Recombinant Zebrafish ALDOAB

• Cat.No.: ALDOAB-12421Z
• Product Overview: Recombinant Zebrafish ALDOAB full length or partial length protein was expressed.

Specification

• Source: Mammalian Cells
• Species: Zebrafish
• Tag: His
• Form: Liquid or lyophilized powder
• Endotoxin: < 1.0 eu per μg of the protein as determined by the LAL method.
• Purity: >80%
• Notes: This item requires custom production and lead time is between 5-9 weeks. We can custom produce according to your specifications.
• Storage: Store it at +4 oC for short term. For long term storage, store it at -20 oC～-80 oC.
• Storage Buffer: PBS buffer

Gene Information

• Gene Name: aldoab aldolase a, fructose-bisphosphate, b [ Danio rerio (zebrafish) ]
• Official Symbol: ALDOAB
• Gene ID: 406496
• mRNA Refseq: NM_213215
• Protein Refseq: NP_998380
• UniProt ID: Q6P043

Reviews

07/10/2019

I greatly appreciate their commitment to ensuring my research is a success.

03/11/2019

The ALDOAB Protein is a protein of exceptional quality that surpasses my expectations and fulfills all my experimental requirements.

09/13/2018

The ALDOAB Protein offers a wide range of applications, making it highly versatile for various experimental settings.

04/28/2017

Its purity and consistency are of the highest standards, allowing for precise and reliable results in my research endeavors.

Q&As

Are there any known genetic mutations in ALDOAB?

Yes, mutations in the ALDOAB gene are associated with hereditary fructose intolerance. These mutations lead to a deficiency in ALDOAB activity, resulting in the accumulation of fructose-1-phosphate and causing symptoms upon fructose consumption.

Is ALDOAB associated with any diseases?

Yes, mutations in the ALDOAB gene are associated with a rare genetic disorder called hereditary fructose intolerance. This condition leads to a deficiency in ALDOAB activity, resulting in the inability to fully metabolize fructose and leading to severe symptoms upon fructose consumption.

Can ALDOAB be a potential therapeutic target?

While ALDOAB deficiency is linked to hereditary fructose intolerance, there is currently no therapeutic intervention targeting this specific enzyme. However, managing the condition involves a strict fructose-free diet.

How is ALDOAB deficiency diagnosed?

ALDOAB deficiency is typically diagnosed through genetic testing. This involves analyzing the ALDOAB gene for mutations or variations that can lead to reduced or absent enzyme activity. Additionally, blood tests can be performed to measure the levels of fructose-1-phosphate, which is typically elevated in individuals with hereditary fructose intolerance.

How is hereditary fructose intolerance treated?

The primary treatment for hereditary fructose intolerance is the complete elimination of fructose, sucrose, and sorbitol from the diet. This includes avoiding fruits, fruit juices, honey, and foods with high levels of fructose and sucrose as ingredients. A registered dietitian can help create a suitable dietary plan.

Is there any research investigating the potential role of ALDOAB in cancer?

Research on the potential role of ALDOAB in cancer is limited. However, some studies have suggested that altered fructose metabolism, for which ALDOAB is involved, may play a role in cancer progression and metabolism. Further research is needed to fully understand the significance of ALDOAB in cancer biology.

What are the symptoms of hereditary fructose intolerance?

Symptoms of hereditary fructose intolerance can vary but commonly include gastrointestinal distress like abdominal pain, nausea, vomiting, and diarrhea after consuming fructose or foods and beverages containing fructose. Other symptoms may include low blood sugar levels, jaundice, liver dysfunction, and failure to thrive in infants.

Is ALDOAB being studied as a biomarker?

ALDOAB is not typically studied as a biomarker, as its levels alone may not provide significant diagnostic or prognostic information. However, its deficiency can be diagnosed through genetic testing in individuals suspected of having hereditary fructose intolerance.

How is ALDOAB regulated in cells?

ALDOAB expression is regulated at the gene transcription level, influenced by factors such as dietary fructose intake and hormonal regulation.

Is there a cure for ALDOAB deficiency?

Currently, there is no cure for ALDOAB deficiency or hereditary fructose intolerance. However, the condition can be managed effectively through strict dietary modifications. Avoiding foods and beverages high in fructose, sucrose, and sorbitol can prevent symptoms and complications associated with the condition.

Can ALDOAB activity be modulated by drugs or other compounds?

As of now, there are no known drugs or compounds specifically targeting ALDOAB activity. However, given the potential metabolic implications of altered fructose metabolism, it is an area of interest for potential therapeutic interventions in the future.

Is ALDOAB an essential enzyme for overall metabolism?

While ALDOAB is not considered essential for overall metabolism, its deficiency in hereditary fructose intolerance can lead to significant health issues. In individuals without hereditary fructose intolerance, other enzymes can compensate for ALDOAB's role in fructose metabolism.

Is ALDOAB present in other tissues apart from the liver?

While ALDOAB is primarily found in the liver, it may be present in lower levels in other tissues as well. Some research suggests its expression in tissues such as the kidney, intestines, and pancreatic islets, albeit at lower levels compared to the liver.

Does ALDOAB have any other functions besides fructose metabolism?

ALDOAB is primarily known for its role in fructose metabolism. However, some studies suggest that it may have non-glycolytic functions, including modulating cell signaling pathways and cellular stress responses, but further research is needed to fully understand these potential roles.

Can ALDOAB deficiency be diagnosed in adulthood?

ALDOAB deficiency, or hereditary fructose intolerance, is typically diagnosed in childhood when fructose-containing foods are introduced into the diet. However, in some cases, individuals may not exhibit symptoms until later in life. Genetic testing can be done to confirm the diagnosis at any age.

Are there any known complications or long-term effects of ALDOAB deficiency?

The primary complication of ALDOAB deficiency is hereditary fructose intolerance. If left untreated, this condition can lead to severe liver damage, resulting in liver failure. It can also cause growth retardation, malnutrition, and in rare cases, neurological issues. However, with proper management through dietary modifications, these complications can be minimized or avoided.

Can ALDOAB deficiency be inherited?

Yes, ALDOAB deficiency, also known as hereditary fructose intolerance, is an autosomal recessive disorder, meaning both parents must carry a mutated ALDOAB gene and pass it on to their child for the disorder to develop. If only one parent carries the mutation, the child will be a carrier but will not have the deficiency.

Are there any alternative treatments for hereditary fructose intolerance?

The main treatment for hereditary fructose intolerance is a strict diet that avoids fructose, sucrose, and sorbitol-containing foods and beverages. There are currently no alternative treatments, but research is ongoing to explore potential therapeutic options or interventions.