AKT3
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Official Full Name
v-akt murine thymoma viral oncogene homolog 3 (protein kinase B, gamma)
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Overview
The protein encoded by this gene is a member of the AKT, also called PKB, serine/threonine protein kinase family. AKT kinases are known to be regulators of cell signaling in response to insulin and growth factors. They are involved in a wide variety of biological processes including cell proliferation, differentiation, apoptosis, tumorigenesis, as well as glycogen synthesis and glucose uptake. This kinase has been shown to be stimulated by platelet-derived growth factor (PDGF), insulin, and insulin-like growth factor 1 (IGF1). Alternatively splice transcript variants encoding distinct isoforms have been described. -
Synonyms
AKT3; v-akt murine thymoma viral oncogene homolog 3 (protein kinase B, gamma); PKBG; PRKBG; STK-2; PKB-GAMMA; RAC-gamma; RAC-PK-gamma; DKFZp434N0250; RAC-gamma serine/threonine-protein kinase; PKB gamma; OTTHUMP00000037911; OTTHUMP00000037912; protein kinase Akt-3; protein kinase B gamma; serine threonine protein kinase, Akt-3;
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- Involved Pathway
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- AKT3 Related Signal Pathway
AKT3 involved in several pathways and played different roles in them. We selected most pathways AKT3 participated on our site, such as AKT phosphorylates targets in the cytosol, AKT phosphorylates targets in the nucleus, AKT-mediated inactivation of FOXO1A, which may be useful for your reference. Also, other proteins which involved in the same pathway with AKT3 were listed below. Creative BioMart supplied nearly all the proteins listed, you can search them on our site.
Pathway Name | Pathway Related Protein |
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AKT phosphorylates targets in the cytosol | CDKN1B;CDKN1A;CHUK;AKT3 |
AKT phosphorylates targets in the nucleus | CREB1;CREB1B;AKT3 |
AKT-mediated inactivation of FOXO1A | |
AMPK signaling pathway | EEF2;SREBF1;CPT1A;PPP2R2D;EIF4EBP1;CAB39L;PIK3R5;AKT2;CREB3 |
Activation of BAD and translocation to mitochondria | YWHAQ;CDK5RAP2;AKT3 |
Activation of BH3-only proteins | YWHAQ;DYNLL2;AKT3;CDK5RAP2;E2F1;BCL2L11 |
Acute myeloid leukemia | STAT5A;FLT3;MYC;CCNA1;CHUK;SFPI1;EIF4EBP1;IKBKB;ARAF |
Adaptive Immune System | KLRB1A;OSBPL1A;CTSO;NPEPPS;LRR1;FCGR1B;CD200R1;FRS2;CD200 |
AKT3 has several biochemical functions, for example, ATP binding, protein binding, protein kinase activity. Some of the functions are cooperated with other proteins, some of the functions could acted by AKT3 itself. We selected most functions AKT3 had, and list some proteins which have the same functions with AKT3. You can find most of the proteins on our site.
Function | Related Protein |
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ATP binding | RIMKLA;NEK10;SMG1;CAMK1D;MAP3K9;PTK2B;CCT8;CAMK4;PAK2B |
protein binding | SOX1;EDA;ATXN7;DAXX;MPP5;SPC25;PGF;FYB;SF3B2 |
protein kinase activity | MAP3K2;BMPR1BB;CSNK1D;CDK5R1;BMPR1AB;GM7168;PAK2B;GC3;SLKA |
protein serine/threonine kinase activity | NEK5;SYK;MAPK14A;MAPK6;TESK2;SMG1;CDC7;PRKCB;NEK8 |
AKT3 has direct interactions with proteins and molecules. Those interactions were detected by several methods such as yeast two hybrid, co-IP, pull-down and so on. We selected proteins and molecules interacted with AKT3 here. Most of them are supplied by our site. Hope this information will be useful for your research of AKT3.
CASP3; CDC37; saicar; PKM; HSP90AA1; PRKCZ; HSP90AB1; NUDCD1
Gene Family
Research Area
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Customer Reviews (5)
Write a reviewI am confident that utilizing the AKT3 protein will empower me to uncover crucial insights into cellular mechanisms with precision.
The AKT3 protein is an exceptional protein solution that exceeds expectations in terms of quality and suitability for my experimental requirements.
Their expertise and guidance will undoubtedly prove valuable in overcoming hurdles and maximizing the potential of this protein in my research endeavors.
In addition to its outstanding quality, the AKT3 protein comes with exceptional technical support from its manufacturer.
Researchers can confidently rely on this high-quality protein to produce accurate and reproducible results, thereby accelerating their research progress
Q&As (20)
Ask a questionDysregulation 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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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).
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.
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.
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.
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.
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.
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.
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.
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.
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