Request Demo

Last update 23 Jan 2025

APLP2

Last update 23 Jan 2025

Basic Info

Synonyms

Amyloid beta (A4) precursor-like protein 2, amyloid beta precursor like protein 2, Amyloid protein homolog

+ [8]

Introduction

May play a role in the regulation of hemostasis. The soluble form may have inhibitory properties towards coagulation factors. May interact with cellular G-protein signaling pathways. May bind to the DNA 5'-GTCACATG-3'(CDEI box). Inhibits trypsin, chymotrypsin, plasmin, factor XIA and plasma and glandular kallikrein. Modulates the Cu/Zn nitric oxide-catalyzed autodegradation of GPC1 heparan sulfate side chains in fibroblasts (By similarity).

Drugs associated with APLP2

CN117264052

Patent Mining

Target

APLP2

Mechanism-

Active Org.

Hangzhou BIOZON Medical Co., Ltd.

Originator Org.

Hangzhou BIOZON Medical Co., Ltd.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with APLP2

100 Translational Medicine associated with APLP2

0 Patents (Medical) associated with APLP2

349

Literatures (Medical) associated with APLP2

01 Dec 2024·Journal of Biological Chemistry

Familial Alzheimer’s disease mutations in amyloid precursor protein impair calcineurin signaling to NMDA receptors

Article

Author: Tavalin, Steven J

Familial Alzheimer's disease (FAD) is frequently associated with mutations in the amyloid precursor protein (APP), which are thought to lead to cognitive deficits by impairing NMDA receptor (NMDAR)-dependent forms of synaptic plasticity. Given the reliance of synaptic plasticity on NMDAR-mediated Ca²⁺ entry, shaping of NMDAR activity by APP and/or its disease-causing variants could provide a basis for understanding synaptic plasticity impairments associated with FAD. A region of APP (residues 639-644 within APP695) processed by the γ-secretase complex, which generates amyloid β (Aβ) peptides, is a hotspot for FAD mutations. This region bears similarity to a binding motif for calcineurin (CaN), a Ca²⁺/calmodulin-dependent phosphatase. Interaction assays confirm that APP associates with CaN in native tissue as well as in a heterologous expression system. This capacity to bind CaN extends to APP family members amyloid precursor-like protein 1 and amyloid precursor-like protein 2 (APLP1 and APLP2, respectively). Electrophysiological analysis demonstrates that APP and its family members limit NMDAR activity, in a manner consistent with CaN-dependent regulation of NMDAR desensitization. FAD mutations, in this region of APP, impair this regulation and consequently enhance NMDAR activity. Thus, by altering the landscape for CaN regulation of NMDA receptors, FAD mutations in APP may contribute to faulty information processing by modifying the dynamic range and temporal window of a critical signal for synaptic plasticity.

01 Nov 2024·Biochemical and Biophysical Research Communications

A peptide alleviated oxidative damages in the L02 cells and mice liver

Article

Author: Zhang, Zhiyang ; Liu, Bing ; Huang, Hongliang ; Gao, Gan ; Xie, Zhihui ; Wang, Qiheng

The liver is vitally metabolic for a multitude of biochemical reactions. Consequently, it generates many free radicals and reactive oxygen species, rendering it more susceptible to oxidative stress-induced damage. Oxidative stress represents a pivotal factor in the pathogenesis of liver diseases. We screened some antioxidant peptides previously. Here we investigated whether the peptides could attenuate oxidative damage with APPH in L02 cells. The results showed that one of the peptides, sequence FETLMPLWGNK, could decrease the excessive reactive oxygen species, increase antioxidant enzyme activity and protect mitochondrial function, reduce the ratio of apoptosis and S phase cycle arrest, and improve the survival rate of L02 cells damaged by APPH compared to cells of the control group. Then the peptide was evaluated in mice that CCl₄ injured. We found that CCl₄-injured mice had significantly increased serum inflammatory factors and liver injury markers, a large number of inflammatory cell infiltration, and local necrosis in the liver. The peptide could reduce inflammation, and improve liver pathological changes. This phenomenon may be associated with the activation of the Nrf2 signaling pathway. Concurrently, the peptide protects the liver by regulating the expression of proteins related to the mitochondrial apoptosis pathway (p53, Bax, Bcl-2, and Caspase3) and mitophagy-related proteins (PINK1, Parkin, and AMPKα). Therefore, the results indicated that the peptide is an active substance with antioxidant activity and anti-inflammatory effects.

01 Aug 2024·Experimental Gerontology

Quercetin ameliorates cognitive deficit, expression of amyloid precursor gene, and pro-inflammatory cytokines in an experimental models of Alzheimer's disease in Wistar rats

Article

Author: Baziar, Milad ; Akbari, Mehdi ; Asghariazar, Vahid ; Safarzadeh, Elham ; Abolhasani, Rozita ; Ataei, Sina ; Dadkhah, Masoomeh

Chronic stress (CS) is critically involved in the Alzheimer's disease (AD) pathogenesis resulting in cognitive disturbance. Also, amyloid precursor protein (APP) related gens, pro-inflammatory cytokines, and stress increases AD-related pathogenesis through increasing APP, all are important players in the development of AD. Herein, we explore the possible neuroprotective and anti-amnestic effect of quercetin (QUER) on cognitive deficits induced by scopolamine (SCOP) in stressed rats. Stress induction was performed by exposed of rats to 2-h chronic restraint stress for 10 days. Then rats were supplemented with QUER (25 mg/kg/day oral gavage, for 1 month). Ratswere submitted to intraperitoneal (i.p.) injection of SCOP (1 mg/kg) during the final 9 days of QUER supplementation to induce dementia like condition. Following the interventions, behavioral tests [elevated plus maze (EPM) and novel object recognition memory (NORM)] was examined to analysis the cognitive functions. Meanwhile, prefrontal cortex (PFC) and hippocampus of brain were used for gene expression and biochemical studies. Also, the plasma corticosterone (CORT) level was measured. We established that administration of QUER ameliorated the SCOP-related memory impairment. Also, QUER decreased stress related anxiety like behaviors in the EPM. QUER also altered the interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels in both PFC and hippocampus of SCOP treated rats in stress and non-stress conditions. We found that QUER increased APP and amyloid precursor-like protein 2 (APLP2) mRNA expression in both non-stress and stressed rats. Also, our findings imply that QUER suppress the effect of SCOP on cognitive functions. Moreover, decreased APP mRNA expression in the hippocampus were observed following pretreatment of rats with QUER in both stress and non-stress groups. Given that decreased amyloid beta (Aβ) expression in the hippocampus of stressed rats, it can be proposed that elevations in APP mRNA expression by QUER activates non-amyloidogenic pathways leading to reduction in Aβ levels. However, our findings indicate that QUER can be a therapeutic candidate, which exerts an anti-amnesic property against SCOP-induced memory decline. On the other hand, prior QUER administration in stress condition could be a promising approach against AD prevention.

Analysis

Perform a panoramic analysis of this field.

view full example data

Chat with Hiro

Get started for free today!

Accelerate Strategic R&D decision making with Synapse, PatSnap’s AI-powered Connected Innovation Intelligence Platform Built for Life Sciences Professionals.

Start your data trial now!

Synapse data is also accessible to external entities via APIs or data packages. Empower better decisions with the latest in pharmaceutical intelligence.

Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

APLP2

Basic Info

Related

Analysis