| 2011 |
CTRP13 is secreted as a disulfide-linked oligomeric protein, and when co-expressed with CTRP10 forms heteromeric complexes via a mechanism that does not involve conserved N-terminal Cys residues. |
Heterologous expression system, co-expression, biochemical characterization of secreted protein |
The Journal of biological chemistry |
Medium |
21378161
|
| 2011 |
CTRP13 (CTRP13/C1QL3) promotes glucose uptake in adipocytes, myotubes, and hepatocytes via activation of the AMPK signaling pathway, as demonstrated using purified recombinant protein. |
In vitro glucose uptake assay with purified recombinant protein in primary adipocytes, myotubes, and hepatocytes; AMPK activation measured |
The Journal of biological chemistry |
High |
21378161
|
| 2011 |
CTRP13 ameliorates lipid-induced insulin resistance in hepatocytes by suppressing SAPK/JNK stress signaling, and reduces hepatocyte glucose output by inhibiting mRNA expression of gluconeogenic enzymes glucose-6-phosphatase and cytosolic phosphoenolpyruvate carboxykinase. |
In vitro hepatocyte assay with purified recombinant CTRP13; mRNA expression analysis of gluconeogenic enzymes |
The Journal of biological chemistry |
High |
21378161
|
| 2013 |
Central (intracerebroventricular) administration of recombinant CTRP13 suppressed food intake and reduced body weight in mice, establishing C1QL3 as an anorexigenic factor in the brain. |
Central administration of recombinant protein in mice; food intake and body weight measured |
PloS one |
Medium |
23638159
|
| 2013 |
CTRP13 and the orexigenic neuropeptide AgRP reciprocally regulate each other's expression in the hypothalamus: central CTRP13 delivery suppressed Agrp expression, while AgRP delivery increased Ctrp13 expression, suggesting a hypothalamic feedback loop. |
Central delivery of recombinant proteins in mice; qPCR measurement of neuropeptide gene expression in hypothalamus |
PloS one |
Medium |
23638159
|
| 2016 |
C1QL3 expression in neurons is activity-dependent and supports excitatory synapse density in cultured neurons; C1QL3-deficient mice have fewer excitatory synapses and exhibit impaired fear memories and other behavioral abnormalities. |
Conditional and constitutive C1ql3 knockout mice; synapse density quantification in cultured neurons and in vivo; behavioral testing including fear memory assays |
Neuron |
High |
27478018
|
| 2016 |
C1QL3 is a secreted neuronal protein that binds to BAI3 (ADGRB3), an adhesion-class GPCR, and C1QL3 expression in basolateral amygdala neurons projecting to the medial prefrontal cortex is required for formation/maintenance of those efferent synapses. |
Circuit-tracing tools, conditional ablation targeted to specific brain regions, synapse density analysis |
Neuron |
High |
27478018
|
| 2017 |
C1QL3 is robustly expressed in the suprachiasmatic nucleus (SCN); C1ql3 knockout mice have reduced density of excitatory synapses in the SCN and exhibit disrupted circadian behavior including less consolidated activity and period lengthening after a phase-delaying light pulse. |
C1ql3 knockout mice; immunohistochemistry for synapse density; circadian behavioral assays |
Journal of biological rhythms |
Medium |
28553739
|
| 2018 |
CTRP13 reduces CD36 protein levels in macrophages through autophagy-lysosome-dependent degradation at the post-transcriptional level, thereby reducing oxidized LDL uptake and foam-cell formation. |
Primary peritoneal macrophages treated with recombinant CTRP13; autophagy-lysosome pathway blocking experiments; CD36 protein and mRNA analysis; foam cell formation assays |
FASEB journal |
Medium |
30222079
|
| 2019 |
CTRP13 preserves endothelial function in diabetes by increasing GTP cyclohydrolase 1 (GCH1) expression and tetrahydrobiopterin (BH4) levels to ameliorate eNOS coupling; mechanistically, CTRP13 rescues high-glucose-induced inhibition of PKA activity, and increased PKA activity enhances phosphorylation of PPARα and its recruitment to the GCH1 promoter, activating GCH1 transcription. |
Ex vivo aortic relaxation assays in diabetic mice; in vitro HUVEC experiments; PKA activity assay; ChIP for PPARα at GCH1 promoter; recombinant CTRP13 treatment |
Diabetes |
Medium |
31676569
|
| 2019 |
CTRP13 attenuates vascular calcification by repressing phosphorylation of tristetraprolin (TTP), thereby activating TTP, which binds the 3'UTR of Runx2 mRNA and accelerates Runx2 mRNA destabilization and degradation in vascular smooth muscle cells. |
In vitro VSMC calcification assay; Runx2 overexpression rescue; TTP binding assay; mRNA stability analysis; recombinant CTRP13 treatment in CRF rat model |
FASEB journal |
Medium |
31145871
|
| 2020 |
CTRP13 protects rat liver sinusoidal endothelial cells from high-glucose-induced injury by activating the CaMKKβ/AMPK pathway, reducing laminin and caveolin-1 expression; inhibition of CaMKKβ or AMPK abolished the protective effects. |
Lentiviral CTRP13 overexpression in rLSECs; CaMKKβ/AMPK inhibitors (STO-609, Compound C); Western blot and qRT-PCR |
Aging |
Medium |
32554851
|
| 2020 |
CTRP13 mitigates abdominal aortic aneurysm formation; mechanistically, CTRP13 stabilizes NAMPT1 protein by reducing its ubiquitination-proteasome-dependent degradation, and NAMPT1 knockdown blocks the beneficial effects of CTRP13 on vascular inflammation and smooth muscle cell apoptosis. |
Two murine AAA models (AngII in ApoE-/- and CaCl2 in C57BL/6J); recombinant CTRP13 infusion; NAMPT1 knockdown; ubiquitination assays |
Molecular therapy |
Medium |
32966772
|
| 2021 |
C1QL3 mediates a novel cell-cell adhesion complex involving ADGRB3 (BAI3) and two neuronal pentraxins, NPTX1 and NPTXR, as identified by an in vivo interactome study; C1ql3, Nptx1, and Nptxr are highly co-expressed in the same excitatory neurons. |
In vivo interactome study (pulldown/co-IP); single-cell RNA-seq data analysis for co-expression |
FASEB journal |
Medium |
33337553
|
| 2021 |
CTRP13 protects cardiomyocytes from hypoxia/reoxygenation injury via the AMPK/Nrf2/ARE signaling pathway; AMPK inhibition reversed CTRP13-mediated Nrf2/ARE activation, and Nrf2 silencing reversed CTRP13's protective effects against oxidative stress and apoptosis. |
H9c2 cell H/R model; CTRP13 overexpression and silencing; AMPK inhibitor (Compound C); Nrf2 siRNA; recombinant CTRP13 in rat I/R model |
Cell transplantation |
Medium |
34338573
|
| 2023 |
Loss of CTRP13 in mice improves systemic metabolism (reduced body weight, improved glucose tolerance, insulin sensitivity, and triglyceride clearance), reduced hepatic glucose output, lower inflammatory profile in visceral fat and liver, and suppressed lipid synthesis with enhanced lipid catabolism gene expression, suggesting CTRP13 is a negative metabolic regulator. |
Ctrp13 knockout mice on chow and high-fat diet; comprehensive metabolic phenotyping; transcriptomic analyses of multiple tissues; mediation analyses with human METSIM cohort data |
Molecular metabolism |
High |
37844630
|
| 2024 |
C1QL3 is required for formation of chronic morphine withdrawal memories in the basolateral amygdala (BLA); C1QL3 colocalizes with BAI3 in the BLA, and downregulation of C1QL3 in the BLA reduces conditioned place aversion scores; C1QL3 modulates ubiquitination-mediated degradation of PSD95, resulting in decreased PSD95 protein levels as a downstream effector. |
Immunofluorescence colocalization of C1QL3 and BAI3; lentiviral downregulation of C1QL3 in BLA; conditioned place aversion behavioral assay; chemogenetic BLA inhibition; ubiquitination/PSD95 protein analysis |
Biochemical and biophysical research communications |
Medium |
38772224
|
| 2024 |
C1ql3 knockout in rats disrupts neuronal integrity (reduced dendritic arbors and spine density), alters microglial activation (increased ramified microglia, decreased hypertrophic microglia, increased amoeboid microglia and Arg-1 expression after LPS), and impairs short working memory with hyperactive behavior. |
CRISPR/Cas9 C1ql3 KO rats; Golgi staining for dendritic morphology; immunohistochemistry for microglia; MRI; behavioral tests (open field, Morris water maze, Y maze) |
Animal models and experimental medicine |
Medium |
38379452
|
| 2024 |
CTRP13 inhibits ferroptosis of endothelial cells via the GCH1/BH4 signaling pathway, upregulating GPX4 and downregulating ACSL4; silencing GCH1 or inhibiting BH4 abolished the protective effects of CTRP13. |
ApoE-/- mice with C1ql3 overexpression AAV; ox-LDL-treated mouse aortic endothelial cells; GCH1 siRNA knockdown; BH4 inhibition; GPX4 and ACSL4 protein detection |
International immunopharmacology |
Medium |
39541845
|
| 2024 |
CTRP13 prevents HUVEC ferroptosis induced by ox-LDL via the AMPK/KLF4 pathway, reducing ROS overproduction and mitochondrial dysfunction; CTRP13 increased p-AMPK/AMPK and decreased KLF4 expression. |
HUVEC ox-LDL model; CTRP13 recombinant protein treatment; Western blot for p-AMPK, KLF4, GPX4, ACSL4; mitochondrial function assays |
Medical science monitor |
Low |
38273650
|
| 2024 |
CTRP13 reduces endothelial cell proliferation via AMPK (specifically alpha-2 AMPK), reduces cell cycle progression, increases p53 phosphorylation and p21 expression, and reduces Rb phosphorylation; these effects depended on alpha-2 AMPK as shown by adenoviral dominant-negative and wild-type AMPK overexpression. |
HUVEC culture; recombinant CTRP13 treatment; adenoviral DN/WT alpha-1/alpha-2 AMPK overexpression; cell cycle analysis; Western blot |
Cells |
Medium |
39120321
|
| 2025 |
Brain-wide light-sheet microscopy using a novel C1ql3-2HA epitope-tagged knock-in mouse revealed an expanded neuroanatomical map of endogenous C1QL3 expression in cortical and subcortical regions and the retina; super-resolution STED microscopy localized C1QL3-2HA to hippocampal mossy fiber synapses positioned between pre- and post-synaptic markers; native PAGE determined the endogenous oligomeric state of C1QL3. |
Epitope-tagged knock-in mouse (C1ql3-2HA); native PAGE for oligomeric state; brain-wide light-sheet microscopy; dual immunohistochemistry; super-resolution STED microscopy |
bioRxivpreprint |
Medium |
41959109
|
| 2025 |
Conditional deletion of C1ql3 from neurons specifically in the prefrontal cortex of adult mice was not sufficient to impair attentional set-shifting behavior, indicating C1ql3's role in cognitive flexibility requires expression in other brain circuits and/or neurodevelopmental processes. |
Conditional C1ql3 deletion in PFC neurons of adult mice; attentional set-shifting behavioral assay |
Neuroscience letters |
Medium |
40541605
|