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Related Concept Videos

Internal Receptors01:31

Internal Receptors

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Many cellular signals are hydrophilic and therefore cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind to internal, or intracellular, receptors that reside within the cell. Many mammalian steroid hormones use this mechanism of cell signaling, as does nitric oxide (NO) gas.
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Receptor-mediated Endocytosis01:39

Receptor-mediated Endocytosis

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Overview
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Enzyme-linked Receptors01:00

Enzyme-linked Receptors

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Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
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G-protein Coupled Receptors01:21

G-protein Coupled Receptors

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G-protein coupled receptors are ligand binding receptors that indirectly affect changes in the cell. The actual receptor is a single polypeptide that transverses the cell membrane seven times creating intracellular and extracellular loops. The extracellular loops create a ligand specific pocket which binds to neurotransmitters or hormones. The intracellular loops holds onto the G-protein.
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Types of Receptors: Internal Receptors01:07

Types of Receptors: Internal Receptors

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Many cellular signals are hydrophilic and cannot pass through the plasma membrane. However, small or hydrophobic signaling molecules can cross the hydrophobic core of the plasma membrane and bind intracellular receptors that reside within the cell cytoplasm or nucleus. Many mammalian steroid hormones and nitric oxide (NO) gas use this cell signaling mechanism.
Similar to membrane-bound receptors, the binding of a ligand to the intracellular receptor of causes a conformational change in the...
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Types of Receptors: Cell Surface Receptors01:28

Types of Receptors: Cell Surface Receptors

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Cell-surface receptors, also known as transmembrane receptors, are cell surface, membrane-anchored (integral) proteins that bind to external ligand molecules. This type of receptor spans the plasma membrane and performs signal transduction, converting an extracellular signal into an intracellular signal. Ligands that interact with cell-surface receptors do not have to enter the cell that they affect. Cell-surface receptors are also called cell-specific proteins or markers because they are...
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Live Imaging of Chemokine Receptors in Zebrafish Neutrophils During Wound Responses
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The chemokine receptor CX

Erfan Ahadzadeh1, Alva Rosendahl1, Daniel Czesla1

  • 1III. Department of Medicine, University Hospital Hamburg-Eppendorf , Hamburg , Germany.

American Journal of Physiology. Renal Physiology
|September 13, 2018
PubMed
Summary

The fractalkine receptor CX3CR1 plays a protective role in hypertensive kidney injury by modulating inflammatory cell infiltration. CX3CR1 deficiency worsens renal damage, suggesting its inhibition should be avoided in hypertension.

Keywords:
CXCR1albuminuriaangiotensin IIcardiac damagepodocyterenal damage

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Area of Science:

  • Immunology
  • Nephrology
  • Cardiovascular Research

Background:

  • The role of the fractalkine receptor CX3CR1 in hypertension-induced organ damage remains unclear.
  • CX3CR1 is expressed on various immune cells, including dendritic cells, macrophages, NK cells, and T cells.

Purpose of the Study:

  • To investigate the function of CX3CR1 in hypertensive renal and cardiac injury.
  • To determine the impact of CX3CR1 deficiency on inflammatory cell infiltration in the kidney during hypertension.

Main Methods:

  • Utilized CX3CR1GFP/+ reporter mice to assess CX3CR1 expression on renal leukocytes.
  • Employed an aggravated hypertension model involving unilateral nephrectomy, angiotensin II infusion, and a high-salt diet in wild-type and CX3CR1-deficient mice.
  • Analyzed renal injury markers, including albuminuria, glomerular damage, podocyte density, and cardiac damage indicators.

Main Results:

  • CX3CR1 deficiency altered renal immune cell composition, reducing dendritic cells and increasing macrophages and neutrophils.
  • CX3CR1-deficient mice showed exacerbated albuminuria, glomerular injury, and reduced podocyte density despite similar blood pressure.
  • Cardiac damage was comparable between wild-type and CX3CR1-deficient mice.

Conclusions:

  • CX3CR1 exerts protective effects in hypertensive renal injury by regulating inflammatory cell infiltration.
  • Targeting CX3CR1 may be detrimental in hypertension, potentially promoting renal injury.