Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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 (show TLR4 Proteins)-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 (show TNF Proteins).
immune-induced degradation does not require CSN5 (show COPS5 Proteins)
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 (show CD24 Proteins)-miR (show MLXIP Proteins)-124-3p, hsa (show CD24 Proteins)-miR (show MLXIP Proteins)-129-5p and hsa (show CD24 Proteins)-miR (show MLXIP Proteins)-378 induced an increase in both expression and activity of CPT1A (show CPT1A Proteins), CACT and CrAT (show CRAT Proteins) in malignant prostate cells.
The antiport mode of transport, typical of mitochondrial carriers such as CAC (show CA2 Proteins), 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 (show CPT2 Proteins) 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 (show SLC25A25 Proteins)* genes and includes functional information.
Results show Steroid Receptor Coactivator (show SRA1 Proteins)-3 (SRC-3 (show NCOA3 Proteins)) 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 (show PSG1 Proteins) sites in HepG2 cells and only the Sp1 (show PSG1 Proteins) site in HEK293 and SK-N-SH cells have a critical role in the transcriptional regulation of the CAC (show CA2 Proteins) 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 50-flanking region of the Cact gene contains a consensus sequence for ERRalpha (show ESRRA Proteins). This sequence binds ERRa (show ESRRA Proteins) both in vivo and in vitro and is required for the activation of Cact expression by the PGC-1/ERR (show SLC7A1 Proteins) axis
Data show that the upregulation of CACT by PPARalpha (show PPARA Proteins) and PPARdelta (show PPARD Proteins) 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