Recombinant Human ALDOB Protein, Myc/DDK-tagged, C13 and N15-labeled
Cat.No. : | ALDOB-5893H |
Product Overview : | ALDOB MS Standard C13 and N15-labeled recombinant protein (NP_000026) with a C-terminal MYC/DDK tag, was expressed in HEK293 cells. |
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Description : | Fructose-1,6-bisphosphate aldolase (EC 4.1.2.13) is a tetrameric glycolytic enzyme that catalyzes the reversible conversion of fructose-1,6-bisphosphate to glyceraldehyde 3-phosphate and dihydroxyacetone phosphate. Vertebrates have 3 aldolase isozymes which are distinguished by their electrophoretic and catalytic properties. Differences indicate that aldolases A, B, and C are distinct proteins, the products of a family of related 'housekeeping' genes exhibiting developmentally regulated expression of the different isozymes. The developing embryo produces aldolase A, which is produced in even greater amounts in adult muscle where it can be as much as 5% of total cellular protein. In adult liver, kidney and intestine, aldolase A expression is repressed and aldolase B is produced. In brain and other nervous tissue, aldolase A and C are expressed about equally. There is a high degree of homology between aldolase A and C. Defects in ALDOB cause hereditary fructose intolerance. |
Source : | HEK293 |
Species : | Human |
Tag : | Myc/DDK |
Molecular Mass : | 39.3 kDa |
AA Sequence : | MAHRFPALTQEQKKELSEIAQSIVA NGKGILAADESVGTMGNRLQRIKVE NTEENRRQFREILFSVDSSINQSIG GVILFHETLYQKDSQGKLFRNILKE KGIVVGIKLDQGGAPLAGTNKETTI QGLDGLSERCAQYKKDGVDFGKWRA VLRIADQCPSSLAIQENANALARYA SICQQNGLVPIVEPEVIPDGDHDLE HCQYVTEKVLAAVYKALNDHHVYLE GTLLKPNMVTAGHACTKKYTPEQVA MATVTALHRTVPAAVPGICFLSGGM SEEDATLNLNAINLCPLPKPWKLSF SYGRALQASALAAWGGKAANKEATQ EAFMKRAMANCQAAKGQYVHTGSSG AASTQSLFTACYTYTRTRPLEQKLI SEEDLAANDILDYKDDDDKV |
Purity : | > 80% as determined by SDS-PAGE and Coomassie blue staining |
Stability : | Stable for 3 months from receipt of products under proper storage and handling conditions. |
Storage : | Store at -80 centigrade. Avoid repeated freeze-thaw cycles. |
Concentration : | 50 μg/mL as determined by BCA |
Storage Buffer : | 100 mM glycine, 25 mM Tris-HCl, pH 7.3. |
Gene Name : | ALDOB aldolase, fructose-bisphosphate B [ Homo sapiens (human) ] |
Official Symbol : | ALDOB |
Synonyms : | ALDOB; aldolase B, fructose-bisphosphate; fructose-bisphosphate aldolase B; aldolase 2; liver-type aldolase; aldolase B, fructose-bisphosphatase; ALDB; ALDO2; |
Gene ID : | 229 |
mRNA Refseq : | NM_000035 |
Protein Refseq : | NP_000026 |
MIM : | 612724 |
UniProt ID : | P05062 |
Products Types
◆ Recombinant Protein | ||
ALDOB-1325R | Recombinant Rabbit ALDOB Protein (2-364 aa), His-tagged | +Inquiry |
Aldob-1596M | Recombinant Mouse Aldob Protein, Myc/DDK-tagged | +Inquiry |
ALDOB-326R | Recombinant Rabbit ALDOB Protein (2-364 aa), His-SUMO-tagged | +Inquiry |
ALDOB-456H | Recombinant Human ALDOB Protein, GST-tagged | +Inquiry |
ALDOB-9567H | Recombinant Human ALDOB, His-tagged | +Inquiry |
◆ Lysates | ||
ALDOB-8911HCL | Recombinant Human ALDOB 293 Cell Lysate | +Inquiry |
Related Gene
For Research Use Only. Not intended for any clinical use. No products from Creative BioMart may be resold, modified for resale or used to manufacture commercial products without prior written approval from Creative BioMart.
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Q&As (6)
Ask a questionHereditary fructose intolerance is caused by a genetic mutation in the ALDOB gene, which leads to a deficiency or complete absence of the ALDOB protein. Without functioning ALDOB protein, the body is unable to properly metabolize fructose, leading to a build-up of toxic byproducts and causing the symptoms of HFI.
Yes, there are multiple mutations identified in the ALDOB gene that can cause hereditary fructose intolerance. These mutations can vary in their severity and impact on the function of the ALDOB protein.
Yes, mutations in the ALDOB gene can have other health implications. In some cases, mutations that cause a partial deficiency of the ALDOB protein may lead to a milder form of fructose intolerance or cause symptoms only when excessive amounts of fructose are consumed. Additionally, there is some evidence to suggest that ALDOB gene mutations may be associated with an increased risk of developing certain types of liver diseases. However, further research is needed to fully understand the potential implications.
Yes, prenatal testing is available for hereditary fructose intolerance. It involves analyzing fetal DNA obtained through procedures like chorionic villus sampling (CVS) or amniocentesis to identify mutations in the ALDOB gene. This allows for early detection of the condition, aiding in family planning and preparation for managing the condition after birth.
The ALDOB protein is primarily involved in fructose metabolism, but it also has other functions. It plays a role in gluconeogenesis, a process in which the liver produces glucose from non-carbohydrate sources. It is also involved in maintaining the balance of sugar molecules in the body and supporting normal liver function.
Hereditary fructose intolerance is typically diagnosed through a combination of clinical symptoms, biochemical testing, and genetic testing. Symptoms of the condition may include abdominal pain, nausea, vomiting, and low blood sugar levels. Biochemical testing involves measuring the levels of certain metabolites, such as fructose and its byproducts, in the blood or urine. Genetic testing can confirm the presence of specific mutations in the ALDOB gene.
Customer Reviews (3)
Write a reviewIt has been extensively used in protein-protein interaction studies, enzymatic assays, and structural analyses, showcasing its reliability and adaptability in diverse research areas.
With the ALDOB Protein, I have the confidence to generate critical insights and drive significant advancements in my field.
I am certain of obtaining reliable and reproducible results, enabling me to contribute to scientific progress and make new discoveries.
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