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Lumber defects, which can affect both the appearance and structural integrity of wood, include a variety of growth and manufacturing flaws. Growth defects such as knots and knotholes occur where branches were once attached to the tree trunk, with knotholes forming when these knots fall out. Other natural defects include decay and insect damage, which compromise the wood's strength and durability.
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Hormones—or any molecule that binds to a receptor, known as a ligand—that are lipid-insoluble (water-soluble) are not able to diffuse across the cell membrane. In order to be able to affect a cell without entering it, these hormones bind to receptors on the cell membrane. When a first messenger, a hormone, binds to a receptor, a signal cascade is set off, causing second messengers, proteins inside the cell, to become activated, resulting in downstream effects.
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Updated: Feb 7, 2026

Dissection of Midgut and Salivary Glands from Ae. aegypti Mosquitoes
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Calcium signaling defects underlying salivary gland dysfunction.

Indu Ambudkar1

  • 1Secretory Physiology Section, Molecular Physiology and Therapeutics Branch, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD, USA.

Biochimica Et Biophysica Acta. Molecular Cell Research
|July 15, 2018
PubMed
Summary

Salivary gland fluid secretion relies on calcium signaling. Defects in calcium pathways, particularly Store-Operated Calcium Entry (SOCE), cause dry mouth (xerostomia) in Sjögren

Keywords:
Ca2+ signalingInositol trisphosphate receptorIrradiationPrimary Sjögren's syndromeReactive oxygen speciesSalivary gland dysfunctionStore-operated Ca2+ entry

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Area of Science:

  • Physiology
  • Molecular Biology
  • Cell Biology

Background:

  • Saliva is crucial for oral health, and its secretion is regulated by intracellular calcium ([Ca2+]i).
  • Xerostomia (dry mouth) results from impaired salivary secretion, leading to oral health complications.
  • Store-Operated Calcium Entry (SOCE) is essential for the [Ca2+]i signals that trigger salivary fluid secretion.

Purpose of the Study:

  • To discuss recent studies identifying defects in calcium signaling mechanisms.
  • To explore the role of SOCE, Orai1, TRPC1, STIM1, and STIM2 in salivary gland function.
  • To understand the molecular basis of salivary dysfunction in radiation treatment and Sjögren's syndrome.

Main Methods:

  • Review of recent studies on calcium signaling in salivary glands.
  • Focus on the molecular components of the SOCE pathway (Orai1, TRPC1, STIM1, STIM2).
  • Analysis of how these mechanisms are affected in radiation-induced xerostomia and Sjögren's syndrome.

Main Results:

  • Depletion of endoplasmic reticulum (ER) Ca2+ stores activates SOCE via STIM proteins interacting with Orai1 and TRPC1 channels.
  • STIM2 may fine-tune cellular responses to agonist stimulation.
  • Defects in these critical Ca2+ signaling pathways are implicated in salivary gland dysfunction.

Conclusions:

  • Understanding calcium signaling defects is key to addressing xerostomia.
  • Dysfunctional SOCE contributes to salivary gland impairment in conditions like Sjögren's syndrome and after radiation therapy.
  • Further research into these mechanisms could lead to therapeutic interventions.