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Related Concept Videos

Transcription Attenuation in Prokaryotes02:42

Transcription Attenuation in Prokaryotes

Transcriptional attenuation occurs when RNA transcription is prematurely terminated due to the formation of a terminator mRNA hairpin structure.  Bacteria use these hairpins to regulate the transcription process and control the synthesis of several amino acids including histidine, lysine, threonine, and phenylalanine. Transcription attenuation takes place in the non-coding regions of mRNA.
There are several different mechanisms used to attenuate transcription. In ribosome mediated...
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a rapamycin-insensitive companion...
Repressible Operon: trp Operon01:21

Repressible Operon: trp Operon

The trp operon in Escherichia coli exemplifies a repressible operon. It regulates the synthesis of tryptophan through repressor-mediated transcriptional control and attenuation. This dual regulatory mechanism ensures tryptophan biosynthesis occurs only when needed, conserving cellular resources.Structure of the trp OperonThe trp operon consists of five structural genes (trpE, trpD, trpC, trpB, and trpA) that encode enzymes for tryptophan biosynthesis. These genes are transcribed as a single...
TGF - β Signaling Pathway01:16

TGF - β Signaling Pathway

The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors are of three kinds RI, RII, and RIII. The RI...
The Unfolded Protein Response01:37

The Unfolded Protein Response

The ER is the hub of protein synthesis in a cell. It has robust systems to quality control protein folding and also for degradation of terminally misfolded proteins. Under normal conditions, a small proportion of misfolded proteins that cannot be salvaged need to be transported to the cytoplasm by the ER-associated degradation or ERAD pathways. However, if the ERAD cannot handle the misfolded proteins, the cell activates the unfolded protein response or UPR to adjust the protein folding...
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...

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Related Experiment Video

Updated: May 10, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Regulatory feedback loop between TP73 and TRIM32.

L Gonzalez-Cano1, A-L Hillje, S Fuertes-Alvarez

  • 1Instituto de Biomedicina (IBIOMED), Department of Molecular Biology, Universidad de León, Campus de Vegazana, León 24071, Spain.

Cell Death & Disease
|July 6, 2013
PubMed
Summary
This summary is machine-generated.

The p73 transcription factor and TRIM32 form a novel feedback loop regulating neural development and cancer. This interaction impacts p73 activity, offering potential therapeutic targets for central nervous system disorders and oncogenesis.

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Analysis of Termination of Transcription Using BrUTP-strand-specific Transcription Run-on (TRO) Approach
12:12

Analysis of Termination of Transcription Using BrUTP-strand-specific Transcription Run-on (TRO) Approach

Published on: March 12, 2017

Related Experiment Videos

Last Updated: May 10, 2026

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis
08:34

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Analysis of Termination of Transcription Using BrUTP-strand-specific Transcription Run-on (TRO) Approach
12:12

Analysis of Termination of Transcription Using BrUTP-strand-specific Transcription Run-on (TRO) Approach

Published on: March 12, 2017

Area of Science:

  • Molecular Biology
  • Neuroscience
  • Oncology

Background:

  • The p73 transcription factor, a member of the p53 family, plays crucial roles in neurogenesis, embryonic development, and differentiation.
  • p73 activity is regulated by multiple mechanisms, including transcriptional and post-translational modifications.

Purpose of the Study:

  • To identify and characterize a novel regulatory loop involving TAp73 and the E3 ubiquitin ligase TRIM32.
  • To elucidate the functional implications of this p73-TRIM32 interaction in neural progenitor cells and its relevance to oncogenesis.

Main Methods:

  • Investigated the transcriptional regulation of TRIM32 by p73, including TAp73 activation and DNp73 repression.
  • Examined the physical interaction between TRIM32 and TAp73.
  • Assessed the effect of TRIM32 on TAp73 ubiquitination, degradation, and transcriptional activity.

Main Results:

  • TRIM32 is identified as a direct transcriptional target of p73 in neural progenitor cells.
  • TRIM32 physically interacts with TAp73, promoting its ubiquitination and degradation.
  • This interaction impairs TAp73-dependent transcriptional activity, establishing a feedback loop.

Conclusions:

  • A novel feedback regulatory loop between p73 and TRIM32 is identified, impacting p73 activity.
  • This loop has significant implications for central nervous system development and oncogenesis.
  • The p73-TRIM32 axis represents a potential therapeutic target for related diseases.