Recombinant Full Length Dog Aquaporin-2(Aqp2) Protein, His-Tagged
Cat.No. : | RFL-8058CF |
Product Overview : | Recombinant Full Length Dog Aquaporin-2(AQP2) Protein (P79144) (1-109aa), fused to N-terminal His tag, was expressed in E. coli. |
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Source : | E.coli expression system |
Species : | Canis lupus familiaris (Dog) (Canis familiaris) |
Tag : | His |
Form : | Lyophilized powder |
Protein length : | Full Length (1-109) |
AA Sequence : | SVAFSRAVFAEFLATLLFVFFGLGS ALNWPQALPSVLQIAMAFGLGIGTL VQALGHVSGAHINPAVTVACLVGCH VSFLRAAFYVAAQLLGAVAGAALLH EITPPHVRG |
Purity : | Greater than 90% as determined by SDS-PAGE. |
Applications : | SDS-PAGE |
Notes : | Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week. |
Storage : | Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles. |
Storage Buffer : | Tris/PBS-based buffer, 6% Trehalose, pH 8.0 |
Reconstitution : | We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference. |
Gene Name : | AQP2 |
Synonyms : | AQP2; Aquaporin-2; AQP-2; ADH water channel; Aquaporin-CD; AQP-CD; Collecting duct water channel protein; WCH-CD; Water channel protein for renal collecting duct; Fragment |
UniProt ID : | P79144 |
Gene Name : | AQP2 |
Synonyms : | AQP2; Aquaporin-2; AQP-2; ADH water channel; Aquaporin-CD; AQP-CD; Collecting duct water channel protein; WCH-CD; Water channel protein for renal collecting duct; Fragment |
UniProt ID : | P79144 |
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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 (26)
Ask a questionYes, AQP2-related disorders can be inherited. Some forms of nephrogenic diabetes insipidus (NDI) are caused by genetic mutations in the AQP2 gene, which can be inherited from one or both parents. These genetic mutations result in impaired or absent functional AQP2 channels, leading to the development of NDI.
Yes, AQP2-related disorders can be inherited. Some forms of nephrogenic diabetes insipidus (NDI) are caused by genetic mutations in the AQP2 gene, which can be inherited from one or both parents. These genetic mutations result in impaired or absent functional AQP2 channels, leading to the development of NDI.
Yes, AQP2-related disorders can affect individuals of any age. Some forms of AQP2 dysfunction, like congenital nephrogenic diabetes insipidus (NDI), may be present from birth and can affect infants and young children. On the other hand, acquired forms of NDI can develop later in life due to factors such as medication side effects, genetic mutations, kidney damage, or other medical conditions. It is important to consider the potential presence of AQP2-related disorders in individuals of all ages who present with symptoms such as excessive thirst, frequent urination, and electrolyte imbalances.
Yes, AQP2-related disorders can affect individuals of any age. Some forms of AQP2 dysfunction, like congenital nephrogenic diabetes insipidus (NDI), may be present from birth and can affect infants and young children. On the other hand, acquired forms of NDI can develop later in life due to factors such as medication side effects, genetic mutations, kidney damage, or other medical conditions. It is important to consider the potential presence of AQP2-related disorders in individuals of all ages who present with symptoms such as excessive thirst, frequent urination, and electrolyte imbalances.
Yes, AQP2 undergoes several post-translational modifications, including phosphorylation and ubiquitination. Phosphorylation plays a critical role in the intracellular trafficking and translocation of AQP2 to the cell membrane, while ubiquitination is involved in the degradation of AQP2.
Yes, lifestyle modifications can be helpful in managing AQP2-related disorders, especially in conditions like nephrogenic diabetes insipidus (NDI). These modifications may include ensuring adequate fluid intake to prevent dehydration, dietary adjustments to maintain electrolyte balance, and avoiding excessive alcohol and caffeine consumption, which can increase urine production. It is always important to consult with a healthcare professional for personalized recommendations based on the specific condition and individual needs.
Yes, lifestyle modifications can be helpful in managing AQP2-related disorders, especially in conditions like nephrogenic diabetes insipidus (NDI). These modifications may include ensuring adequate fluid intake to prevent dehydration, dietary adjustments to maintain electrolyte balance, and avoiding excessive alcohol and caffeine consumption, which can increase urine production. It is always important to consult with a healthcare professional for personalized recommendations based on the specific condition and individual needs.
AQP2 dysfunction can result in an imbalance of electrolytes such as sodium and potassium. In conditions like nephrogenic diabetes insipidus (NDI), where AQP2 is impaired, there is impaired water reabsorption and excessive urinary output. This can lead to dehydration and subsequent electrolyte imbalances, including hyponatremia (low sodium levels) and hyperkalemia (high potassium levels).
AQP2 dysfunction can result in an imbalance of electrolytes such as sodium and potassium. In conditions like nephrogenic diabetes insipidus (NDI), where AQP2 is impaired, there is impaired water reabsorption and excessive urinary output. This can lead to dehydration and subsequent electrolyte imbalances, including hyponatremia (low sodium levels) and hyperkalemia (high potassium levels).
The potential complications and long-term effects of AQP2-related disorders can vary depending on the specific condition and its severity. In conditions like nephrogenic diabetes insipidus (NDI), if left untreated or poorly managed, there is an increased risk of dehydration, electrolyte imbalances, and kidney damage. These complications can lead to symptoms such as fatigue, muscle weakness, dizziness, and in severe cases, kidney failure. It is important for individuals with AQP2-related disorders to receive proper medical care and ongoing management to prevent and address these potential complications.
The potential complications and long-term effects of AQP2-related disorders can vary depending on the specific condition and its severity. In conditions like nephrogenic diabetes insipidus (NDI), if left untreated or poorly managed, there is an increased risk of dehydration, electrolyte imbalances, and kidney damage. These complications can lead to symptoms such as fatigue, muscle weakness, dizziness, and in severe cases, kidney failure. It is important for individuals with AQP2-related disorders to receive proper medical care and ongoing management to prevent and address these potential complications.
AQP2 plays a vital role in the urine concentrating mechanism in the kidneys. When vasopressin is released, AQP2 translocates from intracellular vesicles to the apical membrane of collecting duct cells. This process increases the permeability of water, allowing it to be reabsorbed from the urine back into the bloodstream, concentrating the urine.
AQP2 plays a vital role in the urine concentrating mechanism in the kidneys. When vasopressin is released, AQP2 translocates from intracellular vesicles to the apical membrane of collecting duct cells. This process increases the permeability of water, allowing it to be reabsorbed from the urine back into the bloodstream, concentrating the urine.
Mutations or dysregulation of AQP2 can lead to several disorders related to water balance, including nephrogenic diabetes insipidus (NDI). This condition impairs the kidney's ability to concentrate urine, resulting in excessive thirst and urination.
Yes, research on AQP2-related disorders is ongoing. Scientists are studying various aspects such as the molecular mechanisms behind AQP2 regulation, the development of targeted therapies for AQP2 dysfunction, and the identification of genetic mutations associated with these disorders. Furthermore, advancements in genetic testing techniques have allowed for better diagnosis and classification of AQP2-related disorders, leading to improved patient management and personalized treatment approaches.
Yes, research on AQP2-related disorders is ongoing. Scientists are studying various aspects such as the molecular mechanisms behind AQP2 regulation, the development of targeted therapies for AQP2 dysfunction, and the identification of genetic mutations associated with these disorders. Furthermore, advancements in genetic testing techniques have allowed for better diagnosis and classification of AQP2-related disorders, leading to improved patient management and personalized treatment approaches.
Yes, mutations in the AQP2 gene can cause hereditary nephrogenic diabetes insipidus (NDI), a condition characterized by the inability of the kidneys to concentrate urine. These mutations can affect AQP2 synthesis, trafficking, or function, leading to decreased water reabsorption and excessive urination.
Currently, there is no known cure for AQP2-related disorders. However, effective management and treatment approaches can significantly improve the quality of life for individuals with these conditions. Depending on the specific disorder, treatments may include medication, dietary modifications, fluid management, and addressing any underlying causes or contributing factors. Ongoing research aims to develop more targeted therapies and interventions to better manage and potentially reverse AQP2 dysfunction, but as of now, the focus is on symptom management and preventing complications.
Currently, there is no known cure for AQP2-related disorders. However, effective management and treatment approaches can significantly improve the quality of life for individuals with these conditions. Depending on the specific disorder, treatments may include medication, dietary modifications, fluid management, and addressing any underlying causes or contributing factors. Ongoing research aims to develop more targeted therapies and interventions to better manage and potentially reverse AQP2 dysfunction, but as of now, the focus is on symptom management and preventing complications.
Several physiological conditions can affect AQP2 expression. For example, dehydration stimulates the release of vasopressin, leading to increased AQP2 expression and water reabsorption. On the other hand, excessive water intake or the use of certain medications, such as diuretics, can suppress AQP2 expression, resulting in increased urine output.
Targeting AQP2 could potentially be useful in the treatment of certain water balance disorders. For instance, pharmacological agents that enhance AQP2 expression or function may be beneficial in patients with nephrogenic diabetes insipidus. However, further research is needed to develop specific and safe therapeutic strategies.
AQP2 is a specific member of the aquaporin family, characterized by its expression primarily in the kidney and involvement in water reabsorption. It differs from other aquaporin proteins in terms of its tissue distribution, regulation, and function.
The treatment options for AQP2-related disorders depend on the specific condition. In nephrogenic diabetes insipidus (NDI), medication options may include thiazide diuretics, which reduce urine production, or nonsteroidal anti-inflammatory drugs (NSAIDs) that can increase the responsiveness of the kidneys to vasopressin. In some cases, dietary adjustments and fluid management are also prescribed. However, the specific treatment plan will be determined by a healthcare professional and tailored to the individual patient's needs.
The treatment options for AQP2-related disorders depend on the specific condition. In nephrogenic diabetes insipidus (NDI), medication options may include thiazide diuretics, which reduce urine production, or nonsteroidal anti-inflammatory drugs (NSAIDs) that can increase the responsiveness of the kidneys to vasopressin. In some cases, dietary adjustments and fluid management are also prescribed. However, the specific treatment plan will be determined by a healthcare professional and tailored to the individual patient's needs.
Certain compounds, such as synthetic vasopressin analogs (vasopressin agonists) or vasopressin receptor antagonists, can modulate AQP2 expression or function indirectly by affecting the release or binding of vasopressin. These medications are used in the treatment of water balance disorders or conditions where AQP2 dysregulation is involved.
Vasopressin release is triggered by changes in blood osmolality or volume. When the osmolality increases or blood volume decreases, osmoreceptors or baroreceptors in the body signal the release of vasopressin. Vasopressin then binds to its receptor in the kidney, activating the intracellular cAMP signaling pathway. This pathway leads to phosphorylation of AQP2 and its subsequent translocation to the cell membrane, increasing water reabsorption.
Customer Reviews (5)
Write a reviewThis can be particularly important in clinical trials to ensure accurate and reliable results.
Their prompt assistance and guidance contribute to enhancing the success and efficiency of my work with the AQP2 protein.
Manufacturers may provide documentation of the protein's validation, which includes information about its purity, concentration, stability, and potential contaminants.
They can assist in identifying the most suitable experimental protocols or provide recommendations for optimal usage.
Manufacturers can provide researchers with purified and validated AQP2 protein, ensuring its quality and reliability for use in experiments and trials.
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