CALN1

Last update 23 Jan 2025

Basic Info

Synonyms

CABP8, Calcium-binding protein 8, CALN1

+ [3]

Introduction

Negatively regulates Golgi-to-plasma membrane trafficking by interacting with PI4KB and inhibiting its activity. May play a role in the physiology of neurons and is potentially important in memory and learning.

100 Clinical Results associated with CALN1

100 Translational Medicine associated with CALN1

0 Patents (Medical) associated with CALN1

Literatures (Medical) associated with CALN1

01 Mar 2024·The Journals of Gerontology: Series AQ1 · MEDICINE

Genetic Pleiotropy Between Pulmonary Function and Age-Related Traits: The Long Life Family Study

Q1 · MEDICINE

Article

Author: Santanasto, Adam J ; Province, Michael A ; Nygaard, Marianne ; Wang, Lihua ; Wojczynski, Mary K ; Daw, E Warwick ; Anema, Jason A ; Feitosa, Mary F

AbstractBackgroundPulmonary function (PF) progressively declines with aging. Forced expiratory volume in the first second (FEV1) and forced vital capacity (FVC) are predictors of morbidity of pulmonary and cardiovascular diseases and all-cause mortality. In addition, reduced PF is associated with elevated chronic low-grade systemic inflammation, glucose metabolism, body fatness, and low muscle strength. It may suggest pleiotropic genetic effects between PF with these age-related factors.MethodsWe evaluated whether FEV1 and FVC share common pleiotropic genetic effects with interleukin-6, high-sensitivity C-reactive protein, body mass index, muscle (grip) strength, plasma glucose, and glycosylated hemoglobin in 3 888 individuals (age range: 26–106). We employed sex-combined and sex-specific correlated meta-analyses to test whether combining genome-wide association p values from 2 or more traits enhances the ability to detect variants sharing effects on these correlated traits.ResultsWe identified 32 loci for PF, including 29 novel pleiotropic loci associated with PF and (i) body fatness (CYP2U1/SGMS2), (ii) glucose metabolism (CBWD1/DOCK8 and MMUT/CENPQ), (iii) inflammatory markers (GLRA3/HPGD, TRIM9, CALN1, CTNNB1/ZNF621, GATA5/SLCO4A1/NTSR1, and NPVF/C7orf31/CYCS), and (iv) muscle strength (MAL2, AC008825.1/LINC02103, AL136418.1).ConclusionsThe identified genes/loci for PF and age-related traits suggest their underlying shared genetic effects, which can explain part of their phenotypic correlations. Integration of gene expression and genomic annotation data shows enrichment of our genetic variants in lung, blood, adipose, pancreas, and muscles, among others. Our findings highlight the critical roles of identified gene/locus in systemic inflammation, glucose metabolism, strength performance, PF, and pulmonary disease, which are involved in accelerated biological aging.

01 Dec 2023·Cell Reports

Apolipoproteins L1 and L3 control mitochondrial membrane dynamics

Article

Author: Cornet d'Elzius, Alexandre ; Heo, Paul ; Lecordier, Laurence ; Pincet, Frédéric ; Hennig, Dorle ; Pérez-Morga, David ; Pays, Etienne ; Graversen, Jonas H ; Skytthe, Maria Kløjgaard

Apolipoproteins L1 and L3 (APOLs) are associated at the Golgi with the membrane fission factors phosphatidylinositol 4-kinase-IIIB (PI4KB) and non-muscular myosin 2A. Either APOL1 C-terminal truncation (APOL1Δ) or APOL3 deletion (APOL3-KO [knockout]) reduces PI4KB activity and triggers actomyosin reorganization. We report that APOL3, but not APOL1, controls PI4KB activity through interaction with PI4KB and neuronal calcium sensor-1 or calneuron-1. Both APOLs are present in Golgi-derived autophagy-related protein 9A vesicles, which are involved in PI4KB trafficking. Like APOL3-KO, APOL1Δ induces PI4KB dissociation from APOL3, linked to reduction of mitophagy flux and production of mitochondrial reactive oxygen species. APOL1 and APOL3, respectively, can interact with the mitophagy receptor prohibitin-2 and the mitophagosome membrane fusion factor vesicle-associated membrane protein-8 (VAMP8). While APOL1 conditions PI4KB and APOL3 involvement in mitochondrion fission and mitophagy, APOL3-VAMP8 interaction promotes fusion between mitophagosomal and endolysosomal membranes. We propose that APOL3 controls mitochondrial membrane dynamics through interactions with the fission factor PI4KB and the fusion factor VAMP8.

01 Mar 2023·Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology

[Bioinformatic analysis of the clinical significance of calneuron 1 (CALN1) in glioma and its correlation with immune cell infiltration].

Article

Author: Zhang, Han ; Zhang, Jinhao ; Wang, Tao

Objective To analyze the clinical significance of calneuron 1 (CALN1) expression in glioma and its role in tumor immune cell infiltration by bioinformatics. Methods The expression of CALN1 gene in glioma in the Cancer Genome Atlas (TCGA) database was analyzed by Xiantao Academic Online. Kaplan-Meier survival analysis was used to evaluate its prognostic value, and receiver operating characteristic (ROC) curve was employed to evaluate its clinical diagnostic efficiency. Gene Set Enrichment Analysis (GSEA) was adopted to identify the potential mechanism of CALN1 in glioma. The relationship between CALN1 mRNA and glioma immune cell infiltration was discussed. Results The expression of CALN1 decreased significantly in glioma, and its expression level was negatively correlated with tumor grade. Compared with the control group, the expression level of CALN1 in isocitrate dehydrogenase mutant and 1p/19q co-deletion gliomas increased significantly. Glioma patients with low expression of CALN1 had poor prognosis and significantly reduced overall survival, disease specific survival and progression-free interval. ROC curve analysis showed that CALN1 expression level had good clinical diagnostic value. The results of GSEA gene enrichment suggested that the expression level of CALN1 was negatively correlated with mitosis and neutrophil degranulation. Immunoinfiltration analysis showed that T helper type 2 (Th2) cells, macrophages and neutrophils were significantly increased in the group with low expression of CALN1. Conclusion The expression level of CALN1 in glioma is positively correlated with the prognosis. The abnormal decrease of CALN1 expression may lead to the invasion of tumor-promoting immune cells. CALN1 can be used as a potential prognostic marker and therapeutic target for glioma.

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