Vitamin D, Calbindin, and calcium signaling: Unraveling the Alzheimer's connection.

Acharya, M; Singh, N; Gupta, G; Tambuwala, MM; Aljabali, AAA; Chellappan, DK; Dua, K; Goyal, R

Vitamin D, Calbindin, and calcium signaling: Unraveling the Alzheimer's connection.

Acharya, M Singh, N Gupta, G Tambuwala, MM Aljabali, AAA Chellappan, DK Dua, K

Goyal, R

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Publisher:: Elsevier
Publication Type:: Journal Article
Citation:: Cell Signal, 2024, pp. 111043
Issue Date:: 2024-01-09

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Field	Value	Language
dc.contributor.author	Acharya, M
dc.contributor.author	Singh, N
dc.contributor.author	Gupta, G
dc.contributor.author	Tambuwala, MM
dc.contributor.author	Aljabali, AAA
dc.contributor.author	Chellappan, DK
dc.contributor.author	Dua, K https://orcid.org/0000-0002-7507-1159
dc.contributor.author	Goyal, R
dc.date.accessioned	2024-02-01T00:13:28Z
dc.date.available	2024-01-08
dc.date.available	2024-02-01T00:13:28Z
dc.date.issued	2024-01-09
dc.identifier.citation	Cell Signal, 2024, pp. 111043
dc.identifier.issn	0898-6568
dc.identifier.issn	1873-3913
dc.identifier.uri	http://hdl.handle.net/10453/175166
dc.description.abstract	Calcium is a ubiquitous second messenger that is indispensable in regulating neurotransmission and memory formation. A precise intracellular calcium level is achieved through the concerted action of calcium channels, and calcium exerts its effect by binding to an array of calcium-binding proteins, including calmodulin (CAM), calcium-calmodulin complex-dependent protein kinase-II (CAMK-II), calbindin (CAL), and calcineurin (CAN). Calbindin orchestrates a plethora of signaling events that regulate synaptic transmission and depolarizing signals. Vitamin D, an endogenous fat-soluble metabolite, is synthesized in the skin upon exposure to ultraviolet B radiation. It modulates calcium signaling by increasing the expression of the calcium-sensing receptor (CaSR), stimulating phospholipase C activity, and regulating the expression of calcium channels such as TRPV6. Vitamin D also modulates the activity of calcium-binding proteins, including CAM and calbindin, and increases their expression. Calbindin, a high-affinity calcium-binding protein, is involved in calcium buffering and transport in neurons. It has been shown to inhibit apoptosis and caspase-3 activity stimulated by presenilin 1 and 2 in AD. Whereas CAM, another calcium-binding protein, is implicated in regulating neurotransmitter release and memory formation by phosphorylating CAN, CAMK-II, and other calcium-regulated proteins. CAMK-II and CAN regulate actin-induced spine shape changes, which are further modulated by CAM. Low levels of both calbindin and vitamin D are attributed to the pathology of Alzheimer's disease. Further research on vitamin D via calbindin-CAMK-II signaling may provide newer insights, revealing novel therapeutic targets and strategies for treatment.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	Elsevier
dc.relation.ispartof	Cell Signal
dc.relation.isbasedon	10.1016/j.cellsig.2024.111043
dc.rights	info:eu-repo/semantics/closedAccess
dc.subject	0601 Biochemistry and Cell Biology, 1116 Medical Physiology
dc.subject.classification	Biochemistry & Molecular Biology
dc.subject.classification	3101 Biochemistry and cell biology
dc.title	Vitamin D, Calbindin, and calcium signaling: Unraveling the Alzheimer's connection.
dc.type	Journal Article
utslib.location.activity	England
utslib.for	0601 Biochemistry and Cell Biology
utslib.for	1116 Medical Physiology
pubs.organisational-group	University of Technology Sydney
pubs.organisational-group	University of Technology Sydney/Faculty of Health
utslib.copyright.status	closed_access	*
dc.date.updated	2024-02-01T00:12:29Z
pubs.publication-status	Published online

Abstract:

Calcium is a ubiquitous second messenger that is indispensable in regulating neurotransmission and memory formation. A precise intracellular calcium level is achieved through the concerted action of calcium channels, and calcium exerts its effect by binding to an array of calcium-binding proteins, including calmodulin (CAM), calcium-calmodulin complex-dependent protein kinase-II (CAMK-II), calbindin (CAL), and calcineurin (CAN). Calbindin orchestrates a plethora of signaling events that regulate synaptic transmission and depolarizing signals. Vitamin D, an endogenous fat-soluble metabolite, is synthesized in the skin upon exposure to ultraviolet B radiation. It modulates calcium signaling by increasing the expression of the calcium-sensing receptor (CaSR), stimulating phospholipase C activity, and regulating the expression of calcium channels such as TRPV6. Vitamin D also modulates the activity of calcium-binding proteins, including CAM and calbindin, and increases their expression. Calbindin, a high-affinity calcium-binding protein, is involved in calcium buffering and transport in neurons. It has been shown to inhibit apoptosis and caspase-3 activity stimulated by presenilin 1 and 2 in AD. Whereas CAM, another calcium-binding protein, is implicated in regulating neurotransmitter release and memory formation by phosphorylating CAN, CAMK-II, and other calcium-regulated proteins. CAMK-II and CAN regulate actin-induced spine shape changes, which are further modulated by CAM. Low levels of both calbindin and vitamin D are attributed to the pathology of Alzheimer's disease. Further research on vitamin D via calbindin-CAMK-II signaling may provide newer insights, revealing novel therapeutic targets and strategies for treatment.

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http://hdl.handle.net/10453/175166