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Literature summary for 2.7.1.138 extracted from
- Down-regulation of ceramide kinase via proteasome and lysosome pathways in PC12 cells by serum withdrawal its protection by nerve growth factor and role in exocytosis (2020), Biochim. Biophys. Acta, 1867, 118714 .
Cloned(Commentary)
| Cloned (Comment) | Organism |
|---|---|
| recombinant expression of HA-tagged enzyme CerK in PC-12 cells, A-549cells, and HEK-293 T cells, quantitative real-time PCR analysis of CerK mRNA | Homo sapiens |
Protein Variants
| Protein Variants | Comment | Organism |
|---|---|---|
| additional information | knockdown of CerK is performed with shRNA to silence CerK (shCerK, target sequence GTT (TATCGAGTCAAGAAAT)). Establishment of a stable CerK-knockdown cell line (shCerK) and a HA-tagged CerK expressing cell line using a retroviral vector. Serum withdrawal causes ubiquitination of HA-tagged CerK protein and downregulates both HA-tagged CerK protein and ceramide 1-phosphate formation within 6 h, and these downregulations are abolished by co-treatments with NGF or proteasome inhibitors such as MG132 and clasto-lactacystin. Treatment with the proteasome inhibitors increases HA-tagged CerK in puncture structures, possibly endosomes and/or vesicles, in cells. Treatment with the lysosome inhibitors reduces serum withdrawal-induced downregulation of HA-tagged CerK protein but not ceramide 1-phosphate formation. When knockdown or overexpression of CerK is performed, Ca2+-induced release of [3H] noradrenaline is reduced or enhanced, respectively, but neurite extension is not modified. There is a positive correlation between noradrenaline release and formation of ceramide 1-phosphate and/or HA-tagged CerK levels in NGF- and clasto-lactacystin-treated cells | Homo sapiens |
Inhibitors
| Inhibitors | Comment | Organism | Structure |
|---|---|---|---|
| N-[2-(benzoylamino)-6-benzothiazolyl]-tricyclo[3.3.1.13,7] decane-1-carboxamide | NVP-231, a potent inhibitor of CerK | Homo sapiens |
Localization
| Localization | Comment | Organism | GeneOntology No. | Textmining |
|---|---|---|---|---|
| neurite | - |
Homo sapiens | - |
- |
| synaptic vesicle | - |
Homo sapiens | 8021 | - |
Metals/Ions
| Metals/Ions | Comment | Organism | Structure |
|---|---|---|---|
| Mg2+ | required | Homo sapiens |  |
Natural Substrates/ Products (Substrates)
| Natural Substrates | Organism | Comment (Nat. Sub.) | Natural Products | Comment (Nat. Pro.) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + ceramide | Homo sapiens | - |
ADP + ceramide 1-phosphate | - |
? | |
Organism
| Organism | UniProt | Comment | Textmining |
|---|---|---|---|
| Homo sapiens | Q8TCT0 | - |
- |
Posttranslational Modification
| Posttranslational Modification | Comment | Organism |
|---|---|---|
| phosphoprotein | activity of CerK is regulated by post-translational modifications including phosphorylation | Homo sapiens |
| ubiquitination | levels of CerK are downregulated by the ubiquitin/proteasome and lysosome pathways and the former pathway-sensitive pool of CerK is suggested to be linked with exocytosis in PC12 cells | Homo sapiens |
Source Tissue
| Source Tissue | Comment | Organism | Textmining |
|---|---|---|---|
| brain | - |
Homo sapiens | - |
| additional information | in nerve growth factor (NGF)-treated cells, HA-tagged CerK is mainly localized in punctuate structures, possibly endosomes and/or vesicles, in the cytoplasm in both the bottom and nucleus phases, and HA-tagged CerK exists in the extended neurites observed in the bottom phase | Homo sapiens | - |
| neuron | - |
Homo sapiens | - |
Substrates and Products (Substrate)
| Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
|---|---|---|---|---|---|---|
| ATP + ceramide | - |
Homo sapiens | ADP + ceramide 1-phosphate | - |
? | |
| additional information | activity of CerK in cells is measured by the formation of NBD-C1P from a substrate NBD-ceramide | Homo sapiens | ? | - |
- |
|
Synonyms
| Synonyms | Comment | Organism |
|---|---|---|
| CERK | - |
Homo sapiens |
Temperature Optimum [°C]
| Temperature Optimum [°C] | Temperature Optimum Maximum [°C] | Comment | Organism |
|---|---|---|---|
| 37 | - |
assay at | Homo sapiens |
pH Optimum
| pH Optimum Minimum | pH Optimum Maximum | Comment | Organism |
|---|---|---|---|
| 7.4 | - |
assay at | Homo sapiens |
Cofactor
| Cofactor | Comment | Organism | Structure |
|---|---|---|---|
| ATP | - |
Homo sapiens | |
General Information
| General Information | Comment | Organism |
|---|---|---|
| malfunction | knockdown of CerK and overexpression of HA-tagged CerK down- and upregulated the formation of ceramide-1-phosphate (C1P), respectively. When knockdown or overexpression of CerK is performed, Ca2+-induced release of [3H] noradrenaline is reduced or enhanced, respectively, but neurite extension is not modified. A limited change in cellular sphingolipid levels by knockdown of CerK. The levels of ceramide, sphingomyelin, and monohexosylceramide, including their total levels and levels of their subspecies with irrespective of N-acyl chain lengths, and those of sphingosine, sphingomyelin 1-phosphate, and their dihydro-forms are not affected by the CerK knockdown in PC12 cells | Homo sapiens |
| metabolism | involvement of the lysosome pathway in CerK levels and ceramide 1-phosphate formation | Homo sapiens |
| physiological function | ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P). The activity of CerK is regulated by post-translational modifications including phosphorylation, CerK has a role in neuronal functions | Homo sapiens |
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