Abstract
Identification of potential pathological biomarkers has proved to be essential for understanding complex and fatal diseases, such as cancer and neurodegenerative diseases. Ion channels are involved in the maintenance of cellular homeostasis. Moreover, loss of function and aberrant expression of ion channels and transporters have been linked to various cancers, and to neurodegeneration. The Chloride Intracellular Channel 1 (CLIC1), CLIC1 is a metamorphic protein belonging to a partially unexplored protein superfamily, the CLICs. In homeostatic conditions, CLIC1 protein is expressed in cells as a cytosolic monomer. In pathological states, CLIC1 is specifically expressed as transmembrane chloride channel. In the following review, we trace the involvement of CLIC1 protein functions in physiological and in pathological conditions and assess its functionally active isoform as a potential target for future therapeutic strategies.
Highlights
Identification of potential pathological biomarkers has proved to be essential for understanding complex and fatal diseases, such as cancer and neurodegenerative diseases
Chloride Intracellular Channel 1 (CLIC1) protein has been described in several papers associated to different pathological states, from neurodegenerative processes to solid tumors
CLIC1 is better described icant probe to change among groups to date, it cannot be sufficient to predict neurodegenerative progression throughout Alzheimer’s Disease
Summary
In 2009, Qiu et al published that, the deletion of Clic gene in mouse did not cause embryonic lethality, mice developed a mild bleeding disorder with a higher platelet number and longer bleeding times compared to control group [21] The authors propose this mechanism to be related to platelet P2Y12 receptor. P2Y12R requires free thiol groups (Cys and Cys270) to elicit its function In this picture, CLIC1 would participate in the control of redox environments which, in turn, may induce platelet activation [21]. Relatively abundant levels of CLIC proteins have been found in human bronchial epithelial cells primary cultures It has been shown CLIC1 to be able to modulate cAMP-induced chloride currents [22]. Cl- conductance, proposing the possibility to potentiate CLIC1 functional activity as a possible therapeutic strategy in conditions of impaired chloride homeostasis as cystic fibrosis [22]
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