Related Experiment Video

Updated: Aug 13, 2026

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
10:21

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells

Published on: February 21, 2018

Modulation of Fos-mediated AP-1 transcription by the promyelocytic leukemia protein

S Vallian1, J A Gäken, E B Gingold

  • 1Division of Laboratory Medicine, The University of Texas M.D. Anderson Cancer Center, Houston 77030, USA.

Oncogene
|July 22, 1998
PubMed

Insights

Promyelocytic leukemia (PML) protein interacts with Fos to enhance AP-1 transcriptional activity. This interaction, disrupted in acute promyelocytic leukemia (APL), may explain PML's growth suppressor function.

Area of Science:

  • Molecular Biology
  • Oncology
  • Cell Biology

Background:

  • Promyelocytic leukemia (PML) protein's growth suppressor function is impaired in acute promyelocytic leukemia (APL) due to t(15;17) translocation.
  • Sequence homology between PML and Fos suggests a potential role for PML in AP-1 activity.

Purpose of the Study:

  • To investigate the functional interaction between PML and Fos.
  • To determine PML's role in AP-1-mediated transcriptional activity.

Main Methods:

  • Cotransfection assays with GAL4/Fos and PML constructs.
  • Deletion analysis of Fos and PML domains.
  • Immunoprecipitation and electrophoretic mobility shift assays (EMSA).

Main Results:

  • PML cooperates with Fos to stimulate AP-1 transcriptional activity.
  • Specific domains of PML (RING-finger, B1, nuclear localization) and Fos (C-terminal) are crucial for this cooperation.
  • PML is associated with the AP-1 complex.
  • PMLRARalpha enhances GAL4/Fos activity, which is abrogated by retinoic acid.

Conclusions:

  • PML is involved in the AP-1 complex and modulates Fos-mediated transcription.
  • This modulation may contribute to PML's growth suppressor function, offering insights into APL pathogenesis.

More Related Videos

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence10:09

Methods for Evaluating the Role of c-Fos and Dusp1 in Oncogene Dependence

Published on: January 7, 2019

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Related Concept Videos

RNA Polymerase II Accessory Proteins02:36

RNA Polymerase II Accessory Proteins

Proteins that regulate transcription can do so either via direct contact with RNA Polymerase or through indirect interactions facilitated by adaptors, mediators, histone-modifying proteins, and nucleosome remodelers. Direct interactions to activate transcription is seen in bacteria as well as in some eukaryotic genes. In these cases, upstream activation sequences are adjacent to the promoters, and the activator proteins interact directly with the transcriptional machinery. For example, in...
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...
Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

Nuclear protein sorting regulates nucleus composition and gene expression, crucial for determining the fate of a eukaryotic cell. Hence, the entry and exit of molecules across the nuclear envelope is a tightly controlled process. Nuclear protein sorting can be inhibited by one of the following ways: 1) masking cargo signal sequences, 2) modifying the nuclear receptor's affinity for cargo, 3) controlling the nuclear pore size, 4) retaining the cargo during its transit to the cytosol or the...
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...
MAPK Signaling Cascades01:07

MAPK Signaling Cascades

Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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...