How Do You Spell INBRED CFTR MOUSE?

Pronunciation: [ˈɪnbɹɛd sˌiːˌɛftˌiːˈɑː mˈa͡ʊs] (IPA)

The correct spelling of "Inbred CFTR Mouse" can be a bit tricky due to its complex phonetics. The word "Inbred" is pronounced as "ɪnˈbrɛd" while "CFTR" is spelled out as "/ˌsiːefˈtiːɑːr/". Lastly, "Mouse" is pronounced as "maʊs". The term refers to mice used in biomedical research with the cystic fibrosis gene knocked out. This genetic modification causes the mouse to express symptoms very similar to those of human cystic fibrosis patients.

INBRED CFTR MOUSE Meaning and Definition

  1. The term "Inbred CFTR Mouse" refers to a specific strain of laboratory mice that has been selectively bred to carry a genetic mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR gene is responsible for producing a protein involved in regulating the movement of chloride ions across cell membranes. Mutations in this gene can lead to the development of cystic fibrosis, a genetic disorder characterized by the production of thick, sticky mucus that affects various organs such as the lungs, pancreas, and liver.

    Inbred CFTR mice are called "inbred" because they come from a relatively closed population in which mating occurs between close relatives for multiple generations. Inbreeding helps to achieve a high degree of genetic uniformity within the population, making these mice nearly genetically identical to one another. This allows researchers to conduct experiments with genetically uniform cohorts, minimizing the confounding effects of genetic variation on study results.

    These mice are highly valuable tools in biomedical research because they recapitulate many of the features observed in human cystic fibrosis patients. The Inbred CFTR mouse model provides a means for investigating the underlying mechanisms of cystic fibrosis, studying disease progression, evaluating potential therapeutic interventions, and testing the efficacy of new drugs. By using Inbred CFTR mice, researchers can gain insights into the pathophysiology of cystic fibrosis and work towards developing more effective treatments for this debilitating disease.

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