| 1999 |
CACNG4 was identified as a novel calcium channel gamma subunit gene located on chromosome 17, discovered through low-stringency genomic sequence analysis of regions syntenic to CACNG1 and CACNG2, establishing it as a member of the voltage-dependent Ca2+ channel gamma subunit gene family generated by tandem and chromosome duplication. |
Genomic sequence analysis, gene family identification by synteny |
Genome research |
Medium |
10613843
|
| 2005 |
CACNG4 has seizure-suppressing activity in the corticothalamic circuit; homozygous Cacng4 knockout mice appear phenotypically normal, but combining the Cacng4 null allele with stargazer (Cacng2) mutant alleles exacerbates or induces absence seizures, demonstrating overlapping in vivo functions between CACNG4 and CACNG2 and restricting CACNG4 expression to the thalamus within the corticothalamic loop. |
Targeted gene disruption (knockout mouse), genetic epistasis (double mutant with Cacng2 alleles), seizure phenotype analysis, expression analysis |
Proceedings of the National Academy of Sciences of the United States of America |
High |
15677329
|
| 2002 |
Chick CACNG4 is expressed in differentiating neurons and myoblasts during early development, with expression timing correlating precisely with the onset of neuronal differentiation in cranial and dorsal root ganglia and in the myotome, suggesting a role in modulating calcium channels during cellular differentiation. |
In situ hybridization, developmental expression analysis in chick embryo |
Developmental biology |
Medium |
11884034
|
| 2020 |
CACNG4 promotes breast cancer metastasis by closing the channel pore to inhibit calcium influx, thereby altering calcium signaling through key survival and metastatic pathway genes including AKT2, HDAC3, RASA1, and PKCζ; CACNG4 overexpression alters cell motility in vitro, induces malignant transformation in 3D culture, and increases lung-specific metastasis in vivo. |
In vitro 2D and 3D assays, intracellular calcium influx assays, chick-CAM model, mouse metastasis model, gain/loss-of-function experiments, calcium channel blocker treatment |
EBioMedicine |
High |
32062352
|
| 2022 |
CACNG4 (CaVγ4) is required for pancreatic beta-cell maintenance of its differentiated state; Cacng4 knockout mice exhibit impaired fasting glucose and impaired glucose tolerance with blunted glucose-stimulated insulin secretion. CaVγ4 deletion reduces expression of the transcription factor MafA (on mRNA and protein levels), and CaMKII mediates the regulatory pathway linking CaVγ4 to MafA, as confirmed in mouse islets, human donor islets, and INS-1 832/13 cells. |
Cacng4 knockout mouse (in vivo glucose tolerance and insulin secretion assays), gene expression analysis (mRNA and protein), CaMKII pathway investigation, human islet RNA-seq validation, INS-1 cell line experiments |
Biomedicines |
High |
35453520
|
| 2025 |
CUEDC1 directly modulates CACNG4 to enhance PI3K/AKT pathway activation, thereby facilitating glycolysis (via GLUT1 upregulation) and tumor growth in ER-positive breast cancer; this CUEDC1/CACNG4/PI3K axis was identified by RNA-seq, ChIP, and dual-luciferase reporter assays, with MAZ transcription factor upregulating CUEDC1 transcription. |
Dual-luciferase reporter assay, RNA-seq, chromatin immunoprecipitation (ChIP), metabolic glycolysis assays, mouse xenograft model, western blotting, qRT-PCR |
Cellular & molecular biology letters |
Medium |
41315933
|
| 2023 |
CACNG4 is upregulated in cancer stem cells (CSCs) of hepatocellular carcinoma (HCC); pharmacological inhibition of CACNG4 with amlodipine at low concentrations preferentially reduced CSC viability, markedly decreased tumorsphere formation, and reduced the ALDH1A1-high cell population, indicating a role for CACNG4 in maintaining the CSC state. |
FACS sorting of ALDH1A1-high cells, microarray gene expression analysis, tumorsphere formation assay, cytotoxicity assay with amlodipine (CACNG4 inhibitor) |
Anticancer research |
Medium |
37909988
|
| 2026 |
In Graves' orbitopathy, exosomal miR-221-5p suppresses CACNG4/AMPK signaling in orbital fibroblasts, driving proinflammatory, profibrotic, and adipogenic phenotypes; partial rescue of these pathogenic phenotypes by miR-221-5p inhibition confirmed the functional centrality of CACNG4 suppression in this pathway. |
Exosome isolation and characterization, primary human orbital fibroblast functional assays, miR-221-5p inhibition, in vivo mouse GO model, single-cell RNA sequencing, histopathology, MRI |
Experimental eye research |
Medium |
42203012
|