Cocaine esterase Antibodies

Cocaine esterase (CES2)

Involved in the detoxification of xenobiotics and in the activation of ester and amide prodrugs (PubMed:9169443). Shows high catalytic efficiency for hydrolysis of cocaine, 4- methylumbelliferyl acetate, heroin and 6-monoacetylmorphine (PubMed:9169443).

Hydrolyzes aspirin, substrates with big alcohol group and little acyl group and endogenous lipids like triacylglycerol (PubMed:28677105). .

Gene Information

Human
Gene Name:	CES2
Uniprot:	O00748
Entrez:	8824

Family

Belongs to:
type-B carboxylesterase/lipase family

Alternative Names

carboxylesterase 2 (intestine, liver); Carboxylesterase 2; carboxylesterase 2EC 3.1.1.1; CE-2; CE-2PCE-2; CES2; CES2A1; EC 3.1.1; EC 3.1.1.84; hCE-2; iCE; intestinal carboxylesterase; liver carboxylesterase-2; PCE-2

Molecular Weight

Mass (kDA):
61.807 kDA

Genomic Context

Human
Location:	16q22.1
Sequence:	16; NC_000016.10 (66934471..66945096)

Tissue Specificity

Preferentially expressed in intestine with moderate expression in liver. Within the intestine, highest expression is found in small intestine with lower expression in colon and rectum.

Subcellular Localizations

Endoplasmic reticulum lumen.

Diseases

• Malignant Neoplasms
• Neoplasms
• Colorectal Cancer
• Colorectal Neoplasms
• Diarrhea
• Malignant Tumor Of Colon
• Colonic Neoplasms
• Hepatotoxicity
• Lymphoma
• Mammary Neoplasms
• Dysequilibrium Syndrome
• Adenocarcinoma
• Liver Carcinoma

• Hypertrophy
• Inflammation
• Atherosclerosis
• Palmar-plantar Erythrodysesthesia Syndrome
• Carcinoma
• Ovarian Neoplasm
• Influenza

Pathways

• Transport
• Intestinal Absorption
• Cell Death
• Cell Growth
• Secretion
• Cell Proliferation
• Circadian Rhythm
• Cytokine Secretion
• Conjugation
• Localization
• Rna Capping
• Nuclear Division
• Response To Irinotecan

• Reverse Transcription
• Sensitization
• Translation
• Sperm Motility
• Reverse Cholesterol Transport
• Cholesterol Transport
• Excretion

PTMs

• Phosphorylation
• Hydroxylation
• Glycosylation

• Cleavage
• Oxidation
• Acylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/CES2

Best Uses Of The CES2 Marker

CES2 comes from the large group of carboxylesterases. It is used in the detection of cancer, apoptosis, and tumors. In this article, we will discuss how this marker is used. In addition, we will discuss the benefits and limitations of this marker. To get the most out of this tool, you need to understand how it works.

It is used in order to detect apoptosis

It can be difficult to determine if apoptosis has occurred because the apoptotic body is dead. However, this marker is not perfect. It is not able to detect apoptosis within all cells and may not be able to distinguish between necrosis and apoptosis. Thus, researchers have used a more sensitive and specific marker, the CES2 marker.

Apoptosis involves the translocation (or translocation) of PS from cells' cytoplasmic membranes to their cell surfaces. This lipid scramblase enzyme binds to PS on the outer leaflet of apoptotic cells, producing an "eat me signal." Phagocytes are able to recognize apoptotic tissues and engulf them live. This requires consideration of cell membrane integrity.

Executioner caspase activity is a measure of a cell's point of no return. Executioner caspase-3/7 activity most often is measured with a standard multimode plate reader. The enzyme is responsible for inactivating PARP DNA repairs and producing fragments of p89/p24. This activity results in cells undergoing morphological changes that mimic apoptosis.

Although CES2 can be used as a universal marker for apoptosis and is sensitive enough to detect changes in other processes, CES2 can also be used to detect changes that are not directly related to apoptosis. You can trigger apoptosis by either directly stimulating mitochondria or by targeting certain adaptor protein functions.

Confocal microscopy allows researchers to examine cell death dynamics, and assess DNA damage. Fluorescence microscopic is especially useful in the detection of apoptosis. This allows researchers visualize the nucleus modifications that distinguish apoptotic and necrotic cells. FM is also sensitive to autophagy detection by colocalizing LC3 markers and lysosomal marks.

Apoptosis is also associated with several other morphological changes. Autophagy is marked by the formation of autophagosomes, which contain the ATG12-ATG5-ATG16L1 complex and LC3-II. Autophagosomes are fusions of lysosomes. Similar to autophagosomes, apoptosis is triggered by the condensation of nuclei and the formation apoptotic body.

It is used for the detection of tumors

The CES2 marker, an immunogen, is expressed in the stroma cells of cancer cells. It has been shown that this gene is expressed in higher levels in CCA, CCCA, and ICCA. We don't know how CES2 is upregulated in cancer cell cells. Further studies are needed to better understand how CES2 expression is regulated in cancer cells.

The stroma from CCA tumor cells is expressed in PDAC cell line lines. This heterogeneous expression indicates the active proteins. MS covers the CES2 peptide within all compartments. This confirms that CES2 a active protein. Western blot analysis confirms that CES2 protein expression. This immunoreactivity can be used to detect tumors.

Researchers are currently studying how the CES2 gene contributes to activation of prodrugs in cancer cells. Irinotecan is known for inducing genes involved in inflammation like STAT1, MX1, IFI27 & IL-8. These gene expression results suggest CES2 might be a marker to predict CCA patients' response.

The CES2 marker is most commonly found in biliary carcinomas. However, it can also be detected in non-neoplastic biliary Epithelium. The CES2 immunoreactivity in CCA tumor cells decreased stepwise with cholangiocarcinogenesis. CES2 expression levels were higher in normal biliary epithelium than in high-grade biliary neoplasia or invasive CCA.

The sequence of TP53 gene was performed using a genetic analysis device called an ABI3130xl. Five percent had mutations in TP53. CES2 mRNA levels were comparable in tumors without and with TP53 mutations. This suggests that TP53 mutations are not required for CES2 to be expressed in tumors. If irinotecan doesn't work, then CES2 mRNA expression is a good indicator of the tumor’s response to treatment.

CES2 is able to detect tumors both in vitro and in vivo. It can also identify the location in a patient’s body of inflammatory cells. Unlike cytotoxic chemotherapy CES2 can target tumor cells in a variety different settings. However, CES2 should be expressed in a clinical setting to identify cancer cells. Its higher expression is linked to a greater risk for metastatic cancers.

An alternative strategy to detect the tumor is to use siRNA to knockdown CES2, and immunoreactivity in CCA cells lines. SiRNAs that specifically target CES2 are used in this instance. These siRNAs are derived from human library. The CES2 marker was cloned into a pLenti-C-Myc-DDK-IRESPuro vector. The empty vector was used to control.