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Facts about Aldo-keto reductase family 1 member B10.
May be responsible for detoxification of reactive aldehydes from the digested food until the nutrients are passed on to other organs. .
Human | |
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Gene Name: | AKR1B10 |
Uniprot: | O60218 |
Entrez: | 57016 |
Belongs to: |
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aldo/keto reductase family |
AKR1B10; AKR1B11; AKR1B12; Aldo-keto Reductase 1B10; aldo-keto reductase family 1 member B10; aldo-keto reductase family 1, member B10 (aldose reductase); aldo-keto reductase family 1, member B11 (aldose reductase-like); AldoketoReductase 1B10; aldose reductase-like 1; aldose reductase-like peptide; Aldose reductase-like; Aldose reductase-related protein; ALDRLn; ARL1; ARL-1SI reductase; ARP; EC 1.1.1; EC 1.1.1.-; EC 1.1.1.21; hARP; HIS; HSI; MGC14103; Small intestine reductase
Mass (kDA):
36.02 kDA
Human | |
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Location: | 7q33 |
Sequence: | 7; NC_000007.14 (134527567..134541412) |
Found in many tissues. Highly expressed in small intestine, colon and adrenal gland.
Lysosome. Secreted. Secreted through a lysosome-mediated non-classical pathway.
The AKR1B10 marker is a member of the aldoketo reductase protein family. SEQ ID NOs 4, and 5 identify the ARL-1 proteins. Its amino acids sequence is identical to that of the AKR1B10 Gene Sequence, which is identical with the AKR1B10 Gene in GenBank. Cao et al. Their results were published by J Biol. Chem. 273, 11429-11435.
Boster Bio AKR1B10 Marker (ARL-1 Marker) inhibits apoptosis of breast cancer cells by reducing cytotoxicity using a sandwich ELISA assay. This test detects secreted AKR1B10 from tissue culture media. It reduces the cytotoxicity and toxicity of breast cancer cells derived primarily by HCT-8, MCF-7, or BT-20.
Boster Bio AKR1B10 reduces cytotoxicity in cancer cells by reducing levels of aldoketo reductase. Western blot analysis revealed that methotrexate (6-mercaptopurine, thioguanine) are the antimetabolites. AKR1B10 also inhibits melphalan activity, busulfan activity, and dibromomannitol.
The aldoketo reductase B10(AKR1B10) enzyme can be used to detoxify the body. It can lower levels of carbonyls including nitrile and unsaturated fatty acid, as well as 4-hydroxynonenal. It also protects the host cells from cytotoxic and toxic carbonyls.
The ARL-1 Protein functions in the gastrointestinal system. It is found in terminally differentiated colon epithelia. ARL-1 expression has been significantly reduced in colon cancer cell lines. This suggests that ARL-1 could play an important role in protecting tissues against the harmful effects of reactive carbonyl compounds. However, it is not clear how ARL-1 regulates gastrointestinal toxicities.
The purified protein underwent SDS-PAGE. Western blot analysis was performed using antibodies to AR and ARL-1. Western blot analysis showed that the BosterBio AKR1B10 marked reduces cytotoxicity among cancer cells. For more information, please visit Boster Biologic AKR1B10Marker page.
The AKR1B10 antigens used in the manufacturing of the AKR1B10 mark are human antibodies that are specific to the ARL-1 proteins, also known under the AKR1B10. These monoclonal antigens recognize proteins and peptides, and bind with the epitope defined using amino acid sequences. These antibodies can either be produced by immunizing animals or using a protein molecule.
AKR1B10, also known as aldosterone reducer, is a member the AKR1B enzyme family. It is a highly reactive oxidoreductase that reduces various cytotoxic carbonyl compounds found in human cells. It protects cells and reduces all trans and 9-cis hydroxyl groups.
The levels of AKR1B10 found in breast cancer tissues was higher than those found in non-cancerous material. Overexpression of the protein was associated with lymph node metastasis and tumor size. It was found to negatively correlate with p53 protein expression in breast cancer cell lines. It promotes cell growth. In laboratory experiments, AKR1B10 overexpression induced invasion and migration of MCF-7 cells, while knockdown prevented these processes.
Western blot analysis was used to determine the expression of AKR1B10 within pancreatic cancer cells. It was done in six pancreatic adenocarcinoma cells, including HPDE6E6E7 and Hep2G. AKR1B10 overexpression was evident in all six pancreatic adenocarcinomas. The protein also decreased activity of membrane-bound KRAS protein.
Transfection of AKR1B10 mimics into a BPH-1 cells line confirmed AKR1B10 mRNA expression. The AKR1B10–mimics-group had the highest AKR1B10 levels compared to all other groups. The inhibitor group displayed the lowest levels of expression. Cell proliferation was higher in the AKR1B10–mics, while apoptosis rates were highest in this group.
However, AKR1B10 doesn't directly affect the growth of breast carcinoma cells. Inhibiting apoptosis. The p53-induced apoptosis of cancer cells is inhibited when AKR1B10 is decreased in colorectal cells. Inhibition of the AKR1B10 marker has also been associated with increased migratory potential in breast cancer cells.
Although not every tumor expresses AKR1B10 in all cases, some reports have shown that it is expressed in lung and larynx tissue. Additionally, the gene is associated to tumor size, lymph node metastasis and the prognosis. Further research is needed to determine if AKR1B10 gene suppression is beneficial. Although there are not many reports on AKR1B10’s role in lung carcinoma, this study may shed some light on the mechanisms that AKR1B10 is expressed in the larynx.
AKR1B10 not only activates NF-kB but also plays multiple roles during tumor development. In addition to tumor growth, it is also involved in the development of acquired chemoresistance. The AKR1B10 biomarker is a good indicator of the progression breast cancer. PI3K inhibits NF-kBp65 phosphorylation and suppresses expression of breast cancer-related proteins by inhibiting AKR1B10.
An enzyme-linked immunosorbent assay was used to determine AKR1B10 activity of a cell culture specimen. USCN ELISA Kits were used. The ELISA method involved centrifuging a cell at 1,000xg for 20 minute, and then adding dilutions (standard and sample) to the wells. Next, we added the Substrate Solution, Detection Reagents, and Stop Solution. After this, the optical density was measured using a BioTek Instruments Inc. microplate reader at 450 nm.
The blood levels of AKR1B10 were higher in the research group than the control group. It was found to correlate positively and positively with PSA (EGF), IL-6, IL-6a, TNFa, and TNFa. However, the statistical significance of this relationship between PSA1B10 AKR1B10 is not clear. Researchers concluded that the AKR1B10 genes are not the cause of cancer, but are indicators of the presence other cancer markers.
The current study suggests that AKR1B10 may play a role in prostate cancer. The gene is found in the cytoplasmic cells of prostate epithelial cell s. This was further confirmed by the current study. Furthermore, the results showed that AKR1B10 inhibits both apoptosis (proliferation) and cell death. Thus, the AKR1B10 gene is an important regulator of prostate cancer progression.
AKR1B10 offers a superior diagnostic value for early-stage HCC than AFP, especially in patients who have AFP-negative disease. Further research is required to confirm these findings. Once AKR1B10 is validated, it may become an important diagnostic tool for HCC. HCC will affect many patients. Early detection can be crucial for a patient's survival.
AKR1B10 is known to regulate the production phosphatidylinositol (3.4)-bisphosphate in breast cancer cells. Activated PI3K creates PIP3 (from PIP2). AKR1B10 expression was associated with increased PIP3 levels in MCF-7 and BT-20 cells. These findings suggest that AKR1B10 may be a potential therapeutic target for breast cancer.
PMID: 9565553 by Cao D., et al. Identification and characterization of a novel human aldose reductase-like gene.
PMID: 9765596 by Hyndman D.J., et al. Sequence and expression levels in human tissues of a new member of the aldo-keto reductase family.
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