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Related Concept Videos

M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Inhibition of CDK Activity02:34

Inhibition of CDK Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...
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.

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Related Experiment Video

Updated: Jul 7, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

Mc Cance syndrome.

Saâd Sbihi1, Karima Benbouazza, Najia Hajjaj-Hassouni

  • 1Department of Rheumatology B, El Ayachi Hospital, Rabat-Salé University Centre, 1, rue de plage, 10000 Rabat, Morocco. saadsbihi@yahoo.fr

Clinical Rheumatology
|February 5, 2008
PubMed
Summary

This case report details a 17-year-old boy with vitamin D-resistant rickets (VRR), likely due to a PHEX gene mutation. Treatment focuses on normalizing phosphate levels with calcium and vitamin D supplementation.

Area of Science:

  • Pediatric Endocrinology
  • Medical Genetics
  • Radiology

Background:

  • Vitamin D-resistant rickets (VRR) presents a diagnostic challenge, often linked to genetic anomalies affecting phosphate metabolism.
  • Early identification and management are crucial to prevent long-term skeletal complications.

Observation:

  • A 17-year-old Moroccan male exhibited growth delay and characteristic bone deformities consistent with VRR.
  • Radiographic findings included demineralization, metaphyseal enlargement, and deformities in the thorax, legs, and wrists.
  • Biochemical analysis revealed severe hypophosphatemia, normal phosphaturia, reduced phosphate reabsorption, normal hydroxyvitamin D, and low calciuria.

Findings:

  • Clinical and laboratory data strongly suggested X-linked hypophosphatemia, a condition caused by mutations in the Phosphate regulating gene with Homology to Endopeptidase on the X chromosome (PHEX) gene.

Related Experiment Videos

Last Updated: Jul 7, 2026

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

Published on: April 13, 2015

  • While no family history was reported, genetic studies in parents and siblings would be beneficial for comprehensive diagnosis.

    • Implications:

    • This case highlights the importance of considering genetic causes like PHEX mutations in late-onset VRR.
    • Effective management involves phosphate normalization through calcic and vitamin D supplementation to prevent hypophosphatemic bone disease and secondary hyperparathyroidism.