Recombinant Human AKT1 cell lysate
Cat.No. : | AKT1-677HCL |
Product Overview : | Human AKT1 / PKB / PKBα derived in Baculovirus-Insect cells. The whole cell lysate is provided in 1X Sample Buffer.Browse all transfected cell lysate positive controls |
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Source : | Baculovirus-Insect Cells |
Species : | Human |
Preparation method : | Transfected cells were cultured for 48hrs before collection. The cells were lysed in modified RIPA buffer with cocktail of protease inhibitors. Cell debris was removed by centrifugation and then centrifuged to clarify the lysate. The cell lysate was boiled for 5 minutes in 1 x SDS sample buffer (50 mM Tris-HCl pH 6.8, 12.5% glycerol, 1% sodium dodecylsulfate, 0.01% bromophenol blue) containing 5% b-mercaptoethanol, and lyophilized. |
Lysis buffer : | Modified RIPA Lysis Buffer: 50 mM Tris-HCl pH 7.4, 150 mM NaCl, 1mM EDTA, 1% Triton X-100, 0.1% SDS, 1% Sodium deoxycholate, 1mM PMSF |
Quality control Testing : | 12.5% SDS-PAGE Stained with Coomassie Blue |
Recommended Usage : | 1. Centrifuge the tube for a few seconds and ensure the pellet at the bottom of the tube.2. Re-dissolve the pellet using 200μL pure water and boiled for 2-5 min.3. Store it at -80°C. Recommend to aliquot the cell lysate into smaller quantities for optimal storage. Avoid repeated freeze-thaw cycles.Notes:The lysate is ready to load on SDS-PAGE for Western blot application. If dissociating conditions are required, add reducing agent prior to heating. |
Stability : | Samples are stable for up to twelve months from date of receipt at -80°C |
Storage Buffer : | 50 mM Tris-HCl pH 7.4, 150 mM NaCl, 1mM EDTA, 1% Triton X-100, 0.1% SDS, 1% Sodium deoxycholate, 1mM PMSF |
Storage Instruction : | Lysate samples are stable for 12 months from date of receipt when stored at -80°C. Avoid repeated freeze-thaw cycles. Prior to SDS-PAGE fractionation, boil the lysate for 5 minutes. |
Tag : | Non |
Gene Name : | AKT1 v-akt murine thymoma viral oncogene homolog 1 [ Homo sapiens ] |
Official Symbol : | AKT1 |
Synonyms : | AKT1; v-akt murine thymoma viral oncogene homolog 1; RAC-alpha serine/threonine-protein kinase; AKT; PKB; PRKBA; RAC; PKB alpha; RAC-PK-alpha; proto-oncogene c-Akt; protein kinase B alpha; rac protein kinase alpha; PKB-ALPHA; RAC-ALPHA; MGC99656; |
Gene ID : | 207 |
mRNA Refseq : | NM_001014431 |
Protein Refseq : | NP_001014431 |
MIM : | 164730 |
UniProt ID : | P31749 |
Chromosome Location : | 14q32.32-q32.33 |
Pathway : | AKT phosphorylates targets in the cytosol, organism-specific biosystem; AKT phosphorylates targets in the nucleus, organism-specific biosystem; AKT-mediated inactivation of FOXO1A, organism-specific biosystem; Activation of BAD and translocation to mitochondria, organism-specific biosystem; Activation of BH3-only proteins, organism-specific biosystem; Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; |
Function : | ATP binding; ATP binding; enzyme binding; identical protein binding; kinase activity; nitric-oxide synthase regulator activity; nucleotide binding; phosphatidylinositol-3,4,5-trisphosphate binding; phosphatidylinositol-3,4-bisphosphate binding; protein binding; protein kinase activity; protein serine/threonine kinase activity; protein serine/threonine kinase activity; |
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Write a reviewThe manufacturer's dedicated and knowledgeable support team is readily available to address any concerns, provide guidance, and offer timely solutions.
Q&As (13)
Ask a questionYes, several drugs and agents have been developed to specifically target AKT1. These include small molecule inhibitors that directly target the kinase activity of AKT1. Examples of AKT1 inhibitors currently under investigation or in clinical trials include MK-2206, ipatasertib, and capivasertib. These inhibitors aim to block the activation of AKT1 and disrupt its downstream signaling pathways.
Yes, there are inhibitors that specifically target the activity of AKT1 protein. Small molecule inhibitors, such as MK-2206 and GSK690693, have been developed to block AKT1 activation and downstream signaling. These inhibitors are being studied as potential therapeutic agents for cancer treatment. Additionally, certain natural compounds, including resveratrol and curcumin, have been reported to inhibit AKT1 activity and exhibit anti-tumor effects.
Mutations in AKT1 have been implicated in certain diseases. For example, somatic mutations in AKT1 have been found in a subset of human cancers, such as breast, ovarian, and colorectal cancers. These mutations can lead to constitutive activation of AKT1, contributing to tumor development. Moreover, germline mutations in AKT1 have been linked to a rare genetic disorder called Proteus syndrome, characterized by asymmetric and progressive overgrowth of various tissues.
Yes, combining AKT1 inhibitors with other therapies is being investigated as a potential strategy for cancer treatment. AKT1 inhibition can enhance the efficacy of conventional chemotherapy agents or targeted therapies. For example, combining AKT1 inhibitors with inhibitors of the phosphoinositide 3-kinase (PI3K)/mTOR pathway, which upstream regulates AKT1, could provide a more comprehensive blockade of the pathway. Additionally, AKT1 inhibitors have also been tested in combination with immune checkpoint inhibitors to enhance immune response against tumors. Such combination approaches aim to improve treatment outcomes and overcome drug resistance mechanisms.
AKT1 signaling regulates numerous downstream targets involved in diverse cellular processes. Some of the well-known targets include the mammalian target of rapamycin (mTOR), which plays a role in protein synthesis and cell growth, and the pro-apoptotic protein Bad, which AKT1 phosphorylates to prevent apoptosis. AKT1 also phosphorylates and inactivates the transcription factor Forkhead box protein O (FOXO), which regulates genes involved in apoptosis, cell cycle arrest, and oxidative stress response. Other downstream targets of AKT1 include glycogen synthase kinase 3 (GSK3), nuclear factor-kappa B (NF-kB), and endothelial nitric oxide synthase (eNOS), among others.
Yes, AKT1 protein has the potential to be a therapeutic target for conditions beyond cancer. Due to its role in insulin signaling and glucose metabolism, targeting AKT1 activity could be beneficial in treating metabolic disorders such as type 2 diabetes. Strategies aimed at increasing AKT1 activity and sensitivity to insulin are being explored.
Targeting AKT1 mutations is an active area of research for therapeutic development. Due to the involvement of AKT1 in cancer progression, efforts are being made to develop specific inhibitors that can selectively target mutant AKT1 forms. Clinical trials are being conducted to investigate the efficacy of AKT inhibitors in patients harboring AKT1 mutations in various cancers. However, further research is still needed to fully understand the implications and potential therapeutic strategies for AKT1 mutations.
AKT1 protein is involved in numerous cellular processes. Some of its key functions include promoting cell survival by inhibiting apoptosis (programmed cell death), regulating cell growth and proliferation, and participating in glucose metabolism. It is also involved in the regulation of protein synthesis, cell cycle progression, DNA repair, and cellular migration.
Yes, certain natural compounds and dietary factors have been found to modulate AKT1 activity. For example, resveratrol, a polyphenol found in grapes and red wine, has been shown to inhibit AKT1 signaling and induce apoptosis in cancer cells. Curcumin, a compound found in turmeric, has also been reported to inhibit AKT1 activation and suppress tumor growth.
AKT1 protein is activated by a process called phosphorylation. When growth factor receptors, such as insulin receptors or receptor tyrosine kinases, are stimulated by their ligands, it triggers the activation of phosphoinositide 3-kinase (PI3K). PI3K then converts phosphatidylinositol 4,5-bisphosphate (PIP2) into phosphatidylinositol 3,4,5-trisphosphate (PIP3). PIP3 acts as a second messenger and recruits AKT1 to the cell membrane.
Yes, AKT1 mutations can contribute to drug resistance in cancer treatment. Mutations in AKT1 can lead to constitutive activation of its signaling pathway, rendering cancer cells resistant to targeted therapies that rely on inhibiting AKT1. For example, tumors with activating mutations in AKT1 may not respond to AKT1 inhibitors. Additionally, mutations in AKT1 or its upstream regulators such as PI3K can bypass the inhibitory effects of targeted therapies.
The activity of AKT1 protein is regulated through various mechanisms. In addition to phosphorylation, which activates AKT1, there are several factors that can modulate its activity. One important regulator is phosphatase and tensin homolog (PTEN), which dephosphorylates PIP3 and limits AKT1 activation. Other regulatory proteins, such as protein phosphatase 2A (PP2A) and protein kinase C (PKC), can also influence AKT1 activity by dephosphorylating or phosphorylating AKT1, respectively.
Dysregulation of AKT1 has been associated with various diseases and conditions. Apart from its prominent role in cancer, altered AKT1 signaling has been implicated in metabolic disorders such as diabetes and obesity. Reduced AKT1 activity is observed in insulin resistance, whereby insulin stimulation of AKT1-mediated glucose uptake is impaired. AKT1 dysregulation has also been linked to neurological disorders, including Alzheimer's disease and schizophrenia. Abnormal AKT1 signaling has been implicated in synaptic dysfunction, neuronal survival, and cognitive impairment associated with these conditions. Further research is needed to fully understand the mechanisms and implications of AKT1 dysregulation in these diseases.
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