ADAM10 Cancer Research Results

ADAM10, A Disintegrin And Metalloproteinase Domain-Containing Protein 10: Click to Expand ⟱
Source:
Type:
ADAM10 (A Disintegrin And Metalloproteinase Domain-Containing Protein 10) plays a critical protective role in Alzheimer’s disease (AD) due to its function as an α-secretase, an enzyme involved in the non-amyloidogenic processing of the amyloid precursor protein (APP).
-By preventing Aβ accumulation, ADAM10 indirectly reduces amyloid plaques.br> -Downregulation of ADAM10 is observed in AD brains.
-ADAM10 levels are especially diminished in individuals with an APOE4 genotype
Scientific Papers found: Click to Expand⟱
3859- ALC,    Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment
- Review, AD, NA
*ROS↓, decreases the oxidative stress associated with aging
*ADAM10↑, treatment with ALC caused an increase in the level of ADAM10

7521- CA,    Protective effects of caffeic acid and caffeic acid phenethyl ester against acrolein-induced neurotoxicity in HT22 mouse hippocampal cells
- in-vitro, AD, HT22
*neuroP↑, CA/CAPE significantly attenuated acrolein-induced neurotoxicity, ROS accumulation, and GSH depletion.
*ROS↓,
*GSH↑,
*Akt↑, CA/CAPE showed protective effects against acrolein by modulating MAPKs and Akt/GSK3β signaling pathways.
*GSK‐3β↑,
*BACE/β-secretase↓, CA/CAPE restored the changes of β-secretase (BACE-1) and/or activation of α-secretase (ADAM-10) induced by acrolein.
*p38↓, CA/CAPE inhibited the activation of p38 and JNK1 while promoted the activation of ERK and Akt/GSK3 caused by acrolein
*RAGE↓, In our study, ADAM-10 and LR-11 were decreased while BACE-1 and RAGE were increased after the exposure of acrolein for 24 h (Fig. 3). Of interest, these changes were almost restored by both CA and CAPE
*ADAM10↑,

3855- CAP,    Capsaicin consumption reduces brain amyloid-beta generation and attenuates Alzheimer’s disease-type pathology and cognitive deficits in APP/PS1 mice
- in-vivo, AD, NA
*Risk↓, capsaicin-rich diet consumption was associated with better cognition and lower serum Amyloid-beta (Aβ) levels in people aged 40 years and over.
*Aβ↓, intake of capsaicin, the pungent ingredient in chili peppers, reduced brain Aβ burden and rescued cognitive decline in APP/PS1 mice
*p‑tau↓, capsaicin alleviated other AD-type pathologies, such as tau hyperphosphorylation, neuroinflammation and neurodegeneration.
*Inflam↓,
*neuroP↑,
*cognitive↑, Dietary capsaicin rescues cognition impairment in APP/PS1 mice
*ADAM10↑, capsaicin treatment increased the maturation of ADAM10 and thereby precluded Aβ generation
*PPARα↑, capsaicin also upregulated the levels of PPARα, which could activate ADAM10-mediated proteolysis of APP

3856- CUR,    Curcumin induces IL-6 receptor shedding via the ADAM10 proteinase
- in-vitro, AD, NA
*ADAM10↑, Herein, we report that membrane-modulating agents including curcumin, enhance IL-6R shedding in human monocytes via a mechanism involving a disintegrin and metalloprotease 10 (ADAM10).
*Inflam↓, therapeutic intervention using membrane-active compounds, such as curcuminoids, for diseases such as inflammation and cancer.

3862- CUR,  RES,    The metalloproteinase ADAM10: A useful therapeutic target?
- Review, AD, NA
*SIRT1↑, Therefore, the Sirt1 activators curcumin and resveratrol are tested for their clinical impact on ADAM10 expression in AD.
*ADAM10↑,

7829- FA,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*BioAv↑, Ferulic acid (4-hydroxy-3-methoxycinnamic acid) is abundant in some cereal grains and shows relatively higher absorption in the gastrointestinal mucosa compared to other phenolic acids
*cognitive↓, oral administration of ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks improved the mild cognitive impairment in populations aged 65−85 years old.
*Dose↝, ferulic acid (200 mg/d plus 40 mg of Angelica archangelica extract) daily for 48 weeks
*neuroP↑, ferulic acid might possess great neuroprotective potential in the neurodegenerative diseases.
*Aβ↓, ferulic acid reduced Aβ plaque deposits via inhibiting β-secretase (BACE1) activity and cleavage, as well as enhancing α-secretase (ADAM10) activity and cleavage in APP/PS1 mice
*BACE/β-secretase↓,
*ADAM10↑,
*Ac-histone H3↑, ferulic acid improved the cholinergic deficits as indicated by the increased ACh level in the cortex of Aβ1−42 -injected (i.c.v.) mice after ferulic acid treatmen
*BloodF↑, rerulic acid improved the cerebral blood flow (CBF) and insulin resistance, which helped to reduce the progression of AD pathology
*IRes↑,
*memory↑, while ferulic acid treatment (20 mg/kg, p.o.) improved the capillary hypofunction and reduced the memory deficits of APP/PS1 mice.
*Dose↝, Notably, the effective doses of ferulic acid in rodents were 5.3−30 mg/kg when administered for more than 4 weeks, which could be achieved through daily intake of appropriate amount of mung bean

4302- Gins,    Panax ginseng: A modulator of amyloid, tau pathology, and cognitive function in Alzheimer's disease
- Review, AD, NA
*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/β-secretase↓, 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,

7782- ISL,  BUT,  SCP,    Butein, isoliquiritigenin, and scopoletin attenuate neurodegeneration via antioxidant enzymes and SIRT1/ADAM10 signaling pathway
- in-vitro, AD, SH-SY5Y
*Inflam↓, Plant polyphenols, namely butein, isoliquiritigenin, and scopoletin, have been shown to exhibit various biological activities including anti-inflammatory, antimicrobial, and antioxidant activities.
*AntiBio↑,
*antiOx↑,
*Apoptosis↓, pretreatment of SH-SY5Y cells with 5 μM of butein, isoliquiritigenin, or scopoletin protected against the cell death induced by H2O2, and decreased the levels of apoptotic cells and ROS.
*ROS↓,
*SIRT1↑, levels of SIRT1, FoxO3a, ADAM10, BCL-2, and antioxidant enzymes (catalase and SOD2) were maintained in the cells pretreated with butein, isoliquiritigenin, or scopoletin
*FOXO3↑, Butein, isoliquiritigenin, and scopoletin ameliorated H2O2-induced neurotoxicity by reducing ROS, balancing antioxidants and activating SIRT1-FoxO3a-ADAM10 pathway.
*ADAM10↑,
*Bcl-2↝,
*Catalase↑,
*SOD2↑,
*neuroP↑, Taken together, the data suggest that these polyphenolic compounds could be potential candidates for prevention and/or treatment of neurodegeneration.
*GSR↑, neuroprotective and anti-inflammatory effects in vitro and cognitive enhancing effects in vivo by maintaining SOD, glutathione reductase, and glutathione peroxidase as well as by restoring the content of glutathione.
*GPx↑,
*GSH↑,

7828- Myr,  MBS,    Neuroprotective Potential of Mung Bean (Vigna radiata L.) Polyphenols in Alzheimer's Disease: A Review
- Review, AD, NA
*BBB↑, myricetin was able to cross the BBB, and thus exhibited neuroprotective activity in AD.
*neuroP↑,
*cognitive↑, myricetin (10 mg/kg, i.p.) improved the cognitive deficits and increased the density of hippocampal CA3 pyramidal neurons of STZ-injected (i.c.v.) rats
*Aβ↓, myricetin reduced the production of Aβ peptides by enhancing the activity of α-secretase (ADAM10) and βsecretase (BACE-1).
*ADAM10↑,
*BACE/β-secretase↝,
*IronCh↑, myricetin chelated mental irons and inhibited iron uptake into the brain, thus inhibiting excessive metal-induced Aβ aggregation
*Iron↓,
*AChE↓, inhibitory effect of myricetin on AChE in a model induced by injection (i.p.) of scopolamine, a neurotoxin that could easily penetrate BBB
*ROS↓, suppressing Aβ production and aggregation, oxidative stress, and AChE activity

3858- RES,    Alpha-Secretase ADAM10 Regulation: Insights into Alzheimer’s Disease Treatment
- Review, AD, NA
*neuroP↑, exerts neuroprotective and antioxidant properties
*antiOx↑,
*LDL↓, RSV decreases total cholesterol concentration in hypercholesterolemic rats
*ADAM10↑, RSV under experimental conditions in CHO (chinese hamster ovary) cells expressing human APP695 containing a Swedish mutation showed a significant increase in ADAM10 expression,

3863- RES,  MEL,  VitA,RetA,    Target Enzymes Considered for the Treatment of Alzheimer's Disease and Parkinson's Disease
- Review, AD, NA - Review, Park, NA
*ADAM10↑, resveratrol, with a polyphenol framework found in grape skin, peanut, and pomegranates, has been reported to be applied for the treatment of ND to enhance ADAM10 expression indirectly.
*ADAM10↑, In short, ADAM10 activity could be elevated by biological molecules such as XBP-1, SOX-2, PAX2, and melatonin.
*ADAM10↑, Small molecules such as bryostatin-1, retinoic acid, acitretin, Am80, and phlogacantholide C and multiple natural products (i.e., resveratrol, gemfibrozil, and etazolate) have been reported as upregulators of ADAM10.

4284- RES,    Resveratrol induces dephosphorylation of Tau by interfering with the MID1-PP2A complex
- in-vitro, AD, HEK293 - NA, Stroke, NA - in-vivo, AD, NA
*p‑tau↓, Resveratrol induces dephosphorylation of Tau
*PP2A↑, resveratrol, a polyphenol, significantly induces PP2A activity and reduces Tau phosphorylation at PP2A-dependent epitopes.
*neuroP↑, resveratrol is more and more being established as a neuroprotective drug after ischemic brain injury and in neurodegenerative disorders including Parkinson’s Disease13,14, AD15,16 and Huntington’s Disease
*antiOx↑, resveratrol has anti-oxidant activity19,20, inhibits cycloxygenase activity21,22, ribonucleotide reductase23, protein kinase C24, DNA polymerase 25 and has antiestrogenic properties26,27 and anti-platelet activity
COX2/PTGS2↓,
*AntiAg↑,
*SIRT1↑, it activates Sirt1, an NAD+-dependent protein deacetylase28,29 and also has been demonstrated to activate AMP kinase (AMPK)30,31, an important glucose sensor that inhibits acetyl-CoA carboxylase, thereby increasing oxidation of fatty acids and decre
*AMPK↑,
*Acetyl-CoA↓,
*FAO↑,
*ADAM10↑, Resveratrol has been suggested to induce the α-secretase ADAM10, which outcompetes BACE1 and thereby reduces Aβ-production
*BACE/β-secretase↓,
*Aβ↓,
*memory↑, interestingly, the resveratrol-mediated reduction of Aβ increases life span and improves learning and memory
*Inflam↓, reduces neuroinflammation47 and reduces oxidative stress48.
*ROS↓,


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:


Immune & Inflammatory Signaling(tgid=16) ⓘ

COX2/PTGS2↓, 1,  
Total Targets: 1

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AntiBio↑, 1,   IRes↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 3,   Catalase↑, 1,   GPx↑, 1,   GSH↑, 2,   GSR↑, 1,   Iron↓, 1,   NRF2↑, 1,   ROS↓, 5,   SOD2↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

Ac-histone H3↑, 1,   Acetyl-CoA↓, 1,   AMPK↑, 1,   CREB↑, 1,   FAO↑, 1,   LDL↓, 1,   PPARα↑, 1,   PPARγ↓, 1,   SIRT1↑, 3,  

Cell Death(tgid=5) ⓘ

Akt↑, 2,   Apoptosis↓, 1,   Bcl-2↝, 1,   MAPK↑, 1,   p38↓, 1,  

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

ERK↑, 1,   FOXO3↑, 1,   GSK‐3β↑, 1,   PI3K↑, 1,  

Migration(tgid=13) ⓘ

AntiAg↑, 1,   APP↓, 1,   PKA↑, 1,   RAGE↓, 1,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 4,  

Synaptic & Neurotransmission(tgid=18) ⓘ

AChE↓, 1,   ADAM10↑, 14,   p‑tau↓, 3,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 5,   BACE/β-secretase↓, 4,   BACE/β-secretase↝, 1,   IDE↑, 1,   PP2A↑, 2,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↑, 1,   Dose↝, 2,   eff↑, 1,  

Clinical Biomarkers(tgid=22) ⓘ

BloodF↑, 1,   RAGE↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↓, 1,   cognitive↑, 3,   memory↑, 3,   neuroP↑, 8,   Risk↓, 1,  
Total Targets: 54

Scientific Paper Hit Count for: ADAM10, A Disintegrin And Metalloproteinase Domain-Containing Protein 10
4 Resveratrol
2 Curcumin
2 Mung Bean Sprouts
1 Acetyl-l-carnitine
1 Caffeic acid
1 Capsaicin
1 Ferulic acid
1 Ginseng
1 Isoliquiritigenin
1 Butein
1 Scopoletin
1 Myricetin
1 Melatonin
1 Vitamin A, Retinoic Acid
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#:1368  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

 

Home Page