |
BC, |
MDA-MB-231 |
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eff↑, In this study, we demonstrate that chlorogenic acid (CGA), a natural antioxidant, significantly enhances beta‐lapachone (β‐Lap)‐induced cell death in cancer cells.
Apoptosis↑, augmented apoptosis induced by CGA is associated with activation of protein kinase A (PKA) in β‐Lap–treated cells
PKA↑,
eff↑, CGA Promotes β‐Lap‐Induced Cell Death in NQO1‐Overexpressing Cancer Cells
*neuroP↑, highlighting neuroprotective mechanisms, such as the inhibition of Aβ production, enhanced Aβ clearance, and suppression of tau hyperphosphorylation.
*Aβ↓,
*p‑tau↓,
*cognitive↑, Research on P. ginseng and its bioactive ginsenosides has shown potential for improving cognitive function in AD models
*eff↑, particularly pronounced effects in individuals lacking apolipoprotein ε4 allele.
*PKA↑, Upregulates the PKA/CREB signaling pathway
*CREB↑,
*BACE↓, Inhibits BACE1 activity
*ADAM10↑, Enhances the expression of ADAM10 and reduces BACE1 expression through the activation of MAPK/ERK and PI3K/AKT
*MAPK↑,
*ERK↑,
*PI3K↑,
*Akt↑,
*NRF2↑, Activates the Nrf2/Keap1 signaling pathway
*PPARγ↓, Inhibits PPARγ phosphorylation and upregulates the expression of IDE
*IDE↑,
*APP↓, downregulates the expression of BACE1 and APP
*PP2A↑, Ginsenoside Rb1 enhances PP2A levels, thereby facilitating tau dephosphorylation and reducing p-tau levels observed in animal studies
*memory↑, The 400 mg dose of ginseng extract significantly improved “Quality of Memory” and “Secondary Memory” at all post-dose time points,
*cognitive↑, HuA-LIP significantly ameliorated cognitive dysfunction and neuronal damage in CIH mice.
*SOD↑, HuA-LIP elevated T-SOD and GSH-Px abilities and decreased MDA content to resist oxidative stress damage induced by CIH.
*GPx↑,
*MDA↓,
*ROS↓,
*Iron↓, HuA-LIP reduced brain iron levels by downregulating TfR1, hepcidin, and FTL expression.
*TfR1/CD71↓,
*FTL↓,
*ERK↑, HuA-LIP activated the PKAα/Erk/CREB/BDNF signaling pathway and elevated MAP2, PSD95, and synaptophysin to improve synaptic plasticity.
*PKA↑,
*CREB↑,
*BDNF↑,
*PSD95↑,
*neuroP↑, HuA-LIP showed a superior performance against neuronal damage induced by CIH.
*eff↑, PEMF exposure increased cell proliferation and adhesion
*mTOR↑, PEMFs contribute to activation of the mTOR pathway via upregulation of the proteins AKT, MAPP kinase, and RRAGA, suggesting that activation of the mTOR pathway is required for PEMF-stimulated osteogenic differentiation.
*Akt↑,
*PKA↑, PEMFs increase the activity of certain kinases belonging to known intracellular signaling pathways, such as the protein kinase A (PKA) and the MAPK ERK1/2
*MAPK↑,
*ERK↑,
*BMP2↑, PEMFs stimulation also upregulates BMP2 expression in association with increased differentiation in mesenchymal stem cells (MSCs
*Diff↑,
*PKCδ↓, Decrease in PKC protein (involved on Adipogenesis)
*VEGF↑, Increase on VEGF (involved on angiogenesis)
*IL10↑, PEMF induced a significant increase of in vitro expression of IL-10 (that exerts anti-inflammatory activity)
*neuroP↑, state of the art evidence on the role of resveratrol (RSV) in neuroprotection is presented
*Inflam↓, Resveratrol (3,5,4′-trihydroxy-trans-stilbene), a polyphenol contained in red wine, peanuts, and some berries, is known for its anti-atherosclerotic, anti-inflammatory, antioxidant, and longevity-promoting properties
*antiOx↑,
*GSH↑, ↑glutathione in brain
*HO-1↑, ↑HO-1 ↓iNOS in hippocampus
*iNOS↓,
*BDNF↑, ↑BDNF, ↑pCREB, ↑PKA, ↑BCl-2 expression, ↓BAX expression, ↓IL-1β, IL-6, in hippocampus
*p‑CREB↑,
*PKA↑,
*Bcl-2↑,
*BAX↓,
*IL1β↓,
*IL6↓,
*MMP9↓, ↓MMP-9 in cerebrospinal fluid
*memory↑, ↑memory performance
*AMPK↑, ↑AMPK, ↑PGC-1, ↓NF-κB / IL-1β / NLRP3 in hippocampus and prefrontal cortex
*PGC-1α↓,
*NF-kB↓,
*Aβ↓, may counteract the formation of neurotoxic Aβ
*SIRT1↑, Resveratrol via SIRT-1 can, therefore, be expected to reduce the level of hyperphosphorylated tau and provide protection against neurodegeneration.
*p‑tau↓,
*PP2A↑, resveratrol by lowering the expression of MID1 ubiquitin ligase increases protein phosphatase 2A (PP2A) activity and promotes tau dephosphorylation by preventing its accumulation
*lipid-P↓, resveratrol abolishes Aβ-induced lipid peroxidation and expression of heme oxygenase-1 (HO-1) reduction;
*NLRP3↓, Researchers achieved a significant reduction in the levels of NF-κB (nuclear factor κ-light-chain enhancer of activated B cell), interleukin 1β and NLRP3 (NOD-, LRR- and pyrin domain-containing protein 3) inflammation markers
*BACE↓, figure 1
Showing Research Papers: 1 to 6 of 6
* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6
Pathway results for Effect on Cancer / Diseased Cells:
Core Metabolism/Glycolysis ⓘ
Warburg↓, 1,
Cell Death ⓘ
Apoptosis↑, 1,
Migration ⓘ
PKA↑, 1,
Drug Metabolism & Resistance ⓘ
eff↑, 2,
Total Targets: 4
Pathway results for Effect on Normal Cells:
Redox & Oxidative Stress ⓘ
antiOx↑, 1, GPx↑, 1, GSH↑, 1, HO-1↑, 1, Iron↓, 1, lipid-P↓, 1, MDA↓, 1, NRF2↑, 1, ROS↓, 2, SOD↑, 1,
Metal & Cofactor Biology ⓘ
FTL↓, 1, TfR1/CD71↓, 1,
Mitochondria & Bioenergetics ⓘ
ATP↑, 1, mitResp↑, 1, PGC-1α↓, 1,
Core Metabolism/Glycolysis ⓘ
AMPK↑, 2, CREB↑, 2, p‑CREB↑, 1, FAO↑, 1, FASN↓, 1, PGM1?, 1, PKM2↓, 1, PPARγ↓, 1, SIRT1↑, 1,
Cell Death ⓘ
Akt↑, 2, BAX↓, 1, Bcl-2↑, 1, BMP2↑, 1, iNOS↓, 1, MAPK↑, 2,
Proliferation, Differentiation & Cell State ⓘ
Diff↑, 1, ERK↑, 3, mTOR↑, 1, PI3K↑, 1,
Migration ⓘ
APP↓, 1, MMP9↓, 1, PKA↑, 5, PKCδ↓, 1,
Angiogenesis & Vasculature ⓘ
VEGF↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL10↑, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 2, NF-kB↓, 1,
Synaptic & Neurotransmission ⓘ
ADAM10↑, 1, BDNF↑, 2, PSD95↑, 1, p‑tau↓, 2,
Protein Aggregation ⓘ
Aβ↓, 2, BACE↓, 2, IDE↑, 1, NLRP3↓, 1, PP2A↑, 2,
Drug Metabolism & Resistance ⓘ
eff↑, 2,
Clinical Biomarkers ⓘ
IL6↓, 1,
Functional Outcomes ⓘ
cognitive↑, 2, memory↑, 2, neuroP↑, 3,
Infection & Microbiome ⓘ
Sepsis↓, 1,
Total Targets: 60
Scientific Paper Hit Count for: PKA, protein kinase A
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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