Recombinant Mouse Alas2 Protein, His-tagged
|Product Overview :
|Recombinant Mouse Alas2 Protein (Ala361-Ala587) with N-His tag was expressed in E. coli.
- Gene Information
- Related Products
|Enables 5-aminolevulinate synthase activity. Involved in erythrocyte differentiation; heme biosynthetic process; and hemoglobin biosynthetic process. Acts upstream of or within cellular iron ion homeostasis. Located in mitochondrion. Is expressed in several structures, including alimentary system; brain; genitourinary system; hemolymphoid system gland; and liver and biliary system. Human ortholog(s) of this gene implicated in cutaneous porphyria; erythropoietic protoporphyria; hemochromatosis; sideroblastic anemia; and sideroblastic anemia 1. Orthologous to human ALAS2 (5'-aminolevulinate synthase 2).
|Molecular Mass :
|Predicted Molecular Mass: 28.7 kDa
Accurate Molecular Mass: 29 kDa
|Protein length :
|Positive Control; Immunogen; SDS-PAGE; WB.
|The thermal stability is described by the loss rate. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37 centigrade for 48h, and no obvious degradation and precipitation were observed. The loss rate is less than 5% within the expiration date under appropriate storage condition.
|Avoid repeated freeze/thaw cycles. Store at 2-8 centigrade for one month. Aliquot and store at -80 centigrade for 12 months.
|Storage Buffer :
|PBS, pH7.4, containing 0.01% SKL, 1 mM DTT, 5% Trehalose and Proclin300.
|Reconstitute in sterile water to a concentration of 0.1-1.0 mg/mL. Do not vortex.
|Gene Name :
|Alas2 aminolevulinic acid synthase 2, erythroid [ Mus musculus (house mouse) ]
|Official Symbol :
|ALAS2; aminolevulinic acid synthase 2, erythroid; 5-aminolevulinate synthase, erythroid-specific, mitochondrial; delta-ALA synthase 2; erythroid-specific ALAS; 5-aminolevulinic acid synthase 2; delta-aminolevulinate synthase 2; ALAS; ALASE; ALAS-E; Alas-2
|Gene ID :
|mRNA Refseq :
|Protein Refseq :
|UniProt ID :
|◆ Recombinant Protein
|Recombinant Human ALAS2 Protein, His-tagged
|Recombinant Rat ALAS2 Protein, His (Fc)-Avi-tagged
|Recombinant Human ALAS2 protein, His-tagged
|Recombinant Mouse Alas2 protein, His-tagged
|Recombinant Human ALAS2 Protein, GST-tagged
|Recombinant Human ALAS2 cell lysate
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.
Q&As (12)Ask a question
The main risk factor for ALAS2 deficiency is having a family history of the condition. Since it is inherited in an X-linked recessive pattern, males with a family history of ALAS2 deficiency are at a higher risk of being affected. Females with a family history may be carriers of the mutation and have a lower risk of symptoms.
Yes, there is ongoing research and clinical trials related to ALAS2 deficiency. These studies aim to better understand the underlying mechanisms of the condition and develop potential therapeutic strategies. Some areas of focus include gene therapy, targeted drug therapies, and exploring the role of iron metabolism in the disease.
ALAS2 deficiency is inherited in an X-linked recessive pattern. This means that the mutation in the ALAS2 gene is located on the X chromosome. Males who inherit one mutated copy of the gene will develop the condition, while females would usually need to inherit two mutated copies (one from each parent) to be affected. Female carriers of the mutation may have mild symptoms or may be asymptomatic.
Currently, there is no known cure for ALAS2 deficiency. Treatment options mainly focus on managing the symptoms and complications associated with the condition. However, with advancing research and the development of potential therapies, there is optimism for future treatment options that may lead to a cure or significant improvement in the management of ALAS2 deficiency.
Symptoms of ALAS2 deficiency can vary widely, ranging from mild to severe. They may include anemia, fatigue, pale skin, enlarged spleen, liver abnormalities, and problems with iron metabolism. Some individuals may also experience neurologic abnormalities, such as developmental delay or intellectual disability.
ALAS2 deficiency is a genetic disorder, and currently, there are no known methods for preventing it from occurring. However, genetic counseling and prenatal testing may be available for families with a known history of ALAS2 deficiency, allowing them to make informed decisions regarding reproductive choices.
reatment for ALAS2 deficiency is primarily focused on managing the symptoms and complications. This often involves regular blood transfusions to provide red blood cells and reduce anemia. Chelation therapy may be recommended to manage iron overload resulting from transfusions. In some cases, bone marrow transplantation or stem cell transplantation may be considered as a potential curative therapy. It is important for individuals with ALAS2 deficiency to receive regular medical monitoring and follow-up to assess their response to treatment and manage their overall health.
ALAS2 deficiency can be diagnosed through genetic testing to identify mutations in the ALAS2 gene. Additionally, blood tests can be conducted to measure heme synthesis and iron levels in the body. Bone marrow examination may also be performed to assess the morphology and iron content of the red blood cell precursors.
Currently, there is no specific curative treatment for ALAS2 deficiency. Management typically involves supportive care, including blood transfusions to alleviate anemia and iron chelation therapy to reduce iron overload. In some cases, bone marrow transplant or gene therapy may be considered as potential treatment options. Genetic counseling is also recommended for families affected by ALAS2 deficiency to understand the risks of inheritance and explore reproductive options.
The symptoms of ALAS2 deficiency can vary widely depending on the severity of the condition. The most common symptom is anemia, which can range from mild to severe. Other symptoms may include fatigue, weakness, shortness of breath, pale skin, jaundice, enlarged spleen, and a predisposition to developing gallstones. In some cases, individuals may also experience growth delays, delayed puberty, and skeletal abnormalities.
ALAS2 deficiency is a rare disorder, with an estimated prevalence of fewer than 1 in 100,000 individuals. It primarily affects males due to its X-linked inheritance pattern, although females can also be affected as carriers of the mutation. The exact prevalence is unknown, and the condition is more commonly reported in individuals of Mediterranean, African, and Southeast Asian descent.
The severity of ALAS2 deficiency can vary, and individuals with milder forms of the condition may be able to lead relatively normal lives with appropriate medical management and support. However, those with more severe forms may experience significant health challenges and require ongoing medical care. It is crucial for individuals with ALAS2 deficiency to work closely with healthcare professionals to develop an individualized treatment plan and address any complications or symptoms that arise.
Customer Reviews (4)Write a review
the manufacturer's commitment to providing excellent technical support adds an additional layer of confidence to my choice of the ALAS2 protein.
Its remarkable purity and functional attributes make it an optimal choice for my research, ensuring accurate and reliable outcomes.
By relying on the ALAS2 protein, I can approach my research with unwavering confidence in its quality and the unparalleled support extended by its manufacturer.
I am confident that the ALAS2 protein will unravel crucial insights into molecular mechanisms, greatly enhancing the significance and impact of my scientific investigations.
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