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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
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The primary cilium, made up of microtubules, acts as antennae on the cell surfaces for relaying external stimuli into the cells. These fine hair-like structures are present, generally one per cell. These are non-motile cilia in a 9+0 microtubules arrangement, where the central pair of microtubules are absent. The primary cilia arise from the basal body embedded in the cell membrane. Intraflagellar transport (IFT) carries requisite proteins from the cytoplasm to the cilium because the primary...
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Complex microtubule structures are present in resting cells and in dividing cells. In resting cells, they are responsible for maintaining the cellular architecture, tracks for intracellular transport, positioning of organelles, assembly of cilia and flagella. They mediate the bipolar spindle assembly for chromosomal segregation and positioning of the cell division plate in dividing cells. The formation of microtubule complex structures depends on the cell type, cell stage, and cell function.
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Microtubule function and architecture are regulated by an array of specialized proteins called microtubule-associated proteins or MAPs. These proteins are widespread across different organisms and have conserved protein motifs, like the multi-TOG domain for tubulin binding found in the CLASP family of MAPs. Some MAPs are lineage-specific based on their conserved domains. Their functions depend upon the cytoskeletal architecture and cell type they are located within. In-plant cells, a specific...
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The TGF-β signaling pathway regulates cell growth, differentiation, adhesion, motility, and development. TGF-β ligands that induce TGF-β signaling are synthesized in their latent form. Several proteases or cell surface receptors such as integrins act upon the latent form, releasing the active ligand. There are three types of mammalian TGF-βs: (TGF-β1, TGF-β2, and TGF-β3) that bind as homodimers or heterodimers to TGF-β receptors. The TGF-β receptors...
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Label-Free Non-Linear Optics for the Study of Tubulin-Dependent Defects in Central Myelin
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Tuberous Sclerosis Complex.

Monica P Islam1

  • 1Nationwide Children's Hospital, The Ohio State University College of Medicine, 700 Children's Drive, Columbus, OH.

Seminars in Pediatric Neurology
|April 24, 2021
PubMed
Summary

Tuberous Sclerosis Complex (TSC) is a rare neurocutaneous disorder affecting cell growth, leading to tumors in various organs. Early diagnosis by pediatric neurologists is crucial for managing this genetic condition.

Area of Science:

  • Genetics
  • Neurology
  • Oncology

Background:

  • Tuberous Sclerosis Complex (TSC) is a rare neurocutaneous disorder affecting approximately 1 in 6000-10,000 individuals.
  • It is characterized by abnormal cell proliferation and migration, leading to hamartomas in the skin, brain, heart, kidneys, lungs, and eyes.
  • TSC can present with variable severity across a lifetime and between generations.

Purpose of the Study:

  • To provide an overview of Tuberous Sclerosis Complex (TSC), including its pathophysiology, clinical manifestations, and diagnostic challenges.
  • To highlight the role of genetic identification in understanding TSC and developing targeted therapies.

Main Methods:

  • Review of existing literature on Tuberous Sclerosis Complex (TSC).
  • Discussion of diagnostic approaches, particularly in pediatric neurology.

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  • Exploration of the genetic basis and molecular targets related to TSC.

    • Main Results:

    • TSC is a complex genetic disorder with multi-organ involvement.
    • Early diagnosis, often through infantile spasms or epilepsy, is critical.
    • Identification of the mechanistic target of rapamycin (mTOR) pathway has advanced understanding.

    Conclusions:

    • Tuberous Sclerosis Complex (TSC) requires increased recognition due to its underdiagnosis.
    • Understanding the genetic underpinnings of TSC has opened avenues for targeted therapeutic interventions.
    • Continued research into TSC pathophysiology is essential for improving patient outcomes.