Recombinant Mouse AKT3 cell lysate

• Cat.No.: AKT3-001MCL
• Product Overview: Mouse AKT3 (aa 106-479) derived in Baculovirus-Insect cells. The whole cell lysate is provided in 1X Sample Buffer.Browse all transfected cell lysate positive controls

Specification

• Source: Baculovirus-Insect Cells
• Species: Mouse
• 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
• Protein length: 106-479

Gene Information

• Gene Name: Akt3 thymoma viral proto-oncogene 3 [ Mus musculus ]
• Official Symbol: AKT3
• Synonyms: AKT3; thymoma viral proto-oncogene 3; RAC-gamma serine/threonine-protein kinase; PKB gamma; RAC-PK-gamma; protein kinase Akt-3; protein kinase B gamma; Nmf350; AI851531; D930002M15Rik
• Gene ID: 23797
• mRNA Refseq: NM_011785
• Protein Refseq: NP_035915
• Pathway: Acute myeloid leukemia, organism-specific biosystem; Acute myeloid leukemia, conserved biosystem; Adipocytokine signaling pathway, organism-specific biosystem; Adipocytokine signaling pathway, conserved biosystem; Apoptosis, organism-specific biosystem; Apoptosis, conserved biosystem; Apoptosis signaling pathway, organism-specific biosystem
• Function: ATP binding; kinase activity; nucleotide binding; phospholipid binding; protein kinase C binding; protein kinase activity; protein serine/threonine kinase activity; transferase activity; transferase activity, transferring phosphorus-containing groups

Reviews

03/25/2023

I am confident that utilizing the AKT3 protein will empower me to uncover crucial insights into cellular mechanisms with precision.

12/31/2022

The AKT3 protein is an exceptional protein solution that exceeds expectations in terms of quality and suitability for my experimental requirements.

12/22/2020

Their expertise and guidance will undoubtedly prove valuable in overcoming hurdles and maximizing the potential of this protein in my research endeavors.

07/29/2016

In addition to its outstanding quality, the AKT3 protein comes with exceptional technical support from its manufacturer.

02/01/2016

Researchers can confidently rely on this high-quality protein to produce accurate and reproducible results, thereby accelerating their research progress

Q&As

What are the implications of AKT3 dysregulation?

Dysregulation of AKT3 activity is associated with various human diseases, including cancer, diabetes, neurodegenerative disorders, and cardiovascular diseases. Overactivation of AKT3 can promote uncontrolled cell growth and survival, a hallmark of cancer. In contrast, reduced AKT3 activity is linked to insulin resistance and type 2 diabetes.

Is AKT3 exclusively expressed in certain cell types or can it be found in multiple cell types?

AKT3 is not exclusively expressed in specific cell types and can be found in multiple cell types. While it is abundantly expressed in neuronal tissues and plays a role in brain development, AKT3 is also expressed in other cell types, including epithelial cells, endothelial cells, and immune cells.

Are there any known diseases or disorders associated with dysregulation of AKT3?

Yes, dysregulation of AKT3 has been implicated in a variety of diseases and disorders. As mentioned earlier, genetic mutations in AKT3 are associated with diseases such as Proteus syndrome and megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome. Additionally, dysregulation of AKT3 has been observed in various types of cancer, including breast, ovarian, colorectal, and lung cancer, where it promotes cell survival, proliferation, and resistance to therapies. Altered AKT3 activity has also been implicated in neurological disorders such as autism spectrum disorder and epilepsy.

Are there any ongoing clinical trials targeting AKT3?

Yes, there are ongoing clinical trials investigating AKT inhibitors that target the AKT pathway, which includes AKT3. These trials are evaluating the efficacy and safety of AKT inhibitors in various cancer types, such as breast, ovarian, lung, and prostate cancer.

Are there any drugs targeting AKT3 currently available?

As of now, there are no FDA-approved drugs specifically targeting AKT3. However, there are several ongoing preclinical and clinical studies investigating the efficacy of AKT inhibitors that could potentially target AKT3 in various diseases, including cancer. Some of these compounds include MK-2206, AZD5363, GSK2141795, and ipatasertib.

What are the downstream targets of AKT3?

AKT3 phosphorylates and modulates the activity of numerous downstream targets involved in cell survival and growth regulation. Examples include the anti-apoptotic protein Bcl-2, the mammalian target of rapamycin (mTOR), glycogen synthase kinase-3 (GSK-3), and several transcription factors, such as forkhead box O (FOXO) and nuclear factor kappa B (NF-κB).

Is AKT3 expressed in all tissues of the body?

AKT3 is expressed in a wide range of tissues but its expression levels may vary among different tissues. For instance, AKT3 is more abundantly expressed in the brain, heart, and skeletal muscles compared to other tissues. However, it is important to note that the expression levels of AKT3 can be dynamically regulated depending on cellular context, developmental stage, and environmental cues.

Can AKT3 inhibitors be used in combination with other cancer treatments?

Yes, AKT3 inhibitors can potentially be used in combination with other cancer treatments to enhance their efficacy. Preclinical studies have shown that combining AKT inhibitors with chemotherapy drugs or targeted therapies can improve anti-tumor effects. For example, combining AKT inhibitors with HER2-targeted therapies has been explored in HER2-positive breast cancer. Additionally, AKT inhibitors may also sensitize tumors to radiation therapy. However, more research is needed to optimize the combination strategies and determine the most effective treatment regimens.

Can AKT3 inhibitors be used to treat other diseases besides cancer?

AKT3 inhibitors primarily have been studied in the context of cancer treatment, but the AKT pathway is involved in various physiological and pathological processes beyond cancer. As a result, AKT inhibitors have been explored for potential therapeutic applications in other diseases.

Can AKT3 be regulated by other signaling pathways?

Yes, AKT3 can be regulated by various signaling pathways apart from its canonical activation through growth factors. For example, AKT3 can be activated by insulin signaling, which plays a crucial role in glucose metabolism and cellular energy homeostasis. AKT3 can also be influenced by other pathways such as the AMP-activated protein kinase (AMPK) pathway, which regulates cellular energy status, and the Wnt pathway, which is involved in cell proliferation and differentiation.

Are there any genetic mutations associated with AKT3?

Yes, genetic mutations in the AKT3 gene have been identified in rare human diseases. One well-known condition associated with AKT3 mutations is Proteus syndrome, a complex and highly variable disorder characterized by overgrowth of various tissues. AKT3 mutations are also found in a condition called megalencephaly-polymicrogyria-polydactyly-hydrocephalus syndrome (MPPH), which is characterized by overgrowth of the brain, abnormal brain development, and other features.

How is AKT3 activated?

AKT3 is activated through a phosphorylation cascade. Upon stimulation by growth factors or other extracellular signals, phosphoinositide-dependent kinase-1 (PDK1) phosphorylates AKT3 at threonine 308. This partially activates AKT3. Full activation of AKT3 requires phosphorylation at serine 473, which is carried out by the mammalian target of rapamycin complex 2 (mTORC2).

Are there any known alternative splicing variants of AKT3?

Yes, alternative splicing events can generate different isoforms of AKT3. One example is AKT3β, which lacks a portion of the N-terminal regulatory region compared to the full-length AKT3α isoform. These isoforms may have distinct functions and regulatory mechanisms, although further research is needed to fully understand their specific roles.

Are there any specific mutations or alterations in AKT3 that are associated with cancer?

Yes, alterations in AKT3 have been identified in various types of cancer. These alterations include genetic mutations, gene amplifications, and overexpression of AKT3. For example, AKT3 mutations have been reported in certain types of human cancers, such as endometrial cancer and melanoma.

Is AKT3 involved in any cellular processes besides cell survival and growth?

Yes, AKT3 is involved in a variety of cellular processes besides cell survival and growth. It plays a role in regulating cellular metabolism, including glucose uptake and lipid metabolism. AKT3 is also involved in cell migration and invasion, as well as the regulation of cell cycle progression and apoptosis. Additionally, AKT3 has been implicated in neuronal development and synaptic plasticity, playing a role in brain development and function.

Are there any known interactions between AKT3 and other proteins or signaling pathways?

Yes, AKT3 interacts with a wide range of proteins and signaling pathways. It can interact with various upstream activators, such as PI3K, PDK1, and mTORC2, to be phosphorylated and activated. AKT3 can also interact with numerous downstream effectors, including mTOR, GSK3, FOXO transcription factors, and Bad, among others. Additionally, AKT3 can be regulated by cross-talk with other signaling pathways, such as MAPK, NF-κB, and Wnt signaling, which can modulate its activity and downstream functions.

Can AKT3 inhibition alone be sufficient for cancer treatment or is it often combined with other therapies?

While AKT3 inhibition has shown promise as a potential cancer treatment strategy, it is often used in combination with other therapies. The AKT pathway is complex and interconnected with various cellular processes, and targeting only AKT3 may not be sufficient to fully inhibit AKT signaling in all contexts. Additionally, combination therapies can help overcome potential resistance mechanisms and enhance treatment efficacy. Therefore, AKT3 inhibitors are frequently investigated in combination with chemotherapy, targeted therapies, immunotherapy, or radiation therapy to determine the optimal treatment strategies for different cancer types.

Can AKT3 be therapeutically targeted in diseases?

Yes, targeting AKT3 therapeutically is an active area of research, especially in the context of cancer treatment. Several AKT inhibitors are being developed and tested in preclinical and clinical studies with the aim of blocking AKT3-mediated signaling and inhibiting tumor growth. However, it is important to note that AKT is also essential for normal cellular functions, so the development of selective inhibitors that specifically target the disease-associated dysregulation of AKT3 without affecting normal AKT activity is crucial.

Can AKT3 be targeted therapeutically?

AKT3 has been under investigation as a potential target for therapeutic intervention. Inhibitors of AKT3 and its upstream regulators are being developed to selectively inhibit aberrant AKT3 signaling in diseases such as cancer. However, more research is needed to fully understand the complexities of AKT3 signaling and improve the specificity and efficacy of AKT3-targeted therapies.

Are there any potential side effects or limitations associated with AKT3 inhibition?

While AKT3 inhibitors show promise as potential therapeutics, they can also have side effects and limitations. AKT is crucial for normal cellular functions, so inhibiting its activity may affect normal physiological processes.