Related Experiment Video

Updated: Aug 11, 2026

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling
08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

BAP31 and its caspase cleavage product regulate cell surface expression of tetraspanins and integrin-mediated cell

Marina Stojanovic1, Marc Germain, Mai Nguyen

  • 1Department of Biochemistry, McIntyre Medical Sciences Building, McGill University, Montreal, Quebec H3G 1Y6, Canada.

The Journal of Biological Chemistry
|June 11, 2005
PubMed

Insights

BAP31 protein regulates cell surface protein export. Deleting BAP31 impairs cell adhesion and survival, but restoring BAP31 rescues these functions, highlighting its role in cell health.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Protein Trafficking

Background:

  • BAP31 is an endoplasmic reticulum protein crucial for exporting membrane proteins.
  • Tetraspanins CD9 and CD81 are involved in cell surface multiprotein complexes, including integrins.

Purpose of the Study:

  • To investigate the role of BAP31 in cell surface protein expression and cell adhesion.
  • To determine the impact of BAP31 deletion on integrin function and cell survival under serum stress.

Main Methods:

  • Gene deletion of Bap31 in mouse cells.
  • Analysis of cell surface expression of CD9, CD81, and integrins.
  • Assessment of cell adhesion to extracellular matrix under serum starvation.
  • Reconstitution experiments with wild-type BAP31.
  • Inhibition studies using antagonizing antibodies.
  • Experiments with human KB epithelial cells and p20 BAP31.

Main Results:

  • Bap31-null cells show reduced cell surface expression of CD9 and CD81.
  • Integrins alpha5beta1 and alpha(v)beta3 in Bap31-null cells fail to maintain adhesion under serum reduction.
  • Bap31-null cells exhibit increased sensitivity to serum starvation-induced apoptosis.
  • Restoring BAP31 rescues integrin-mediated cell attachment and survival.
  • p20 BAP31 inhibits tetraspanin and integrin-mediated cell attachment in human cells.

Conclusions:

  • BAP31 is essential for proper cell surface expression of tetraspanins and subsequent integrin-dependent cell adhesion and survival.
  • The caspase-8 cleavage product, p20 BAP31, acts upstream of BCL-2 to modulate cell surface protein export and cell attachment.

More Related Videos

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation08:47

Lighting Up the Pathways to Caspase Activation Using Bimolecular Fluorescence Complementation

Published on: March 5, 2018

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex07:17

Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex

Published on: August 2, 2021

Related Concept Videos

Caspases01:24

Caspases

Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside cells.
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Activation of Integrins01:15

Activation of Integrins

Integrins bind ligands and transmit information from outside the cell to inside or vice-versa through an "outside-in signaling" or "inside-out signaling."
In "outside-in signaling," external factors in the extracellular space bind to exposed ligand binding sites on integrins. This causes the inactive protein to undergo a conformational change to become active. Integrins are often clustered on the cell membrane. Repetitive and regularly spaced ligand binding events provide an effective stimulus.
Intracellular Signaling Affects Focal Adhesions01:17

Intracellular Signaling Affects Focal Adhesions

Integrins act both as extracellular input receivers and as intracellular processing activators. As their name suggests, integrins are entirely integrated into the membrane structure. Their hydrophobic membrane-spanning regions interact with the phospholipid bilayer's hydrophobic region. These membrane receptors provide extracellular attachment sites for effectors like hormones and growth factors. They activate intracellular response cascades when their effectors are bound and active.
Some...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...