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Related Concept Videos

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...
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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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Convergence and divergence, and cross-talk between signaling pathways
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Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
Mitogens and the Cell Cycle02:38

Mitogens and the Cell Cycle

Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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The Ras Gene

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Related Experiment Video

Updated: May 13, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

PELP1 oncogenic functions involve CARM1 regulation.

Monica Mann1, Valerie Cortez, Ratna Vadlamudi

  • 1Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX 78229-3900, USA.

Carcinogenesis
|March 15, 2013
PubMed
Summary
This summary is machine-generated.

PELP1 recognizes histone arginine methylation and interacts with CARM1, enhancing estrogen receptor alpha (ERα) activity in breast cancer. Inhibiting PELP1 and CARM1 reduces tumor growth by altering epigenetic modifications.

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Last Updated: May 13, 2026

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants
07:38

Intracellular Phosphoflow Cytometry of Acute Myeloid Leukemia Patient-Derived Xenotransplants

Published on: June 6, 2025

Area of Science:

  • Molecular Biology
  • Epigenetics
  • Oncology

Background:

  • Estrogen receptor alpha (ERα) signaling is crucial in breast cancer.
  • Epigenetic modifications regulate ERα target genes.
  • PELP1 is an ERα coregulator and proto-oncogene overexpressed in breast cancer.

Purpose of the Study:

  • To elucidate the molecular mechanisms of epigenetic deregulation in breast cancer progression.
  • To investigate the role of PELP1 in recognizing and mediating epigenetic changes.
  • To explore the therapeutic potential of targeting PELP1 and associated epigenetic modifiers.

Main Methods:

  • Histone peptide array to profile PELP1's epigenetic interactome.
  • Co-immunoprecipitation to study PELP1-CARM1 interaction.
  • Chromatin immunoprecipitation (ChIP) assays to assess histone methylation at ERα target promoters.
  • In vivo studies using PELP1 knockdown models.
  • Immunohistochemical analysis of human breast tumor tissues.

Main Results:

  • PELP1 recognizes dimethylated histone arginine and lysine residues.
  • PELP1 functionally interacts with CARM1, synergistically enhancing ERα transactivation.
  • PELP1 modulates histone H3 arginine methylation at ERα target gene promoters.
  • CARM1 inhibition or knockdown reduces PELP1's oncogenic functions and in vivo tumorigenesis.
  • Co-overexpression of PELP1 and CARM1 observed in ERα-positive breast tumors.

Conclusions:

  • PELP1 acts as a reader of histone arginine methylation modifications.
  • Deregulation of PELP1 promotes breast cancer proliferation through epigenetic alterations.
  • Targeting PELP1 and arginine methyltransferases offers a potential therapeutic strategy for breast cancer.