Human Amyloid Beta Precursor Protein Binding Protein A3 (APBA3) Protein

Product specifications

Proteins and Peptides

Amyloid Beta Precursor Protein Binding Protein A3 (APBA3)

E. coli

Human

Unconjugated

Molecular Weight: Calculated MW: 31.0 kDa
Concentration: Prior to lyophilization: 200 µg/ml
Sequence Fragment: Asp23-Leu278
Tag: N-terminal His tag

Recombinant

> 97%

10 µg

50 µg

100 µg

200 µg

500 µg

Lyophilized To keep the original salt concentration, we recommend reconstituting to the original concentration prior to lyophilization (see Concentration) in ddH2O. If a lower concentration is required, dilute in PBS, pH 7.4. If a higher concentration is required, the product can be reconstituted directly in PBS, pH 7.4, though please note that this will change the overall salt concentration. The stock concentration should be between 0.1-1.0 mg/ml. Do not vortex.

WB, SDS-PAGE

Prior to lyophilization: PBS, pH 7.4, containing 0.01% Sarcosyl, 1 mM DTT, 5% Trehalose and Proclin-300.

Shipped within 5-7 working days.

Store at 2-8 °C for up to one month. Store at -80 °C for up to one year. Avoid repeated freeze/thaw cycles.

No

O96018

APBA3, MGC:15815, X11L2, mint3, amyloid beta precursor protein binding family A member 3

Protein APBA3

RUO

This product is for research use only.   Not for human consumption, cosmetic, therapeutic or diagnostic use.

Descripción

APBA3, another member of the X11 protein family, is involved in the binding and regulation of the amyloid-beta precursor protein (APP). Unlike other members, APBA3 is highly expressed in a variety of tissues, including brain, heart, and liver, where it regulates both APP trafficking and protein stability. It binds APP through its phosphotyrosine-binding (PTB) domain and modulates its intracellular transport, preventing abnormal amyloid-beta production. APBA3 has additional roles beyond APP regulation, including its participation in vesicular transport, endocytosis, and regulation of apoptotic pathways. The protein is also implicated in immune regulation, where it interacts with components of the Toll-like receptor signaling pathway, suggesting a role in inflammatory responses. Dysregulation of APBA3 expression can contribute to amyloid plaque formation, mitochondrial dysfunction, and oxidative stress, particularly in neurodegenerative disorders such as Alzheimer’s disease. Furthermore, its involvement in cellular apoptosis suggests that APBA3 may also play a role in cancer progression and metabolic disorders. Understanding its mechanisms in APP metabolism and cellular signaling offers promising therapeutic opportunities to target neurodegenerative conditions and inflammatory processes.

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