BAFF/APRIL system
Cytokines

Author: Gianpiero Pescarmona
Date: 27/05/2019

Description

DEFINITION

B-cell activating factor / BAFF also known as tumor necrosis factor ligand superfamily member 13B is a protein that in humans is encoded by the TNFSF13B gene. BAFF is also known as B Lymphocyte Stimulator (BLyS) and TNF- and APOL-related leukocyte expressed ligand (TALL-1) and the Dendritic cell-derived TNF-like molecule (CD257 antigen; cluster of differentiation 257)

A proliferation-inducing ligand /APRIL(protein), also known as tumor necrosis factor ligand superfamily member 13 (TNFSF13), is a protein of the TNF superfamily recognized by the cell surface receptor TACI

Soluble BAFF and APRIL signalling. BAFF and APRIL are type II transmembrane proteins, but BAFF can be processed into a soluble cytokine after cleavage at a furin protease site. APRIL is soluble, having been cleaved intracellularly. BAFF only has weak affinity for BCMA. BAFF-R is essential for survival and maturation of immature B cells. TACI is critical for T-cell-independent responses of B cells to

THE GENES

DatabaseLink
HGNCACADM
Uniprot"URL":

CHEMICAL STRUCTURE AND IMAGES

When relevant for the function

  • Primary structure
  • Secondary structure
  • Tertiary structure
  • Quaternary structure


Protein Aminoacids Percentage
The Protein Aminoacids Percentage gives useful information on the local environment and the metabolic status of the cell (starvation, lack of essential AA, hypoxia)

Protein Aminoacids Percentage (Width 700 px)

SYNTHESIS AND TURNOVER

mRNA synthesis
protein synthesis

post-translational modifications
degradation

CELLULAR FUNCTIONS

cellular localization,
biological function

Overexpression of the Cytokine BAFF and Autoimmunity Risk, 2017

  • A variant in TNFSF13B, encoding the cytokine and drug target B-cell activating factor (BAFF), was associated with multiple sclerosis as well as SLE. The disease-risk allele was also associated with up-regulated humoral immunity through increased levels of soluble BAFF, B lymphocytes, and immunoglobulins. The causal variant was identified: an insertion–deletion variant, GCTGT→A (in which A is the risk allele), yielded a shorter transcript that escaped microRNA inhibition and increased production of soluble BAFF, which in turn up-regulated humoral immunity. Population genetic signatures indicated that this autoimmunity variant has been evolutionarily advantageous, most likely by augmenting resistance to malaria.
  • Enzymes
DatabaseLink
BRENDA - The Comprehensive Enzyme Information System"URL":
KEGG Pathways"URL":
Human Metabolome Database"URL":
  • Cell signaling and Ligand transport
  • Structural proteins

REGULATION

DIAGNOSTIC USE

Attachments
fileuserdate
BAFF_APRIL_ch1.gifgp27/05/2019
BAFF_APRIL_ch2.gifgp27/05/2019
AddThis Social Bookmark Button