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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...
Mismatch Repair01:20

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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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).
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mTOR Signaling and Cancer Progression03:03

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.
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Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
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Related Experiment Video

Updated: Jul 13, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
11:02

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development

Published on: October 30, 2013

Evolution of the human MUC1 oncoprotein.

Sekhar Duraisamy1, Turner Kufe, Selvi Ramasamy

  • 1Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.

International Journal of Oncology
|August 3, 2007
PubMed
Summary

The transmembrane mucin 1 (MUC1) oncogenic function originated from secreted mucins. MUC1 subunits evolved from MUC5B, with the cytoplasmic domain diversifying to gain transforming abilities.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Evolutionary Biology

Background:

  • The mucin (MUC) family includes secreted and membrane-bound forms.
  • Transmembrane mucin 1 (MUC1) is overexpressed in various human carcinomas and hematologic malignancies.
  • MUC1 subunits (MUC1-N and MUC1-C) arise from autocleavage within the SEA domain.

Purpose of the Study:

  • To investigate the evolutionary origin of the MUC1 cytoplasmic domain (MUC1-CD) and its associated transforming sequences.
  • To determine the ancestral relationship between MUC1 and other mucin family members.

Main Methods:

  • Comparative sequence analysis of MUC1 with other mucins.
  • Phylogenetic analysis to trace evolutionary pathways.

Main Results:

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Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins
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Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins

Published on: June 14, 2016

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Last Updated: Jul 13, 2026

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development
11:02

Induction of Invasive Transitional Cell Bladder Carcinoma in Immune Intact Human MUC1 Transgenic Mice: A Model for Immunotherapy Development

Published on: October 30, 2013

Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins
09:24

Mucin Agarose Gel Electrophoresis: Western Blotting for High-molecular-weight Glycoproteins

Published on: June 14, 2016

  • MUC1-CD sequences evolved from repeat regions within the secreted mucin MUC5B.
  • Sequences upstream of the MUC1 SEA domain also originated from MUC5B.
  • MUC1 subunits evolved from secreted gel-forming mucins, with MUC1-CD gaining oncogenic function through diversification.

Conclusions:

  • MUC1 evolved from secreted mucins, specifically MUC5B.
  • The oncogenic potential of MUC1-CD is a result of evolutionary diversification after its origin from MUC5B.
  • Understanding MUC1 evolution provides insights into cancer development.