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Related Concept Videos

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...
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...
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...
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...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
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.

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Mapping the Structure-Function Relationships of Disordered Oncogenic Transcription Factors Using Transcriptomic Analysis
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Published on: June 27, 2020

TAF6delta orchestrates an apoptotic transcriptome profile and interacts functionally with p53.

Emmanuelle Wilhelm1, Mara Kornete, Brice Targat

  • 1RNA Group, Département de Microbiologie et d'Infectiologie, Faculté de Médecine et Sciences de la Santé, Université de Sherbrooke, Sherbrooke, Québec J1H 5N4, Canada.

BMC Molecular Biology
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PubMed
Summary

The TAF6delta protein isoform drives an apoptotic gene expression program, influencing cell death decisions. This pathway interacts with the p53 protein, highlighting a novel connection in cellular regulation.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • TFIID is a crucial transcription factor complex regulating RNA polymerase II (Pol II) transcription.
  • TAF6, a core TFIID subunit, has isoforms TAF6alpha and TAF6delta.
  • TAF6delta is a pro-apoptotic isoform with a distinct histone fold domain, impacting cell fate.

Purpose of the Study:

  • To investigate the global transcriptome effects of endogenous TAF6delta expression.
  • To understand the relationship between TAF6delta and other transcription regulators like TAF9 and p53.

Main Methods:

  • Analysis of global gene expression patterns influenced by TAF6delta.
  • Comparison of TAF6delta-driven gene expression with TAF9/TAF9b depletion data.
  • Testing for physical and functional interactions between TAF6delta and p53.

Main Results:

  • TAF6delta expression orchestrates a transcriptome enriched with apoptotic genes.
  • TAF6delta-mediated gene expression patterns show similarities to, but are distinct from, TAF9/TAF9b depletion effects.
  • A physical and functional interaction between TAF6delta and p53 was demonstrated.

Conclusions:

  • A TAF6delta-driven apoptotic gene expression program was defined.
  • Crosstalk between the p53 and TAF6delta pathways was established.