Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Enzyme-linked Receptors

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...

The JAK-STAT Signaling Pathway

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as SH2...

General Transcription Factors

General Transcription Factors

Tissue-specific transcription factors contribute to diverse cellular functions in mammals. For example, the gene for beta globin, a major component of hemoglobin, is present in all cells of the body. However, it is only expressed in red blood cells because the transcription factors that can bind to the promoter sequences of the beta globin gene are only expressed in these cells. Tissue-specific transcription factors also ensure that mutations in these factors may impair only the function of...

Receptor Tyrosine Kinases

Receptor Tyrosine Kinases

Receptor tyrosine kinases or RTKs are membrane-bound receptors that phosphorylate specific tyrosine on protein substrates. RTKs regulate cellular growth, differentiation, survival, and migration. They contain an extracellular ligand binding domain, a transmembrane domain, and a cytosolic tail with intrinsic kinase activity. Several extracellular signaling molecules activate RTKs in one or more ways and relay the signal downstream. Ligands such as platelet-derived growth factor (PDGF) or...

NF-κB-dependent Signaling Pathway

NF-κB-dependent Signaling Pathway

The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...

Regulation of the Unfolded Protein Response

Regulation of the Unfolded Protein Response

Inositol-requiring kinase one or IRE1 is the most conserved eukaryotic unfolded protein response (UPR) receptor. It is a type I transmembrane protein kinase receptor with a distinctive site-specific RNase activity. As the binding mechanics of the misfolded proteins with the N-terminal domain of IRE-1 are unclear, three binding models — direct, indirect, and allosteric -- are proposed for receptor activation. Nevertheless, it is known that once a misfolded protein associates with IRE1, it...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

Disease-modifying treatment preferences and decision-making in a multiple sclerosis randomized and observational clinical trial (DELIVER-MS).

Multiple sclerosis (Houndmills, Basingstoke, England)·2026

Same author

Diagnostic Challenge: The Case of a 70-Year-Old Man Who Presents With Progressive Vision Loss and Headaches.

Annals of clinical and translational neurology·2025

Same author

Incorporation of the central vein sign into the McDonald criteria.

Multiple sclerosis and related disorders·2024

Same author

Heart meets brain: A 25-year-old with a constellation of neurologic symptoms and heart failure.

Annals of clinical and translational neurology·2024

Same author

Withdrawal: Ceramide stabilizes β-site amyloid precursor protein-cleaving enzyme 1 and promotes amyloid β-peptide biogenesis.

The Journal of biological chemistry·2022

Same author

Association of the Protein-Quality-Control Protein Ubiquilin-1 With Alzheimer's Disease Both <i>in vitro</i> and <i>in vivo</i>.

Frontiers in neuroscience·2022

Search research articles

Related Experiment Video

Updated: Jun 3, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

TrkB Isoforms Differentially Affect AICD Production through Their Intracellular Functional Domains.

Sara Ansaloni¹, Brian P Leung, Neeraj P Sebastian

¹Department of Biology, Drexel University, Philadelphia, PA 19027, USA.

International Journal of Alzheimer'S Disease

|March 23, 2011

Summary

The TrkB receptor gene (NTRK2) influences amyloid precursor protein (APP) metabolism and AICD levels. Different TrkB receptor isoforms exhibit distinct effects on APP processing, impacting neurological pathways.

More Related Videos

qKAT: Quantitative Semi-automated Typing of Killer-cell Immunoglobulin-like Receptor Genes

qKAT: Quantitative Semi-automated Typing of Killer-cell Immunoglobulin-like Receptor Genes

Published on: March 6, 2019

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

Related Experiment Videos

Last Updated: Jun 3, 2026

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

A Guide to Production, Crystallization, and Structure Determination of Human IKK1/α

Published on: November 2, 2018

qKAT: Quantitative Semi-automated Typing of Killer-cell Immunoglobulin-like Receptor Genes

qKAT: Quantitative Semi-automated Typing of Killer-cell Immunoglobulin-like Receptor Genes

Published on: March 6, 2019

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes

Published on: March 12, 2013

Area of Science:

Neuroscience
Molecular Biology
Genetics

Background:

Amyloid precursor protein (APP) metabolism is crucial in neurobiology.
The TrkB receptor, encoded by NTRK2, plays a role in neuronal function.
Dysregulation of APP metabolism is implicated in neurological disorders.

Purpose of the Study:

To investigate how different TrkB receptor isoforms affect APP metabolism.
To elucidate the specific roles of TrkB isoforms (FL, SHC, T) in regulating APP processing and AICD levels.

Main Methods:

Utilized the SH-SY5Y human neuroblastoma cell line.
Employed knockdown and overexpression techniques to study TrkB isoforms.
Analyzed the impact of TrkB isoforms on APP, AICD, and sAPP levels.

Main Results:

TrkB FL isoform increased AICD-mediated transcription and APP levels, while decreasing sAPP levels.
Tyrosine kinase activity, PLC-γ, and SHC-binding sites mediated TrkB FL effects.
TrkB SHC isoform decreased AICD-mediated transcription; TrkB T isoform had no significant effect alone.
TrkB T co-expression abolished TrkB FL effects, while TrkB SHC co-expression partially retained them.

Conclusions:

TrkB isoforms differentially regulate APP metabolism.
The specific TrkB isoform and its signaling pathways are critical determinants of APP processing outcomes.