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It has been shown that Dorsal repressed Ush expression levels to promote hemocytes differentiation, whereas Cactus maintained Ush levels to block differentiation.
CalpA targets free Cactus, which is incorporated into and modulates Toll-responsive complexes in the embryo and immune system.
Dorsal and Cactus maybe necessary for normal function and maintenance of the neuromuscular system. These proteins can respond to synaptic activity.
Cactus acts as an inhibitor of the Rel-transcription factors Dorsal and Dif.
immune-induced degradation does not require CSN5
Dpp signals increase Cactus levels through Calpain A inhibition, thereby interfering with Dorsal activation
we report the first 2 cases of CACTD identified from the mainland China. Apart from a founder mutation c.199-10T>G, we have identified a novel c.1A>G mutation. Patients with Carnitine-acylcarnitine translocase deficiency with a genotype of c.199-10T>G mutation usually presents with a severe clinical phenotype. Early recognition and appropriate treatment is crucial in this highly lethal disorder.
We provide evidence that the downregulation of hsa-miR-124-3p, hsa-miR-129-5p and hsa-miR-378 induced an increase in both expression and activity of CPT1A, CACT and CrAT in malignant prostate cells.
The antiport mode of transport, typical of mitochondrial carriers such as CAC, results from coupling of uniport reactions in opposite directions mediated by specific amino acid residues.
C.576G>A, c.106-2a>t and c.516T>C are novel CACT gene mutations.
CPT2 and CACT are crucial for mitochondrial acylcarnitine formation and export to the extracellular fluids in mitochondrial fatty acid beta-oxidation disorders.
Compares and contrasts all the known human SLC25A* genes and includes functional information.
Results show Steroid Receptor Coactivator-3 (SRC-3) plays a central role in long chain fatty acid metabolism by directly regulating carnitine/acyl-carnitine translocase (CACT) gene expression.
These results show that FOXA and Sp1 sites in HepG2 cells and only the Sp1 site in HEK293 and SK-N-SH cells have a critical role in the transcriptional regulation of the CAC proximal promoter.
A deficiency in CACT was treated with a carnitine diet and administration of medium-chain triglycerides.
The clinical, biochemical, & molecular features of 6 CACT-deficient patients from Italy, Spain, & North America who had significant clinical heterogeneity are reported. 5 novel & 3 previously reported mutations were found.
The modulation of CACT expression has consequences for CPT 1 activity, while the biologic effects of acetyl-carnitine are not associated with a generic supply of energy compounds but to the anaplerotic property of the molecule.
Report the outcome of two siblings with CACT deficiency.
Functional analysis of mutations of residues Pro278 and Ala279 in A. nidulans, together with kinetic data in reconstituted liposomes, suggest a predominant structural role for these amino acids.
PPARalpha regulates the expression of human SLC25A20 via the peroxisome proliferator responsive element.
the 50-flanking region of the Cact gene contains a consensus sequence for ERRalpha. This sequence binds ERRa both in vivo and in vitro and is required for the activation of Cact expression by the PGC-1/ERR axis
Data show that the upregulation of CACT by PPARalpha and PPARdelta may increase the import of acylcarnitine into the mitochondrial matrix during fasting.
This gene product is one of several closely related mitochondrial-membrane carrier proteins that shuttle substrates between cytosol and the intramitochondrial matrix space. This protein mediates the transport of acylcarnitines into mitochondrial matrix for their oxidation by the mitochondrial fatty acid-oxidation pathway. Mutations in this gene are associated with carnitine-acylcarnitine translocase deficiency, which can cause a variety of pathological conditions such as hypoglycemia, cardiac arrest, hepatomegaly, hepatic dysfunction and muscle weakness, and is usually lethal in new born and infants.
, NF-kappa-B inhibitor cactus
, solute carrier family 25 (carnitine/acylcarnitine translocase), member 20
, carnitine/acylcarnitine translocase
, mitochondrial carnitine/acylcarnitine carrier protein
, solute carrier family 25 (mitochondrial carnitine/acylcarnitine translocase), member 20
, solute carrier family 25 member 20
, protein kinase, cAMP-dependent, regulatory, type II, alpha
, carnitine/acylcarnitine carrier protein
, mitochondrial carnitine-acylcarnitine translocase