Recombinant Human ANK1 protein, His & T7-tagged
Cat.No. : | ANK1-1730H |
Product Overview : | Recombinant Human ANK1 aa. (Leu32~Leu369 (Accession # P16157)) fused with N-terminal His & T7 tag was produced in E. coli cells. |
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Source : | E. coli |
Species : | Human |
Tag : | His & T7 |
Form : | Freeze-dried powder |
Molecular Mass : | Predicted Molecular Mass: 40.5kDa |
Protein length : | Leu32~Leu369 (Accession # P16157) |
Endotoxin : | <1.0EU per 1ug (determined by the LAL method) |
Purity : | >95% |
Characteristic : | The isoelectric point is 7.5. |
Applications : | SDS-PAGE; WB; ELISA; IP. |
Stability : | The thermal stability is described by the loss rate of the target protein. The loss rate was determined by accelerated thermal degradation test, that is, incubate the protein at 37°C for 48h, and no obvious degradation and precipitation were observed. (Referring from China Biological Products Standard, which was calculated by the Arrhenius equation.) The loss of this protein is less than 5% within the expiration date under appropriate storage condition. |
Storage : | Avoid repeated freeze/thaw cycles. Store at 2-8°C for one month. Aliquot and store at -80°C for 12 months. |
Storage buffer : | Supplied as lyophilized form in PBS, pH7.4, containing 5% trehalose, 0.01% sarcosyl. |
Reconstitution : | Reconstitute in sterile PBS, pH7.2-pH7.4. |
SDS-PAGE: |
Gene Name : | ANK1 ankyrin 1 [ Homo sapiens (human) ] |
Official Symbol : | ANK1 |
Synonyms : | ANK1; ankyrin 1; ANK; SPH1; SPH2; ankyrin-1; ANK-1; ankyrin 1, erythrocytic; ankyrin-R; erythrocyte ankyrin |
Gene ID : | 286 |
mRNA Refseq : | NM_000037.3 |
Protein Refseq : | NP_000028.3 |
UniProt ID : | P16157 |
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◆ Lysates | ||
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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 (13)
Ask a questionOngoing research on ANK1-related disorders focuses on understanding the underlying molecular mechanisms, exploring the full spectrum of associated symptoms and complications, developing better diagnostic methods, and investigating potential targeted therapies. Researchers are also studying the role of ANK1 in other diseases, such as cardiovascular disorders and neurological conditions.
While ANK1 mutations are most commonly associated with conditions affecting red blood cells, recent studies have also identified their potential involvement in other disorders. For example, ANK1 mutations have been implicated in hereditary spherocytosis-associated gallstones and an increased risk of gallbladder cancer. Moreover, there is evidence suggesting ANK1 gene variations may contribute to susceptibility to certain cardiovascular diseases, such as atrial fibrillation and myocardial infarction. However, further research is required to ascertain the precise role of ANK1 mutations in these conditions.
While ANK1 is well-known for its importance in maintaining the shape and stability of red blood cells, recent research has unveiled its involvement in various other cellular processes. ANK1 has been found in the brain, where it interacts with components of the cytoskeleton and contributes to the organization and function of nerve cells. Additionally, ANK1 is present in skeletal muscles and has been implicated in the development and maintenance of muscle structure. These findings suggest that ANK1 may have diverse functions beyond the red blood cell membrane.
The long-term complications and health risks associated with ANK1-related disorders primarily depend on the specific disorder and its severity. In hereditary spherocytosis and related conditions, individuals may experience chronic anemia, jaundice, gallstones, and an increased risk of serious infections.
At present, there are no specific drugs or compounds available that specifically target ANK1 activity. However, researchers are actively investigating potential small molecules or compounds that could modulate ANK1 function. These studies aim to identify molecules that could interact with ANK1 or associated pathways to potentially develop targeted therapies for diseases associated with ANK1 dysfunction.
The treatment options for ANK1-related disorders depend on the specific disorder and its severity. In milder cases, regular monitoring of blood cell counts and managing symptoms, such as anemia, may be sufficient. For individuals with more severe symptoms, treatment may involve blood transfusions to address chronic anemia or surgical removal of the gallbladder in cases of gallstones. In some cases, splenectomy (surgical removal of the spleen) may be necessary to manage complications such as splenomegaly or to decrease the destruction of red blood cells. Genetic counseling is also recommended for affected individuals and their families to discuss the inheritance pattern and assess the risk of passing on the mutation.
Currently, there are no specific therapies targeting ANK1 protein. However, research efforts are underway to explore potential therapeutic strategies. In the case of hereditary spherocytosis and related disorders, treatment mainly focuses on managing the symptoms, such as anemia, through blood transfusions or splenectomy. Gene therapy approaches that aim to correct or replace the defective ANK1 gene are also being investigated as potential future treatments.
Apart from its role in maintaining cell shape and integrity, ANK1 protein has also been implicated in other cellular processes. It has been shown to interact with various ion channels and transporters, participating in the regulation of cell volume, membrane potential, and signal transduction in specific cell types. Additionally, ANK1 has been identified as a tumor suppressor gene and has been associated with certain types of cancer. However, further research is needed to fully understand these additional roles and their mechanisms.
Yes, there is ongoing research related to ANK1 protein. Scientists are studying the structure and function of ANK1 in more detail to gain a deeper understanding of its role in cellular processes and diseases. They are also investigating potential therapeutic approaches that target ANK1 or associated pathways. Additionally, further research is being conducted to explore the involvement of ANK1 in cancer development and progression.
Mutations in the ANK1 gene can cause various forms of hereditary spherocytosis, a condition characterized by abnormal red blood cell morphology leading to hemolytic anemia. In these cases, the ANK1 protein is either partially or completely deficient, leading to weakened interaction between the cytoskeleton and the plasma membrane, resulting in the loss of cell membrane integrity and increased susceptibility to cell rupture.
Apart from hereditary spherocytosis, ANK1 mutations have been associated with other related conditions, such as hereditary elliptocytosis and pyropoikilocytosis. These conditions involve abnormal red blood cell morphology, similar to spherocytosis. ANK1 mutations have also been linked to a rare neurological disorder known as spinocerebellar ataxia type 37 (SCA37), characterized by progressive cerebellar degeneration and ataxia. Additionally, there is emerging research suggesting a potential role of ANK1 in certain types of cancer, although more studies are needed to establish a clear association.
ANK1-related disorders, such as hereditary spherocytosis, are considered relatively rare. The exact prevalence is difficult to determine, as the disorder can vary in severity and may be underdiagnosed due to mild or atypical symptoms. It has been estimated that hereditary spherocytosis occurs in approximately 1 in 2,000 to 5,000 individuals, with some populations having higher prevalence rates. Other ANK1-related conditions, such as elliptocytosis, are even rarer. However, advances in genetic testing and increased awareness may lead to more accurate prevalence estimates in the future.
Yes, ANK1 mutations can be inherited in an autosomal dominant or autosomal recessive manner. In autosomal dominant inheritance, only one copy of the mutated ANK1 gene is necessary for the disorder to be inherited. This means that if a person has an affected parent, they have a 50% chance of inheriting the mutated gene and developing the disorder. In autosomal recessive inheritance, both copies of the ANK1 gene must be mutated for the disorder to be inherited. This means that both parents must be carriers of a mutated gene, and each child has a 25% chance of inheriting the disorder.
Customer Reviews (4)
Write a reviewWith their support, I can confidently explore the intricacies of ANK1 and make significant contributions to the understanding of its functions in various biological processes.
The manufacturer's excellent technical support, commitment to innovation, and customer-centric approach further reinforce its suitability for my research.
This existing knowledge base provides a solid foundation for designing experiments and interpreting results, ultimately enhancing the efficiency and reliability of trials involving ANK1 protein.
Extensive research has been conducted on ANK1, making it relatively accessible and well-understood in terms of its structure and functions.
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