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Related Concept Videos

Positive Regulator Molecules02:39

Positive Regulator Molecules

Mitotic cell division results in daughter cells that exactly resemble the parent cell. However, errors in the DNA replication or distribution of genetic material may lead to genetic mutations that may be passed down to every new cell formed from the resulting abnormal cell. Propagation of such mutant cells is restricted through checkpoint mechanisms present at different stages of the cell cycle. These checkpoints involve regulator molecules that either promote or demote cell cycle events.
Positive Regulator Molecules01:45

Positive Regulator Molecules

To consistently produce healthy cells, the cell cycle—the process that generates daughter cells—must be precisely regulated.
S-Cdk Initiates DNA Replication02:38

S-Cdk Initiates DNA Replication

The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
Two states at the origin of replication
In eukaryotes, the initiation of replication occurs at many sites on the chromosomes, called the origins of replication.
cAMP-dependent Protein Kinase Pathways01:25

cAMP-dependent Protein Kinase Pathways

Cyclic Adenosine Monophosphate (cAMP) is an essential second messenger that activates protein kinase A (PKA) and regulates various biological processes. A single epinephrine molecule binds to GPCR and activates several heterotrimeric G proteins, each stimulating multiple adenylyl cyclase, amplifying the signal, and synthesizing large numbers of cAMP molecules. Small changes in cAMP concentration affect PKA activity. The binding of four cAMP molecules induces a conformational change in PKA,...
Inhibitors of Viral Protein Synthesis01:30

Inhibitors of Viral Protein Synthesis

Protein synthesis is indispensable for viral replication, as viruses lack the cellular machinery required for this process and must hijack the host's translational apparatus. In response, host cells deploy a critical innate immune defense involving interferons, specialized cytokines that play a central role in inhibiting viral propagation.Upon viral detection, infected cells release interferons that bind to receptors on adjacent uninfected cells, activating the JAK-STAT signaling pathway and...
Hepatitis01:25

Hepatitis

Hepatitis is an inflammatory condition of the liver most commonly caused by hepatotropic viruses (A–E), though non-infectious causes such as alcohol and drugs also exist.Hepatitis AHepatitis A virus (HAV) is a non-enveloped RNA virus of the Picornaviridae family. It is primarily transmitted via the fecal-oral route, typically through ingestion of contaminated food or water. After ingestion, HAV enters the bloodstream through the oropharynx or intestinal epithelium and reaches the liver. The...

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Related Experiment Video

Updated: Jun 18, 2026

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis
10:23

Lipid Droplet Isolation for Quantitative Mass Spectrometry Analysis

Published on: April 17, 2017

Multiple cyclophilins involved in different cellular pathways mediate HCV replication.

L Alex Gaither1, Jason Borawski, Leah J Anderson

  • 1Novartis Institutes of Biomedical Research, Cambridge, MA 02139, USA.

Virology
|November 26, 2009
PubMed
Summary
This summary is machine-generated.

Hepatitis C drug NIM811 inhibits viral replication by targeting multiple cyclophilins and cellular pathways, particularly protein trafficking. Further research is needed to fully understand its mechanism of action.

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Last Updated: Jun 18, 2026

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Area of Science:

  • Virology
  • Molecular Biology
  • Drug Discovery

Background:

  • Cyclophilin inhibitors like DEBIO-025, SCY635, and NIM811 are in clinical trials for hepatitis C.
  • The precise mechanism of action for these cyclophilin inhibitors is not fully elucidated.
  • Human cells express at least 16 cyclophilins involved in various cellular functions.

Purpose of the Study:

  • To identify specific cyclophilins crucial for hepatitis C virus (HCV) replication.
  • To elucidate the mechanism of action of NIM811 in inhibiting HCV.
  • To investigate the cellular pathways affected by NIM811.

Main Methods:

  • Large-scale siRNA screening to identify essential cyclophilins.
  • Chemoproteomic assays using cyclophilin-binding compounds.
  • mRNA profiling of cells containing HCV replicons.

Main Results:

  • Confirmed the role of cyclophilin A in HCV replication.
  • Identified additional cyclophilin-containing pathways involved in HCV.
  • NIM811 demonstrated inhibition of multiple cyclophilins and pathways.
  • Protein trafficking was identified as the most significantly impacted pathway by NIM811.

Conclusions:

  • NIM811 exerts its antiviral effect by inhibiting multiple cyclophilins.
  • The inhibition of protein trafficking is a key mechanism by which NIM811 reduces HCV replication.
  • These findings contribute to understanding cyclophilin inhibitor mechanisms for hepatitis C therapy.