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Regulation of Nuclear Protein Sorting01:45

Regulation of Nuclear Protein Sorting

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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...
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Lipid Catabolism01:25

Lipid Catabolism

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Triglycerides serve as crucial long-term energy storage molecules in microorganisms, providing a dense source of metabolic energy. Their breakdown is mediated by lipases, which hydrolyze triglycerides into glycerol and free fatty acids. Each of these components follows distinct metabolic pathways, ultimately contributing to ATP synthesis and cellular energy homeostasis.Glycerol MetabolismGlycerol, released from triglyceride hydrolysis, is phosphorylated by glycerol kinase to form...
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Overview of Lipid Metabolism01:24

Overview of Lipid Metabolism

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Lipid metabolism is a crucial process in the human body that involves the synthesis and degradation of lipids. This process is essential for energy production, cell membrane formation, and hormone production, among other functions.
Lipolysis: The Breakdown of Lipids:
Lipolysis is the process of breaking down lipids, particularly triglycerides, into glycerol and fatty acids. This process typically occurs in the adipose tissue and is triggered by various hormones, including glucagon and...
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Regulation of Metabolism01:19

Regulation of Metabolism

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Cellular needs and conditions vary from cell to cell and change within individual cells over time. For example, the required enzymes and energetic demands of stomach cells are different from those of fat storage cells, skin cells, blood cells, and nerve cells. Furthermore, a digestive cell works much harder to process and break down nutrients during the time that closely follows a meal compared with many hours after a meal. As these cellular demands and conditions vary, so do the amounts and...
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Master Transcription Regulators02:23

Master Transcription Regulators

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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...
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Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

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Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
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Related Experiment Video

Updated: Jan 11, 2026

Analysis of SCAP N-glycosylation and Trafficking in Human Cells
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Analysis of SCAP N-glycosylation and Trafficking in Human Cells

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The Functional Interaction Between PRDM16 and the SREBP Pathway Controls Lipid Metabolism.

Hafiz Majid Mahmood1, Maria Teresa Bengoechea-Alonso1, Dana E Al-Ansari2

  • 1College of Health and Life Sciences, Hamad Bin Khalifa University, Doha P.O. Box 34110, Qatar.

International Journal of Molecular Sciences
|November 13, 2025
PubMed
Summary
This summary is machine-generated.

PRDI-BF1 and RIZ homology domain containing 16 (PRDM16) inhibits sterol regulatory element-binding protein 1 and 2 (SREBP1/2)-dependent lipid metabolism. PRDM16 inactivation enhances SREBP1/2 activity, increasing lipid synthesis and adipogenesis, impacting metabolic disease.

Keywords:
BATPRDM16SREBPWATadipogenesischolesteroldiabetesinsulin signalinglipid metabolism

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Related Experiment Videos

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Investigation of Beige Fat Biology and Metabolism Using the CRISPR SunTag-p65-HSF1 Activation System
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Area of Science:

  • Biochemistry
  • Molecular Biology
  • Metabolic Research

Background:

  • Dysregulated lipid metabolism is a key factor in cardiovascular disease, obesity, and type 2 diabetes.
  • Sterol regulatory element-binding protein 1 and 2 (SREBP1/2) are critical transcription factors regulating cholesterol and fatty acid synthesis.
  • PRDI-BF1 and RIZ homology domain containing 16 (PRDM16) is known for regulating brown adipose tissue (BAT) and inhibiting white adipogenesis.

Purpose of the Study:

  • To investigate the functional interactions between SREBP1/2 and PRDM16 in lipid metabolism.
  • To determine PRDM16's role in regulating SREBP1/2 transcriptional activity.
  • To explore the implications of PRDM16's influence on lipid metabolism in adipose tissue and metabolic disease.

Main Methods:

  • Co-immunoprecipitation assays to assess protein interactions.
  • Quantitative PCR and Western blotting to measure gene and protein expression.
  • Cell culture experiments using preadipocytes and adipose-derived stem cells, including knockdown models.

Main Results:

  • PRDM16 directly interacts with the nuclear forms of SREBP1/2, inhibiting their transcriptional activity.
  • PRDM16 inactivation significantly upregulates SREBP1/2 target genes involved in fatty acid and cholesterol synthesis.
  • PRDM16 deficiency increases LDL receptor expression and LDL particle uptake, leading to neutral lipid accumulation.
  • PRDM16 inactivation in adipocytes promotes the expression of adipogenic markers.

Conclusions:

  • PRDM16 acts as a novel inhibitor of SREBP1/2-mediated lipid metabolism.
  • PRDM16 plays a crucial role in regulating lipid homeostasis within adipose tissue.
  • Targeting PRDM16 may offer therapeutic strategies for metabolic diseases associated with dysregulated lipid metabolism.