Recombinant Rat Ampd1, His-tagged
Cat.No. : | Ampd1-3429R |
Product Overview : | AMP deaminase 1 (Ampd1) |
- Specification
- Gene Information
- Related Products
Description : | catalyzes the conversion of AMP to IMP in energy metabolism . |
Source : | E. Coli or Yeast |
Species : | Rat |
Tag : | His |
Form : | This item requires custom production and lead time is between 5-9 weeks. We can custom produce according to your specifications. |
Protein length : | 747 |
Purity : | >90% |
Notes : | Small volumes of Ampd1 recombinant protein may occasionally become entrapped in the seal of the product vial during shipment and storage. If necessary, briefly centrifuge the vial on a tabletop centrifuge to dislodge any liquid in the container`s cap. Certain products may require to ship with dry ice. |
Storage : | Store at -20 degree C. For extended storage, store at -20 or -80 degree C. |
Storage Buffer : | PBS pH 7.4, 50% glycerol |
Warning : | This product is for research use only. Not for use in diagnostic or therapeutic procedures. |
Gene Name : | Ampd1 adenosine monophosphate deaminase 1 [ Rattus norvegicus ] |
Official Symbol : | Ampd1 |
Synonyms : | AMPD1; adenosine monophosphate deaminase 1; AMP deaminase 1; Ampd; myoadenylate deaminase; adenosine monophosphate deaminase 1 (isoform M); Ampd01; RATAMPD01; |
Gene ID : | 25028 |
mRNA Refseq : | NM_138876 |
Protein Refseq : | NP_620231 |
Pathway : | Metabolic pathways, organism-specific biosystem; Metabolism, organism-specific biosystem; Metabolism of nucleotides, organism-specific biosystem; Purine metabolism, organism-specific biosystem; Purine metabolism, organism-specific biosystem; Purine metabo |
Function : | AMP deaminase activity; hydrolase activity; metal ion binding; myosin heavy chain binding; |
Products Types
◆ Recombinant Protein | ||
AMPD1-313R | Recombinant Rat AMPD1 Protein, His (Fc)-Avi-tagged | +Inquiry |
AMPD1-334H | Recombinant Human AMPD1 Protein, His (Fc)-Avi-tagged | +Inquiry |
AMPD1-8877H | Recombinant Human AMPD1 protein, MYC/DDK-tagged | +Inquiry |
Ampd1-1615M | Recombinant Mouse Ampd1 Protein, Myc/DDK-tagged | +Inquiry |
AMPD1-11138Z | Recombinant Zebrafish AMPD1 | +Inquiry |
◆ Lysates | ||
AMPD1-8877HCL | Recombinant Human AMPD1 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
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Q&As (16)
Ask a questionCurrently, there is no cure for AMPD1 protein deficiency. Treatment mainly focuses on managing symptoms and minimizing their impact on daily life. Lifestyle modifications, including avoiding triggers, dietary adjustments, and appropriate physical activity, are essential components of management.
AMPD1 protein deficiency is generally considered stable and non-progressive. While symptoms can fluctuate in severity and may worsen with certain triggers, the condition itself does not tend to worsen over time. However, individual experiences may vary, and it is important for individuals to have regular medical follow-ups to monitor their condition.
AMPD1 protein deficiency primarily affects skeletal muscle tissue due to its higher energy demands during exercise. However, there is evidence to suggest that this deficiency may have broader effects, such as impairing cardiac function. Further research is needed to fully understand the potential systemic impact of AMPD1 protein deficiency.
Currently, AMPD1 protein deficiency is not included in routine newborn screening panels. Diagnosis is typically made based on symptoms, genetic testing, and enzymatic activity analysis. However, as research progresses and our understanding of the condition improves, it is possible that it may be included in newborn screening programs in the future.
As of now, there is no cure for AMPD1 protein deficiency. However, ongoing research is being conducted to better understand the condition and explore potential treatment options. Management strategies and lifestyle modifications can help individuals with AMPD1 protein deficiency lead a relatively normal life and minimize symptoms.
While specific clinical trials for AMPD1 protein deficiency may be limited, ongoing research is being conducted to better understand the condition, improve diagnosis, and explore potential therapies. This research includes investigating gene therapy, enzyme replacement therapy, and pharmacological interventions aimed at addressing the underlying metabolic abnormalities associated with the disorder.
With proper management and lifestyle modifications, individuals with AMPD1 protein deficiency can lead relatively normal lives. Understanding and avoiding triggers that may worsen symptoms, such as intense exercise or high-protein diets, can help minimize complications. Regular monitoring and communication with healthcare providers are essential for effectively managing the condition.
The ability to engage in physical exercise may vary among individuals with AMPD1 protein deficiency. It is generally recommended to avoid intense and prolonged exercise, as it can trigger symptoms and increase the risk of muscle damage. Moderate and low-impact activities, such as walking or swimming, may be better tolerated. Each individual's exercise tolerance should be assessed on a case-by-case basis, and guidance from healthcare professionals is crucial.
The most common symptom of AMPD1 protein deficiency is exercise intolerance, which may manifest as muscle cramps, pain, stiffness, and weakness during or after physical exertion. Some individuals may also experience fatigue, myoglobinuria (the presence of myoglobin in the urine), and rhabdomyolysis (breakdown of muscle tissue). The severity of symptoms can vary among individuals.
The diagnosis of AMPD1 protein deficiency typically involves a combination of clinical evaluation, genetic testing, and biochemical analyses. Muscle biopsies may be performed to evaluate enzyme activity levels. Genetic testing can identify mutations in the AMPD1 gene, confirming the diagnosis.
AMPD1 protein deficiency is considered a rare condition. Its prevalence is estimated to be around 1 in 20,000 individuals globally. However, the frequency may vary across different populations.
Research studies and clinical trials related to AMPD1 protein deficiency may be ongoing, but it is essential to consult reputable sources, such as clinical trial registries or research institutes, to get the most up-to-date information. Participating in clinical trials can provide individuals with opportunities to contribute to the advancement of knowledge and potentially access new treatment options.
Yes, mutations in the AMPD1 gene are responsible for AMPD1 protein deficiency. The most common mutation is a substitution of glycine with arginine at position 202 (Gly202Arg). Other mutations have also been identified, and the specific mutation can influence the severity and clinical presentation of the condition.
Symptoms of AMPD1 protein deficiency can vary widely among affected individuals. Common symptoms include muscle pain, weakness, cramps, and fatigue, particularly during or after strenuous exercise. Some individuals may also experience exercise intolerance, muscle breakdown (rhabdomyolysis), or myoglobinuria (the presence of myoglobin in the urine).
Currently, there is no specific treatment for AMPD1 protein deficiency. Management primarily involves avoiding triggers that worsen symptoms, maintaining a balanced diet, and adopting strategies to minimize exercise-induced symptoms. In some cases, medication such as allopurinol or ribose supplements may be used, but their effectiveness can vary among individuals.
In most cases, AMPD1 protein deficiency is not life-threatening. However, severe episodes of muscle breakdown (rhabdomyolysis) can occur, leading to potential complications such as kidney damage. It is important for individuals with the condition to monitor their symptoms and seek medical attention if severe muscle pain, dark urine, or other concerning symptoms arise.
Customer Reviews (4)
Write a reviewTheir dedication to customer satisfaction has been instrumental in overcoming obstacles and achieving successful results in my experiments.
The manufacturer of AMPD1 protein has consistently provided outstanding technical support that has surpassed my expectations.
This protein demonstrates remarkable purity, stability, and specificity, ensuring utmost accuracy and reproducibility in my research endeavors.
I am delighted to express my complete satisfaction with the quality of AMPD1 protein, as it precisely suits my experimental requirements.
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