Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

NF-κB-dependent Signaling Pathway02:26

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...
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...
NF-kB-dependent Signaling Pathway02:26

NF-kB-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...
Targeted Cancer Therapies02:57

Targeted Cancer Therapies

The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
There are several types of targeted therapies against specific...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...

You might also read

Related Articles

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

Sort by
Same author

Emerging Piperazine Derivatives: Synthesis, Characterization, Biological Evaluation, Molecular Docking, and ADMET In silico Studies.

Drug metabolism and bioanalysis·2026
Same author

Democratizing cloud data lake analytics: natural language access to Apache Iceberg via LLM agents.

Frontiers in big data·2026
Same author

Chemo-Diversity Landscape Using Physico-Biochemical, Elemental, and Metabolic Profiling in Different Stages and Accessions of <i>Madhuca longifolia</i> Flowers for Unveiling Their Processing Value and Utilization.

Molecules (Basel, Switzerland)·2026
Same author

Limb occlusion pressure adjusted tourniquet use results in adequate hemostasis in pediatric limb surgeries: a prospective clinical study.

Journal of pediatric orthopedics. Part B·2026
Same author

Gout, Hyperuricemia and Crystal-Associated Disease Network (G-CAN) consensus statement regarding labels and definitions for disease elements in calcium pyrophosphate crystal deposition (CPPD).

Annals of the rheumatic diseases·2026
Same author

Investigating the spatial adaptation for iron and zinc content using AMMI and GGE biplot model in lentil (Lens culinaris L.).

BMC plant biology·2026

Related Experiment Video

Updated: May 21, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

BLM regulates MALT1-driven NF-κB signalling and is targetable in B-cell malignancies.

Ritu Agrawal1,2, Supratim Ghosh3, Nitin Kumar4

  • 1Biotechnology Research and Innovation Council-National Institute of Immunology (BRIC- NII), Aruna Asaf Ali Marg, New Delhi, 110067, India. rituagrawal@nii.ac.in.

Cell Death & Disease
|May 19, 2026
PubMed
Summary

The BLM helicase is crucial for B cell development by maintaining NF-κB signaling via MALT1. Its loss impairs B cells, but its depletion can treat B cell cancers by inhibiting this pathway.

More Related Videos

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

Related Experiment Videos

Last Updated: May 21, 2026

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity
07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

NF-&#954;B-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells
10:57

NF-κB-dependent Luciferase Activation and Quantification of Gene Expression in Salmonella Infected Tissue Culture Cells

Published on: January 12, 2020

Area of Science:

  • Molecular Biology
  • Immunology
  • Cancer Biology

Background:

  • Bloom Syndrome is caused by BLM helicase loss, leading to genomic instability, cancer, and immunodeficiency.
  • BLM helicase is vital for B cell proliferation and development, maintaining NF-κB signaling pathways.

Purpose of the Study:

  • To investigate the role of BLM helicase in B cell development and NF-κB signaling.
  • To explore the therapeutic potential of targeting the BLM-MALT1-NF-κB axis in B cell malignancies.

Main Methods:

  • Utilized BLM knockout mice to study B cell development.
  • Analyzed NF-κB pathway activation, including RelA nuclear translocation.
  • Investigated BLM's interaction with the MALT1 promoter.
  • Assessed the effects of MALT1 reintroduction and IKKβ activation.
  • Examined BLM depletion and MALT1 inhibition in lymphoma and leukemia models.

Main Results:

  • BLM deficiency impairs B cell development by disrupting NF-κB signaling due to reduced MALT1 transcription.
  • Restoring MALT1 or IKKβ function rescues B cell development in BLM-deficient cells.
  • BLM depletion, similar to MALT1 inhibition, suppresses lymphoma and leukemia progression.
  • Malignant B cells are sensitized to chemotherapy upon BLM or MALT1 inhibition.

Conclusions:

  • The BLM-MALT1-NF-κB axis is essential for normal B cell development.
  • Targeting this axis offers therapeutic potential for B cell malignancies.
  • Maintaining a controlled threshold of BLM expression is critical to prevent oncogenesis.