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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

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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...
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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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...
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Positive regulators allow a cell to advance through cell cycle checkpoints. Negative regulators have an equally important role as they terminate a cell’s progression through the cell cycle—or pause it—until the cell meets specific criteria.
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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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Related Experiment Video

Updated: Dec 10, 2025

Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
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BAP1: Not just a BRCA1-associated protein.

Bryan H Louie1, Razelle Kurzrock1

  • 1Center for Personalized Cancer Therapy, University of California San Diego, Moores Cancer Center, 3855 Health Sciences Dr, La Jolla, CA 92037, USA.

Cancer Treatment Reviews
|September 3, 2020
PubMed
Summary

BRCA1-Associated Protein 1 (BAP1) is a tumor suppressor regulating key cellular processes. Mutations in BAP1 drive aggressive cancers and hereditary cancer syndromes, with emerging targeted therapies showing promise.

Keywords:
BAP1CancerImmunotherapyTargeted therapy

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Related Experiment Videos

Last Updated: Dec 10, 2025

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • BRCA1-Associated Protein 1 (BAP1) functions as a tumor suppressor, regulating DNA repair, cell cycle, and chromatin modification.
  • BAP1 mutations are linked to aggressive cancers like uveal melanoma, mesothelioma, and renal cell carcinoma.
  • Germline BAP1 mutations define a hereditary cancer predisposition syndrome with increased early-onset cancer risk.

Purpose of the Study:

  • To provide a concise and current overview of the BAP1 gene in cancer.
  • To survey BAP1's functional roles, cancer-related characteristics, and clinical manifestations.
  • To highlight established and emerging therapeutic strategies for BAP1-mutated cancers.

Main Methods:

  • Review of existing literature on BAP1 function, mutations, and clinical implications.
  • Analysis of therapeutic approaches targeting BAP1's role in DNA repair, chromatin modification, and immune response.
  • Synthesis of information on BAP1-associated cancers and their susceptibility to targeted therapies and immunotherapies.

Main Results:

  • BAP1 mutations are associated with aggressive tumor types and hereditary cancer syndromes.
  • Targeted therapies including HDAC inhibitors, EZH2 inhibitors, PARP inhibitors, and platinum agents show potential.
  • BAP1 alterations may confer immunogenic phenotypes, suggesting susceptibility to cancer immunotherapies.

Conclusions:

  • BAP1 is a critical tumor suppressor gene with significant implications in various cancers.
  • Targeted therapies and immunotherapies represent promising avenues for treating BAP1-mutated cancers.
  • Further research into BAP1's functions and therapeutic targeting is warranted.