Ignet

Gene Information

Gene symbol: APP

Gene name: amyloid beta (A4) precursor protein

HGNC ID: 620

Related Genes

#	Gene Symbol	Number of hits
1	ADIPOQ	1 hits
2	APLP2	1 hits
3	APOE	1 hits
4	BDNF	1 hits
5	CASP3	1 hits
6	CTGF	1 hits
7	GCG	1 hits
8	IAPP	1 hits
9	IDE	1 hits
10	INS	1 hits
11	IRS1	1 hits
12	JUN	1 hits
13	LRP1	1 hits
14	MAPK8	1 hits
15	MAPT	1 hits
16	NTRK2	1 hits
17	PPARG	1 hits
18	PRKAA1	1 hits
19	PSEN1	1 hits
20	SORL1	1 hits
21	VPS35	1 hits
22	VWS	1 hits

Related Sentences

#	PMID	Sentence
1	12515900	Furthermore, GLP-1 can modify processing of the amyloid beta- protein precursor in cell culture and dose-dependently reduces amyloid beta-peptide levels in the brain in vivo.
2	12634421	IDE deficiency resulted in a >50% decrease in Abeta degradation in both brain membrane fractions and primary neuronal cultures and a similar deficit in insulin degradation in liver.
3	15823718	Glycation of Abeta markedly enhances its aggregation in vitro, and the glycation of tau, in addition to hyperphosphorylation, appears to enhance the formation of paired helical filaments.
4	15850385	Deletion of insulin-degrading enzyme (IDE) in mice causes accumulation of cerebral amyloid beta-protein (Abeta), hyperinsulinemia, and glucose intolerance.
5	15850385	Here, we systematically characterize human IDE mRNAs, identify a novel splice form, and compare its subcellular distribution, kinetic properties, and ability to degrade Abeta to the known isoform.
6	16187222	We have recently shown that exposure to low levels of Abeta impairs BDNF trkB signal transduction, suppressing the Ras/ERK, and the PI3-K/Akt pathways but not the PLCgamma pathway.
7	16186174	Finally, using in vitro cellular models of amyloid precursor protein (APP)-processing and Abeta generation/clearance, we confirmed that human recombinant (hr)CTGF may increase Abeta1-40 and Abeta1-42 peptide steady-state levels, possibly through a mechanism that involves gamma-secretase activation and decreased insulin-degrading enzyme (IDE) steady-state levels in a MAP kinase (MAPK)/ phosphatidylinositol 3-kinase (PI-3K)/protein kinase-B (AKT)1-dependent manner.
8	16399206	We review the current evidence, which suggests that hyperinsulinaemia may elevate Abeta through insulin's competition with Abeta for IDE.
9	16574064	Insulin degrading enzyme (IDE), a zinc metalloprotease, can specifically recognize and degrade insulin, as well as several amyloidogenic peptides such as amyloid beta (Abeta) and amylin.
10	16787414	In addition to being a target for diabetes, PPARgamma activation state has recently been shown to modulate beta-amyloid peptide (Abeta) production in cellular models relevant to Alzheimer's disease.
11	17609417	The hepatic clearance of amyloid beta-peptide (1-40) [Abeta(1-40)] from plasma, which is largely mediated by low-density lipoprotein receptor-related protein (LRP-1), is suggested to play a role in preventing Abeta(1-40) accumulation in the brain.
12	17609417	The apparent hepatic uptake of [(125)I]Abeta(1-40) was also induced by insulin in a time-dependent manner.
13	17609417	In conclusion, plasma insulin facilitates LRP-1 translocation to the hepatic plasma membrane from the intracellular pool, resulting in significant enhancement of hepatic Abeta(1-40) uptake from the circulating blood.
14	18407659	The objective of this study is to examine if the neurotoxic oligomeric Abeta interacts with apoE CT and if this association affects the lipoprotein binding function of recombinant human apoE CT.
15	18407659	Site-specific fluorescence labeling of single cysteine-containing apoE CT variants with donor probes were employed to identify the binding of Abeta bearing an acceptor probe by intermolecular fluorescence resonance energy-transfer analysis.
16	19015532	We describe a full structural model for amyloid fibrils formed by the 40-residue beta-amyloid peptide associated with Alzheimer's disease (Abeta(1-40)), based on numerous constraints from solid state NMR and electron microscopy.
17	19387119	Insulin influences Abeta production by modulating alpha-secretase activity and Abeta degradation.
18	19285094	Low-density lipoprotein receptor related protein 1(LRP1) at the blood-brain barrier (BBB) is critical for regulation of Abeta homeostasis in the brain.
19	19672057	We recently demonstrated that adipocyte amyloid precursor protein (APP) expression is upregulated in obesity and correlates with insulin resistance and adipose tissue inflammation.
20	19672057	We conducted a pilot study in which we measured adipocyte APP gene expression and the circulating plasma levels of Abeta40 in 10 obese individuals before and after a 6-month behaviorally based weight loss intervention.
21	19672057	At baseline, adipocyte APP expression correlated significantly with plasma Abeta40 levels and with 2-hour insulin concentrations.
22	19672057	Changes in adipocyte APP expression correlated with changes in plasma Abeta40 levels (R = 0.74, p = 0.01) and changes in 2-hour insulin (R = 0.75, p = 0.01).
23	19672057	The results of this pilot study suggest that increased circulating plasma levels of Abeta peptides in obesity may be due to increased adipocyte APP gene expression.
24	19936237	There is increasing evidence that insulin also plays a role in Alzheimer's disease (AD) as it is involved in the metabolism of beta-amyloid (Abeta) and tau, two proteins that form Abeta plaques and neurofibrillary tangles (NFTs), respectively, the hallmark lesions in AD.
25	20881129	We readily recovered SorCS1:APP, SorCS1:SorL1, and SorCS1:Vps35 complexes from nontransgenic mouse brain.
26	18950899	Abeta was co-localized with amylin in islet amyloid deposits.
27	18950899	LPS increased APP in non-neuronal cells as well.
28	19237574	In addition, we found that glucose deprivation and various tyrphostins, known inhibitors of insulin-like growth factors/insulin receptor tyrosine kinases, do not modulate the effect of metformin on Abeta.
29	19237574	Finally, inhibition of AMP-activated protein kinase (AMPK) by the pharmacological inhibitor Compound C largely suppresses metformin's effect on Abeta generation and BACE1 transcription, suggesting an AMPK-dependent mechanism.
30	16444902	Insulin and IGF-I may modulate brain levels of insulin degrading enzyme, which would also lead to an accumulation of Abeta amyloid.
31	21347323	We found no changes in APP processing however the levels of soluble amyloid beta 40 was reduced in APOE knockout animals treated with pioglitazone.
32	18160637	LR11 is a neuronal sorting protein that reduces amyloid precursor protein (APP) trafficking to secretases that generate beta-amyloid (Abeta).
33	18160637	Because reduced LR11 is known to increase Abeta production and may be a significant genetic cause of LOAD, our results indicate that DHA increases in SorLA/LR11 levels may play an important role in preventing LOAD.
34	19605645	Here, we investigate the role of Abeta oligomer-induced c-Jun N-terminal kinase (JNK) activation leading to phosphorylation and degradation of the adaptor protein insulin receptor substrate-1 (IRS-1).
35	19605645	Here, we report Abeta oligomers significantly increased active JNK and phosphorylation of IRS-1 (Ser616) and tau (Ser422) in cultured hippocampal neurons, whereas JNK inhibition blocked these responses.
36	19605645	These data indicate JNK mediates Abeta oligomer inactivation of IRS-1 and phospho-tau pathology and that dietary treatment with fish oil/DHA, curcumin, or a combination of both has the potential to improve insulin/trophic signaling and cognitive deficits in AD.
37	19046405	Taken together, these data indicate that short-term WD is sufficient to selectively promote cerebral oxidative stress and metabolic disturbances in APP x PS1 knock-in mice, with increased oxidative stress preceding alterations in Abeta.
38	21411544	Insulin infusion significantly suppressed the expression of APP, presenilin-1, presenilin-2, and glycogen synthase kinase-3? in peripheral blood mononuclear cells.
39	21826222	Despite JNK overexpression, cell viability was unaffected probably because of decreases in cleaved caspase3 as well as in SMAC/DIABLO and APP, involved in the induction and amplification of apoptosis.