AKT total + Phospho S473 FLOW Kit
Cat.No. : | Kit-0065 |
Product Overview : | Akt is a serine, threonine protein kinase critical in cellular metabolism, glucose uptake, protein synthesis, cell proliferation, growth, apoptosis, survival, angiogenesis, migration and invasion. It acts downstream of the phosphatidylinositol 3 kinase (PI3K) and it mediates the effects of several growth factors such as platelet-derived growth factor, epidermal growth factor and insulin growth factor. It is activated by phosphorylation on Ser-473, Thr-308 and Tyr-474 and when active it phosphorylates transcription factors (FOXO1), kinases (GSK-3, Raf-1, ASK, Chk1) and other signaling proteins (Bad, MDM2). There are three Akt isoforms (Akt1, Akt2 and Akt3) which share 80% sequence identity also known as PKBα, PKBβ and PKBγ. Akt has been shown to have a role in metabolism, apoptosis and proliferation and therefore it has been proposed to be the candidate "Warburg Kinase". |
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Size : | 50 tests |
Applications : | Flow Cytmore details |
Storage : | Store at +4°C. |
Products Types
◆ Assay kits | ||
Kit-0063 | AKT Activity Assay Kit | +Inquiry |
Kit-0064 | Akt kinase activity Kit | +Inquiry |
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 (21)
Ask a questionThere are three isoforms of AKT: AKT1 (PKBα), AKT2 (PKBβ), and AKT3 (PKBγ). Although they share similar structures and functions, they may have distinct roles in different tissues and cellular contexts.
The use of AKT inhibitors as single agents in cancer therapy has shown limited success due to the complex nature of the AKT signaling pathway and the presence of compensatory pathways. However, combining AKT inhibitors with other targeted therapies or conventional chemotherapy drugs may improve treatment outcomes by targeting multiple pathways simultaneously and overcoming resistance mechanisms.
Several inhibitors targeting AKT are currently being tested in clinical trials for cancer treatment. These include small molecule inhibitors like ipatasertib, capivasertib, and triciribine. Additionally, combinations of AKT inhibitors with other targeted therapies or chemotherapy are being investigated to enhance treatment efficacy.
Yes, there are several small molecule inhibitors that target AKT. These inhibitors can block the activation or activity of AKT and are being actively investigated as potential therapeutic agents for various cancers.
AKT has numerous downstream targets involved in various cellular processes. These targets include proteins involved in cell survival (e.g., BAD, caspase-9, FOXO), cell proliferation (e.g., TSC2, p27Kip1, mTOR), metabolism (e.g., GLUTs, enzymes in glycolysis and lipogenesis), and neuronal function (e.g., proteins involved in neurite outgrowth and synaptic plasticity).
Yes, AKT is involved in modulating immune responses. It participates in signaling pathways triggered by various immune receptors, such as T cell receptors and B cell receptors. AKT activation in immune cells can regulate cell survival, proliferation, differentiation, and cytokine production, thereby contributing to immune system homeostasis and response to pathogens.
AKT activation is tightly regulated by multiple mechanisms. One of the main regulation mechanisms is phosphorylation. AKT is activated by phosphorylation at two critical residues, Thr308 and Ser473. Various kinases, such as phosphoinositide-dependent kinase 1 (PDK1) and mammalian target of rapamycin complex 2 (mTORC2), phosphorylate AKT and initiate its activation.
The AKT signaling pathway can be activated by various factors, including growth factors, hormones, and cytokines. Activation usually occurs through the binding and activation of cell surface receptors, such as receptor tyrosine kinases (e.g., epidermal growth factor receptor or insulin receptor) or G-protein coupled receptors. Binding of these ligands to their receptors leads to receptor dimerization or conformational changes, which activate the intrinsic kinase activity of the receptors. Subsequently, the receptors phosphorylate specific tyrosine residues on themselves (autophosphorylation) or on other signaling molecules.
AKT phosphorylates numerous downstream targets, including but not limited to: mTOR (mammalian target of rapamycin), FOXO (forkhead box O) transcription factors, glycogen synthase kinase 3 (GSK3), and Bcl-2 family members. These targets mediate AKT's effects on cell growth, metabolism, survival, protein synthesis, and apoptosis regulation.
AKT plays a major role in promoting cell survival and protecting cells from apoptosis. It phosphorylates and inhibits pro-apoptotic proteins, such as BAD and caspase-9, while activating anti-apoptotic proteins, such as Bcl-2 and Bcl-XL. AKT also regulates the activity of transcription factors, such as FOXO, which control the expression of genes involved in cell survival and apoptosis.
Yes, AKT is involved in a wide range of physiological processes beyond cancer. It plays roles in embryonic development, insulin signaling and glucose metabolism, neuronal survival and function, inflammation, and immune responses.
Yes, AKT activation can stimulate cell proliferation. It promotes the entry of cells into the cell cycle by phosphorylating and inactivating proteins that negatively regulate the cell cycle, such as tuberous sclerosis complex 2 (TSC2) and p27Kip1. AKT also enhances protein translation and synthesis through direct phosphorylation of targets involved in protein synthesis, such as mTOR.
AKT can be activated by various stimuli, such as growth factors, hormones, and extracellular signals. Activation typically involves phosphorylation of specific amino acid residues within the AKT protein.
Dysregulation of AKT signaling is frequently observed in cancer. Abnormal activation of AKT can promote uncontrolled cell growth, resistance to apoptosis, and metastasis, contributing to tumor development and progression.
Yes, AKT activation is often associated with drug resistance in cancer cells. It can promote cell survival and counteract the effects of chemotherapy and targeted therapies. Consequently, targeting AKT signaling pathways has emerged as a potential strategy to overcome drug resistance and improve treatment outcomes.
AKT plays important roles in neuronal development, survival, and function. It is involved in promoting neurite outgrowth and axon regeneration. AKT signaling also regulates synaptic plasticity and neurotransmitter release. Dysregulation of AKT signaling has been implicated in various neurological disorders, including Alzheimer's disease and Parkinson's disease.
AKT is a promising target for cancer therapy due to its crucial role in cell survival, proliferation, and resistance to treatment. Multiple approaches have been explored to target AKT, including small molecule inhibitors and antibody-based therapies. Small molecule inhibitors, such as allosteric inhibitors and ATP-competitive inhibitors, have been developed to block AKT activity. Additionally, antibody-based therapies, such as monoclonal antibodies targeting AKT or its upstream regulators, have been investigated to inhibit AKT signaling.
Yes, AKT has been implicated in the regulation of aging. Studies have shown that AKT activity can modulate cellular senescence, lifespan, and age-related pathological conditions. AKT's role in regulating processes such as metabolism and cellular stress responses may contribute to its impact on aging.
Several signaling pathways and molecules can activate AKT. Growth factors, such as insulin-like growth factor 1 (IGF-1) and epidermal growth factor (EGF), activate AKT by binding to their receptors and initiating downstream signaling cascades. Phosphatidylinositol 3-kinase (PI3K) is a critical mediator of AKT activation, as it produces phosphatidylinositol (3,4,5)-trisphosphate (PIP3), which recruits AKT to the plasma membrane for phosphorylation and activation.
Yes, dysregulation of the AKT signaling pathway is commonly observed in cancer and can contribute to tumorigenesis. Abnormal activation of AKT can lead to uncontrolled cell proliferation, evasion of apoptosis, enhanced angiogenesis, and increased metastatic potential. AKT pathway alterations, such as activating mutations in AKT genes or genetic alterations in upstream regulators or downstream effectors, are frequently found in various types of cancer.
Yes, mutations or aberrant activation of AKT isoforms have been linked to several genetic disorders. For example, AKT2 mutations are associated with insulin resistance and type 2 diabetes. AKT1 and AKT3 mutations have been found in some cases of Proteus syndrome and megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH).
Customer Reviews (4)
Write a reviewIts high purity and stability ensure reliable and reproducible results, which are paramount for achieving meaningful scientific outcomes.
With the AKT protein's high-quality composition and reliability, researchers can confidently proceed with their studies, knowing that they have access to a protein that consistently delivers accurate results.
Whether measuring analyte concentrations, screening for specific interactions, or monitoring immune responses, this protein's exceptional performance in ELISA experiments is truly commendable.
The AKT protein is renowned for its outstanding quality, making it an optimal choice to fulfill the requirements of my experimental investigations.
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