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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
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Co-activators and Co-repressors02:04

Co-activators and Co-repressors

Gene transcription is regulated by the synergistic action of several proteins that form a complex at a gene regulatory site. This is observed in eukaryotes, where the regulation of gene expression is a complex process. Regulatory proteins in eukaryotes can broadly be classified into two types – regulators that bind directly to specific DNA sequences and co-regulators that associate with regulatory proteins but cannot directly bind to the DNA. These co-regulators are further divided into...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
NF-kB-dependent Signaling Pathway02:26

NF-kB-dependent Signaling Pathway

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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...
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...

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BAG-1 interacts with the p50-p50 homodimeric NF-κB complex: implications for colorectal carcinogenesis.

S L Southern1, T J Collard, B C Urban

  • 1School of Cellular & Molecular Medicine, University of Bristol, Bristol, UK.

Oncogene
|October 4, 2011
PubMed
Summary

The anti-apoptotic protein BAG-1 forms a novel complex with p50-p50 NF-κB, selectively regulating gene expression in colorectal cancer cells. This interaction impacts epidermal growth factor receptor (EGFR) and COX-2, offering potential new strategies for CRC prevention and treatment.

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Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Signaling

Background:

  • Aberrant tumor cell survival is a key challenge in colorectal cancer (CRC).
  • The anti-apoptotic protein BAG-1 is upregulated in CRC and influences cell survival via NF-κB.
  • Understanding BAG-1's precise role in CRC pathogenesis is crucial for developing new therapies.

Purpose of the Study:

  • To identify novel mechanisms by which BAG-1 promotes colorectal cancer cell survival.
  • To investigate the interaction between BAG-1 and NF-κB signaling pathways.
  • To determine the functional relevance of the BAG-1-NF-κB complex in regulating target genes like EGFR and COX-2.

Main Methods:

  • Identification of a novel complex between BAG-1 and p50-p50 NF-κB homodimers.
  • Detection of the BAG-1-p50 complex at regulatory regions of EGFR and COX-2 genes.
  • Utilizing small interfering RNA (siRNA) to suppress BAG-1 expression in CRC cells.
  • Employing NF-κB1 (p105/p50) knock-out mouse embryonic fibroblasts to assess p50 dependency.
  • Measuring ligand-activated EGFR phosphorylation in CRC cells.

Main Results:

  • A novel complex between BAG-1 and p50-p50 NF-κB homodimers was identified, indicating BAG-1's role in an atypical NF-κB pathway.
  • The BAG-1-p50 complex was found at the regulatory sequences of the epidermal growth factor receptor (EGFR) and COX-2 (PTGS2) genes.
  • Suppression of BAG-1 increased EGFR and decreased COX-2 expression in CRC cells.
  • p50 expression was necessary for BAG-1 to suppress EGFR expression, and BAG-1 inhibition enhanced EGFR activation.
  • BAG-1 acts as a selective regulator of p50-p50 NF-κB responsive genes in colorectal tumor cells.

Conclusions:

  • BAG-1 interacts with p50-p50 NF-κB complexes, modulating gene expression in colorectal cancer.
  • This BAG-1-p50 interaction selectively regulates key genes like EGFR and COX-2, contributing to tumor cell survival.
  • Understanding the BAG-1-p50 NF-κB complex offers potential therapeutic targets for colorectal cancer prevention and treatment.