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

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like Cell Adhesion Molecules

Immunoglobulin-like cell adhesion molecules or Ig-CAMs are a versatile group of cell surface glycoproteins belonging to the immunoglobulin protein superfamily. Ig-CAMs possess the characteristic immunoglobulin protein domains and other domains such as the fibronectin type III domain. The Ig domains are glycosylated to varying degrees in different Ig-CAMs.
Ig-CAMs exhibit either homophilic binding (to other Ig-CAMs) or heterophilic binding (to other ligands such as integrins). While most Ig-CAMs...

The Intrinsic Apoptotic Pathway

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...

The Extrinsic Apoptotic Pathway

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...

B Cell Activation and Differentiation

B Cell Activation and Differentiation

The adaptive immune response, a sophisticated defense mechanism, relies on the activation and differentiation of B lymphocytes, or B cells. These processes enable our bodies to mount a tailored response against specific pathogens such as bacteria, free virus particles, toxins, and parasites.
When naive B cells encounter a specific antigen that can bind to the B cell receptor (BCR) on their surface, they undergo sensitization to respond to the antigen's presence. Sensitization begins with...

Receptor Downregulation in MVBs

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 activation may...

Cellular Injury V: Apoptosis and Autophagy

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...

You might also read

Related Articles

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

Sort by

Same author

Gut T cell-independent IgA responses to commensal bacteria require engagement of the TACI receptor on B cells.

Science immunology·2020

Same author

BET inhibition represses miR17-92 to drive BIM-initiated apoptosis of normal and transformed hematopoietic cells.

Leukemia·2016

Same author

Re-activation of mitochondrial apoptosis inhibits T-cell lymphoma survival and treatment resistance.

Leukemia·2016

Same author

Critical B-lymphoid cell intrinsic role of endogenous MCL-1 in c-MYC-induced lymphomagenesis.

Cell death & disease·2016

Same author

PUMA promotes apoptosis of hematopoietic progenitors driving leukemic progression in a mouse model of myelodysplasia.

Cell death and differentiation·2016

Same author

Combined loss of PUMA and p21 accelerates c-MYC-driven lymphoma development considerably less than loss of one allele of p53.

Oncogene·2015

Search research articles

Related Experiment Video

Updated: Jun 14, 2026

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Published on: October 8, 2012

CAML regulates Bim-dependent thymocyte death.

C E Edgar¹, L D Lindquist, D L McKean

¹Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN, USA.

Cell Death and Differentiation

|March 20, 2010

Summary

Calcium-modulating cyclophilin ligand (CAML) is crucial for T lymphocyte development. CAML deficiency increases apoptosis by raising reactive oxygen species (ROS) and is regulated by Bim.

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Related Experiment Videos

Last Updated: Jun 14, 2026

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Examination of Thymic Positive and Negative Selection by Flow Cytometry

Published on: October 8, 2012

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Methods to Assess Beta Cell Death Mediated by Cytotoxic T Lymphocytes

Published on: June 16, 2011

Area of Science:

Immunology
Cell Biology
Molecular Biology

Background:

T lymphocyte differentiation requires precise apoptosis control for immune tolerance and foreign antigen recognition.
The precise signaling pathways governing thymocyte survival and apoptosis remain incompletely understood.

Purpose of the Study:

To investigate the role of calcium-modulating cyclophilin ligand (CAML) in T lymphocyte development and apoptosis.
To elucidate the molecular mechanisms by which CAML regulates thymocyte survival.

Main Methods:

Analysis of thymocyte development and apoptosis in CAML-deficient mice.
Assessment of reactive oxygen species (ROS) levels and sensitivity to cytotoxic stimuli in vitro.
Genetic manipulation including p53 deletion, Fas deficiency, and Bim deletion.

Main Results:

Thymocytes lacking CAML exhibited impaired T-cell development and increased apoptosis.
CAML-deficient thymocytes showed elevated ROS levels and accelerated death upon cytotoxic stress.
Loss of Bim, but not p53 or Fas, significantly rescued the survival of CAML-deficient thymocytes.

Conclusions:

CAML is essential for normal T-cell development by regulating thymocyte apoptosis.
CAML controls thymocyte death pathways involving ROS accumulation and the BH3-only protein Bim.
CAML represents a critical regulator of ROS- and Bim-dependent thymocyte apoptosis.