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Related Concept Videos

The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

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...
Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase01:27

Pharmacogenetics of Phase II Enzymes: N-acetyltransferase, Thiopurine S-methyltransferase, UDP-glucuronosyltransferase

Phase II biotransformation reactions are essential for detoxifying and eliminating xenobiotics, including many pharmaceutical compounds. These reactions typically involve conjugation, the covalent attachment of polar endogenous groups such as glucuronic acid, sulfate, methyl, or acetyl moieties to functional groups introduced during Phase I metabolism. The resulting conjugates are more water-soluble, enabling efficient renal or biliary excretion.The major classes of Phase II enzymes include...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
Cytotoxic T Cells-mediated Immune Response01:27

Cytotoxic T Cells-mediated Immune Response

Cytotoxic T cells are a vital component of the immune system. They have the remarkable ability to identify and target antigens on infected or abnormal cells. These antigens often originate from intracellular pathogens such as viruses or abnormal proteins cancer cells produce.
Immunological surveillance is the ability of immune cells to monitor and eliminate infected cells with intracellular pathogens, neoplastically transformed cells, and cells with non-self antigens. Cytotoxic T cells and NK...

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Related Experiment Video

Updated: Jun 30, 2026

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

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Published on: May 10, 2022

SLC2A9-Mediated Uric Acid Homeostasis Modulates Apoptosis in TNBC.

Peng Chen1, Jiapeng Xu1, Yulong Liang1

  • 1Department of Thyroid, Breast and Hernia Surgery, Third Hospital of Hebei Medical University, Shijiazhuang, Hebei, People's Republic of China.

Breast Cancer (Dove Medical Press)
|June 29, 2026
PubMed
Summary

The solute carrier family 2, member 9 (SLC2A9) gene is downregulated in triple-negative breast cancer (TNBC). SLC2A9 regulates uric acid (UA) metabolism, inhibiting TNBC cell growth and metastasis.

Keywords:
SLC2A9TNBCapoptosisurate transportersuric acid metabolism

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Last Updated: Jun 30, 2026

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates
09:47

Evaluation of Substrate Ubiquitylation by E3 Ubiquitin-ligase in Mammalian Cell Lysates

Published on: May 10, 2022

Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method
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Determination of the Relative Potency of an Anti-TNF Monoclonal Antibody (mAb) by Neutralizing TNF Using an In Vitro Bioanalytical Method

Published on: September 16, 2017

Area of Science:

  • Oncology
  • Metabolic pathways
  • Molecular biology

Background:

  • Triple-negative breast cancer (TNBC) exhibits aggressive behavior and limited therapeutic options.
  • Uric acid (UA) metabolism is increasingly recognized for its role in cancer progression.
  • The specific role of SLC2A9 in TNBC and its connection to UA metabolism require further investigation.

Purpose of the Study:

  • To elucidate the biological function of SLC2A9 in TNBC.
  • To determine the molecular mechanisms by which SLC2A9 influences TNBC cell behavior through UA metabolism.

Main Methods:

  • Bioinformatics analysis identified intersecting genes in TNBC and UA metabolism.
  • In vitro studies established SLC2A9 overexpression and knockdown models in TNBC cell lines.
  • Cellular assays assessed proliferation, apoptosis, migration, and invasion; Western blot analyzed protein expression.

Main Results:

  • SLC2A9 expression was significantly reduced in TNBC tissues and cell lines.
  • SLC2A9 overexpression suppressed TNBC cell proliferation, migration, and invasion, while enhancing apoptosis.
  • SLC2A9 modulated intracellular and extracellular UA levels, impacting apoptosis-related and UA metabolism proteins.

Conclusions:

  • SLC2A9 plays a critical role in regulating the malignant phenotype of TNBC by altering UA homeostasis.
  • SLC2A9's anticancer effects are linked to its UA transport function.
  • SLC2A9 presents potential as a prognostic biomarker and a novel metabolic therapeutic target for TNBC.