Related Experiment Video

Updated: Jan 6, 2026

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice
07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

948

Understanding the role of 14-3-3Ƞ protein in rheumatoid arthritis: from molecular dysregulation to therapeutic

Dhrita Chatterjee1, Kousik Maparu2

  • 1Department of Pharmacology, Sanaka Educational Trust, Durgapur, 713212, West Bengal, India.

Molecular Biology Reports
|September 27, 2025
PubMed

Insights

The 14-3-3η protein is elevated in rheumatoid arthritis (RA) and linked to joint damage. Inhibiting this protein may offer a new therapeutic strategy for RA treatment.

Area of Science:

  • Immunology
  • Biochemistry
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is a chronic autoimmune disease causing joint inflammation and damage.
  • The 14-3-3η protein is implicated in RA pathogenesis.
  • Elevated 14-3-3η levels correlate with RA severity and joint deterioration.

Purpose of the Study:

  • To investigate the role of 14-3-3η protein in rheumatoid arthritis.
  • To explore 14-3-3η as a potential biomarker and therapeutic target for RA.

Main Methods:

  • Detection of 14-3-3η protein levels in synovial fluid and serum of RA patients.
  • Analysis of 14-3-3η interactions with intracellular signaling pathways (MAPK/ERK, SAPK/JNK, JAK-STAT).
  • Preclinical studies evaluating the effects of 14-3-3η inhibition on RA models.

Main Results:

  • High 14-3-3η protein levels were consistently found in RA patients.
  • 14-3-3η enhances pro-inflammatory cytokine production, contributing to joint swelling and bone loss.
  • Inhibition of 14-3-3η reduced synovial inflammation and bone loss in preclinical RA models.

Conclusions:

  • The 14-3-3η protein is a significant factor in RA pathogenesis.
  • Targeting 14-3-3η presents a promising therapeutic avenue for rheumatoid arthritis.
  • 14-3-3η inhibition shows potential as a disease-modifying treatment for RA.
Keywords:
ApoptosisJAK-STATMAPK/ERKRheumatoid arthritis (RA), 14-3-3ηSAPK/JNKSynovial inflammation, autophagy

More Related Videos

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes11:52

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes

Published on: January 27, 2023

4.3K
Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain04:50

Preliminary Study on Acupuncture Combined with Grain-sized Moxibustion for Treating Rheumatoid Arthritis with Finger Joint Pain

Published on: May 16, 2025

770

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

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...
11.7K
T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.1K
Regulation of the Unfolded Protein Response01:31

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...
2.9K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.7K
Inflammatory Response01:28

Inflammatory Response

An inflammatory response is a localized, nonspecific immune reaction that occurs when a tissue is injured. It is characterized by redness, swelling, heat, and pain, which are commonly called the cardinal signs and symptoms of inflammation. Inflammation can sometimes result in a loss of function.
Inflammation can be triggered by various stimuli, such as impact, abrasion, chemical irritation, infections, and extreme hot or cold temperatures. These can damage cells and connective tissue fibers,...
15.8K
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
6.2K