Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
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Drug
Enzyme
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Query: UMLS:C0007758 (
cerebellar ataxia
)
3,609
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The mechanism of store-operated Ca
2+
entry (SOCE) brings extracellular Ca
2+
into cells after depletion of intracellular Ca
2+
stores. Regulation of Ca
2+
homeostasis by SOCE helps control various intracellular signaling functions in both non-excitable and excitable cells. Whereas essential components of the SOCE pathway are well characterized, molecular mechanisms underlying regulation of this pathway need investigation. A class of proteins recently demonstrated as regulating SOCE is septins. These are filament-forming GTPases that assemble into higher order structures. One of their most studied cellular functions is as a molecular scaffold that creates diffusion barriers in membranes for a variety of cellular processes. Septins regulate SOCE in mammalian non-excitable cells and in
Drosophila
neurons. However, the molecular mechanism of SOCE-regulation by septins and the contribution of different subgroups of septins to SOCE-regulation remain to be understood. The regulation of SOCE is relevant in multiple cellular contexts as well as in diseases, such as the
Severe Combined Immunodeficiency
(
SCID
) syndrome and neurodegenerative syndromes like Alzheimer's, Spino-
Cerebellar Ataxias
and Parkinson's. Moreover,
Drosophila
neurons, where loss of SOCE leads to flight deficits, are a possible cellular template for understanding the molecular basis of neuronal deficits associated with loss of either the Inositol-1,4,5-trisphosphate receptor (IP
3
R1), a key activator of neuronal SOCE or the Endoplasmic reticulum resident Ca
2+
sensor STIM1 (Stromal Interaction Molecule) in mouse. This perspective summarizes our current understanding of septins as regulators of SOCE and discusses the implications for mammalian neuronal function.
...
PMID:Regulation of Store-Operated Ca
2+
Entry by Septins. 2801 1