|Positive WB detected in||HepG2 cells, Jurkat cells|
|Positive IHC detected in||human liver cancer tissue, human kidney tissue|
Note: suggested antigen retrieval with TE buffer pH 9.0; (*) Alternatively, antigen retrieval may be performed with citrate buffer pH 6.0
|Positive IF detected in||HepG2 cells|
|Western Blot (WB)||WB : 1:500-1:1000|
|Immunohistochemistry (IHC)||IHC : 1:50-1:500|
|Immunofluorescence (IF)||IF : 1:50-1:500|
|Sample-dependent, check data in validation data gallery|
16912-1-AP targets CES1 in WB, IHC, IF, ELISA applications and shows reactivity with human samples.
|Host / Isotype||Rabbit / IgG|
|Immunogen||CES1 fusion protein Ag10567|
|Full Name||carboxylesterase 1 (monocyte/macrophage serine esterase 1)|
|Calculated molecular weight||566 aa, 62 kDa|
|Observed molecular weight||62 kDa|
|GenBank accession number||BC012418|
|Gene ID (NCBI)||1066|
|Purification Method||Antigen affinity purification|
|Storage Buffer||PBS with 0.02% sodium azide and 50% glycerol pH 7.3.|
|Storage Conditions||Store at -20°C. Stable for one year after shipment. Aliquoting is unnecessary for -20oC storage.|
CES1(liver carboxylesterase 1) is also named as CES2, SES1 and belongs to the type-B carboxylesterase/lipase family. The deduced 567-amino acid protein contains a putative 18-amino acid signal peptide and a characteristic C-terminal endoplasmic reticulum retention signal (HXEL). It is the major hydrolytic enzyme responsible for the metabolism of numerous therapeutic agents as well as endogenous substrates.Westernblot analysis demonstrated that CES1 is expressed in human liver microsomes (HLM) but not in human intestinal microsomes (HIM)(PMID:19185566).
J Proteome Res
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Drug Metab Dispos
Simultaneous absolute protein quantification of carboxylesterases 1 and 2 in human liver tissue fractions using liquid chromatography-tandem mass spectrometry.
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Multifactorial resistance to aminopeptidase inhibitor prodrug CHR2863 in myeloid leukemia cells: down-regulation of carboxylesterase 1, drug sequestration in lipid droplets and pro-survival activation ERK/Akt/mTOR.
ATAD3 gene cluster deletions cause cerebellar dysfunction associated with altered mitochondrial DNA and cholesterol metabolism.