Composition, Activation Mechanisms, and Biological Effects of the AKT Pathway
Composition, Activation Mechanisms, and Biological Effects of the AKT Pathway
The AKT pathway is one of the most central signaling networks governing cell growth, metabolism, survival, and stress adaptation. Its research value does not lie in explaining a single phosphorylation event in isolation, but in revealing how cells integrate receptor tyrosine kinases, PI3K, lipid second messengers, protein kinase cascades, and metabolic regulation into unified biological outputs. Aberrant activation or suppression of the AKT pathway can simultaneously affect tumorigenesis, insulin responsiveness, cardiovascular homeostasis, neurodevelopment, and drug resistance.
Keywords: AKT; PKB; PI3K; PTEN; PDK1; mTORC2; FOXO; GSK3; cell survival; metabolic regulation
1 Basic Framework of the AKT Pathway
1.1 Pathway Positioning
(1) Core functional position
The AKT pathway is positioned between receptor-proximal signaling and terminal cellular functions, serving as a major hub that links growth factor stimulation, nutrient status, energy sensing, and transcriptional regulation.
(2) Types of upstream inputs
The most typical upstream inputs of the AKT pathway include receptor tyrosine kinases, the insulin receptor, IGF receptors, selected G protein-coupled receptors, and integrin-associated signaling. Although these upstream stimuli originate from different entry points, most ultimately converge on the PI3K-PIP3 module to drive AKT activation.
(3) Scope of downstream outputs
AKT does not regulate cell survival alone. Its downstream outputs also include mTORC1 activation, glucose metabolism, protein synthesis, cell cycle progression, inhibition of transcription factors, cell migration, and anti-apoptotic programs.
1.2 Core Components
(1) Lipid signaling layer
PI3K converts the membrane lipid PIP2 into PIP3, and PIP3 serves as the key lipid second messenger that recruits AKT to the plasma membrane.
(2) Kinase layer
AKT itself is not a receptor-proximal kinase. Instead, after PIP3-mediated membrane recruitment, it is activated through phosphorylation at key sites by PDK1 and mTORC2.
(3) Negative regulatory layer
PTEN, SHIP, PP2A, and PHLPP together constitute the negative regulatory network of the AKT pathway and restrict both signaling duration and intensity.
2 Structure and Isoforms of AKT
2.1 Molecular Structure
(1) PH domain
The N-terminus of AKT contains a PH domain that specifically recognizes PIP3 or related phospholipids, thereby allowing AKT to be recruited to the plasma membrane upon pathway activation.
(2) Kinase domain
The central region is a serine/threonine kinase domain responsible for phosphorylation of downstream substrates and represents the catalytic core of AKT.
(3) Regulatory tail
The C-terminal regulatory region contains key phosphorylation sites, among which Ser473 is particularly important for full activation of AKT.
2.2 Isoform Composition
(1) AKT1
AKT1 is most closely associated with cell growth, proliferation, and general survival support, and is the isoform most frequently discussed in tumor biology.
(2) AKT2
AKT2 is more closely linked to metabolic regulation, especially insulin signaling, glucose uptake, and lipid metabolism, and therefore carries greater methodological weight in metabolic disease research.
(3) AKT3
AKT3 is more commonly associated with nervous system development, brain growth, and selected tumor types.
Table 1. Major Functional Biases of AKT Isoforms
Isoform | Major functional bias | Common research settings |
AKT1 | Growth, proliferation, survival | Tumors, cell cycle, drug resistance |
AKT2 | Metabolism, insulin response, glucose uptake | Glucose metabolism, lipid metabolism, insulin resistance |
AKT3 | Neurodevelopment, brain-related regulation | Nervous system development, brain tumors |
3 Classical Activation Mechanism of the AKT Pathway
3.1 Receptor-Proximal Activation
(1) Initiation by receptor tyrosine kinases
After ligands such as insulin, IGF, EGF, and PDGF bind to their receptors, receptor autophosphorylation occurs and adaptor proteins such as IRS and Gab are recruited, thereby providing a docking platform for PI3K.
(2) PI3K activation
Following recruitment to the membrane, Class I PI3K converts PIP2 into PIP3. Enrichment of PIP3 on the inner leaflet of the plasma membrane is one of the decisive events that drives the AKT pathway into an activated state.
3.2 Membrane Recruitment of AKT and Dual-Site Phosphorylation
(1) Membrane recruitment process
AKT recognizes PIP3 through its PH domain and translocates from the cytosol to the plasma membrane, a step that brings AKT into spatial proximity with its upstream activating kinases.
(2) Phosphorylation at Thr308
PDK1 phosphorylates Thr308 within the activation loop of AKT, and this is the key step by which AKT acquires catalytic activity.
(3) Phosphorylation at Ser473
mTORC2 generally mediates phosphorylation of AKT at Ser473. This modification enhances the completeness of the AKT substrate spectrum and the overall activation level. In most cases, concurrent phosphorylation at Thr308 and Ser473 is a more reliable indicator of full AKT activation.
3.3 Spatial Translocation After Activation
(1) Transfer from membrane to cytosol
After activation at the membrane, AKT can leave the membrane compartment and phosphorylate multiple cytosolic substrates related to metabolism and survival.
(2) Nuclear translocation
A portion of activated AKT can enter the nucleus and regulate transcription factors such as FOXO as well as nuclear substrates associated with cell cycle control.
4 Negative Regulatory Mechanisms of the AKT Pathway
4.1 Negative Regulation at the Lipid Level
(1) PTEN
PTEN dephosphorylates PIP3 back to PIP2 and is one of the most central negative regulators of the AKT pathway. Loss of PTEN can lead to PIP3 accumulation and sustained AKT activation.
(2) SHIP family
SHIP phosphatases dephosphorylate PIP3 at different positions, thereby regulating the persistence of PIP3 signaling and cell type-specific responses.
4.2 Negative Regulation at the Protein Level
(1) PP2A
PP2A can dephosphorylate AKT and some of its downstream substrates, thereby reducing pathway strength.
(2) PHLPP
PHLPP directly dephosphorylates AKT at Ser473 and is an important protein phosphatase that limits full AKT activation.
4.3 Feedback Inhibition
(1) mTORC1-S6K negative feedback
Following AKT-mediated activation of mTORC1, S6K can impose negative feedback on IRS proteins, thereby weakening upstream insulin/IGF input. This feedback loop is easily overlooked in AKT pathway studies but is highly important.
(2) Drug-induced feedback remodeling
When mTORC1 is inhibited, the above negative feedback is attenuated, which may instead cause reactivation of upstream AKT signaling. Accordingly, inhibition of the downstream branch alone does not always suppress the entire pathway.
5 Major Downstream Modules of the AKT Pathway
5.1 mTORC1 Axis
(1) Inhibition of TSC2
AKT can phosphorylate TSC2, thereby relieving its inhibitory effect on the Rheb-mTORC1 axis and promoting protein synthesis and cell growth.
(2) Enhancement of protein translation
Activation of S6K and 4E-BP1 downstream of mTORC1 enhances ribosome biogenesis and mRNA translation efficiency, thereby supporting increases in cell size and anabolic activity.
5.2 GSK3 Axis
(1) Inhibition of GSK3
Phosphorylation of GSK3α/β by AKT suppresses its activity and thereby affects glycogen synthesis, cell cycle regulation, and selected transcriptional programs.
(2) Effects on metabolism and differentiation
Following GSK3 inhibition, cells can enhance glycogen synthesis and alter differentiation-related signaling outputs.
5.3 FOXO Axis
(1) Nuclear export of FOXO
After AKT phosphorylates FOXO family transcription factors, FOXO is translocated from the nucleus to the cytoplasm and loses transcriptional activity.
(2) Biological consequences
This process reduces expression of genes involved in cell cycle inhibition, antioxidant responses, and apoptosis promotion. Accordingly, AKT activation is commonly accompanied by enhanced cell survival and altered stress thresholds.
5.4 Apoptosis-Regulatory Axis
(1) Phosphorylation of BAD
AKT can weaken the pro-apoptotic activity of BAD through phosphorylation, thereby increasing cellular tolerance to death-inducing stimuli.
(2) Indirect suppression of the caspase program
AKT does not directly block all caspases, but it globally increases the anti-apoptotic background by regulating BAD, FOXO, and mTOR-associated networks.
5.5 Metabolic Axis
(1) GLUT4 translocation
In the insulin response, AKT promotes GLUT4 translocation through substrates such as AS160/TBC1D4, thereby enhancing glucose uptake.
(2) Integration of glucose and lipid metabolism
AKT also influences glycogen synthesis, lipid synthesis, and suppression of hepatic gluconeogenesis, making it a key node in metabolic homeostasis.
Table 2. Major Downstream Modules and Functional Outputs of AKT
Downstream module | Key substrates/nodes | Major outputs |
mTORC1 axis | TSC2, S6K, 4E-BP1 | Protein synthesis, cell growth |
GSK3 axis | GSK3α/β | Glycogen metabolism, regulation of cell cycle and differentiation |
FOXO axis | FOXO1/3/4 | Enhanced survival, transcriptional suppression |
Anti-apoptotic axis | BAD and others | Increased cell death threshold |
Glucose metabolism axis | AS160/GLUT4 | Enhanced glucose uptake |
6 Biological Functions of the AKT Pathway
6.1 Cell Growth and Proliferation
(1) Control of cell size
Through mTORC1, AKT enhances protein synthesis and biosynthetic metabolism and is therefore an important upstream driver of cell size increase and growth program progression.
(2) Cell cycle progression
AKT promotes the transition from growth arrest to proliferation by suppressing programs associated with cell cycle inhibitory factors.
6.2 Cell Survival and Stress Adaptation
(1) Anti-apoptotic support
After AKT activation, cells show increased tolerance to nutrient deprivation, oxidative stress, and certain pro-apoptotic stimuli.
(2) Regulation of stress thresholds
AKT does not simply increase survival in all contexts. Rather, it jointly alters cellular stress response patterns through coordinated regulation of transcription, metabolism, and translation.
6.3 Metabolic Regulation
(1) Insulin response
In liver, skeletal muscle, and adipose tissue, AKT is one of the most central effector kinases in insulin signaling.
(2) Anabolic bias
AKT activation is generally accompanied by enhanced glucose utilization, increased glycogen synthesis, and reprogramming of lipid synthesis.
6.4 Migration and Invasion
(1) Cytoskeletal regulation
AKT can influence cytoskeletal remodeling and adhesion status through multiple downstream branches.
(2) Significance in pathological remodeling
In tumors and injury repair, the AKT pathway commonly participates in cell migration, invasion, and tissue remodeling.
7 AKT Pathway and Disease
7.1 Tumors
(1) Sustained pathway activation
PIK3CA mutation, PTEN loss, and excessive RTK activation can all result in persistent AKT hyperactivation and represent major molecular features in multiple solid tumors and hematologic malignancies.
(2) Drug resistance and survival advantage
High AKT activity can enhance tumor cell survival, metabolic adaptation, and therapeutic tolerance, and therefore also constitutes an important background for resistance to targeted therapies and chemotherapy.
7.2 Metabolic Diseases
(1) Insulin resistance
Insufficient AKT pathway responsiveness impairs glucose uptake and metabolic regulation and is one of the major mechanistic layers underlying insulin resistance.
(2) Lipid metabolic disorders
AKT abnormalities can also affect adipogenesis, hepatic lipid accumulation, and systemic metabolic reprogramming.
7.3 Cardiovascular and Nervous System Disorders
(1) Cardiomyocyte survival and stress responses
AKT plays important roles in cardioprotection during ischemia, vascular endothelial function, and cardiac compensation.
(2) Neurodevelopment and neuroprotection
AKT3 is particularly associated with brain development, while overall AKT signaling also contributes to neuronal survival and post-injury adaptation.
8 Experimental Investigation and Interpretation of the AKT Pathway
8.1 Common Readouts
(1) Upstream-layer indicators
PI3K activation, PIP3 levels, RTK phosphorylation, and IRS status can be used to determine whether upstream AKT input has been triggered.
(2) Indicators of intrinsic AKT activation
p-AKT Thr308 and p-AKT Ser473 are the most commonly used indicators of AKT activation. In most cases, combined observation of both sites is more informative than analysis of a single site alone.
(3) Downstream functional indicators
p-GSK3β, p-FOXO, p-S6K, p-4E-BP1, and GLUT4 translocation can serve as functional readouts at different output levels.
8.2 Common Experimental Strategies
(1) Growth factor stimulation models
Rapid AKT activation models can be established by stimulating cells with insulin, IGF-1, or EGF.
(2) Inhibitors and genetic interventions
PI3K inhibitors, AKT inhibitors, mTOR inhibitors, or PTEN overexpression/knockdown can be used to dissect hierarchical relationships within the pathway.
(3) Time-course analysis
The AKT pathway displays marked time dependence. Early responses are mainly reflected by AKT phosphorylation itself, whereas later phases gradually transition to transcriptional and functional outputs.
8.3 Common Biases in Result Interpretation
(1) Equating isolated elevation of Ser473 with full AKT activation
An increase in Ser473 does not always indicate complete enhancement of overall AKT function, and interpretation still requires consideration of Thr308 and downstream substrates.
(2) Simplifying AKT activation as equivalent to mTORC1 output
AKT and mTORC1 are closely related, but they are not always fully synchronous. Under some conditions, AKT activation is obvious while mTORC1 output is limited, or vice versa.
(3) Neglecting feedback regulation
If only a single time point is examined, AKT reactivation after feedback remodeling can easily be misinterpreted as drug failure or as an abnormal model phenotype.
Table 3. Key Readouts for Experimental Analysis of the AKT Pathway
Observation level | Common indicators | Methodological significance |
Upstream input layer | RTK, IRS, PI3K, PIP3 | Determines whether receptor-proximal activation has occurred |
AKT intrinsic layer | p-AKT Thr308, p-AKT Ser473 | Determines whether AKT has entered an activated state |
Metabolic output layer | p-AS160, GLUT4, glycogen synthesis | Determines metabolic effects |
Growth output layer | p-S6K, p-4E-BP1, mTORC1 | Determines anabolic growth programs |
Transcription/survival layer | p-FOXO, p-GSK3, BAD | Determines survival and transcriptional regulatory outcomes |
9 Product Tables Related to the AKT Pathway
Table 4. Small-Molecule Modulator Product Table for the AKT Pathway
Product type | Catalog No. | Name | CAS No. | Grade and Purity | Suitable research direction/use |
AKT inhibitor | (E)-Akt inhibitor-IV | 959841-49-7 | 10mM in DMSO | Suitable for AKT pathway inhibition and functional blockade studies | |
AKT inhibitor | (E)-Akt inhibitor-IV | 959841-49-7 | ≥99% | Suitable for AKT pathway inhibition studies | |
AKT inhibitor | 3-BrB-PP1 | 956025-99-3 |
| Suitable for small-molecule AKT inhibition studies | |
AKT1/2 inhibitor | 3CAI | 28755-03-5 | ≥95%(HPLC) | Suitable for inhibition studies of AKT1/AKT2 branches | |
AKT inhibitor | A-443654 | 552325-16-3 | Moligand™, ≥98% | Suitable for AKT inhibition and pathway function validation | |
AKT kinase inhibitor | AKT Kinase Inhibitor | 842148-40-7 | ≥99% | Suitable for studies on inhibition of AKT kinase activity | |
AKT kinase inhibitor | AKT Kinase Inhibitor | 842148-40-7 | 10mM in DMSO | Suitable for AKT kinase inhibition experiments | |
AKT kinase inhibitor | AKT Kinase Inhibitor hydrochloride | 3026697-00-4 | Moligand™, 10 mM in DMSO | Suitable for AKT kinase inhibition experiments | |
AKT kinase inhibitor | AKT Kinase Inhibitor hydrochloride | 3026697-00-4 | ≥99% | Suitable for AKT kinase inhibition studies | |
AKT inhibitor | AKT-IN-1 | 1357158-81-6 | Moligand™, 10 mM in DMSO | Suitable for AKT pathway inhibition studies | |
AKT inhibitor | AKT-IN-2 | 1295514-91-8 |
| Suitable for AKT pathway inhibition studies | |
AKT inhibitor | AKT-IN-3 | 2374740-21-1 | ≥99% | Suitable for AKT pathway inhibition studies | |
AKT inhibitor | AKT-IN-3 | 2374740-21-1 | Moligand™, 10 mM in DMSO | Suitable for AKT pathway inhibition experiments | |
AKT inhibitor | AKT-IN-6 | 1430056-54-4 | Moligand™, 10 mM in DMSO | Suitable for AKT pathway inhibition studies | |
AKT inhibitor | AKT Inhibitor VIII | 612847-09-3 | Moligand™, 10mM in DMSO | Suitable for AKT pathway inhibition experiments | |
AKT inhibitor | AKT Inhibitor VIII | 612847-09-3 | Moligand™, ≥97% | Suitable for AKT pathway inhibition studies | |
Akt/PKB inhibitor | API-1 | 36707-00-3 | ≥96%(HPLC) | Suitable for Akt/PKB inhibition studies | |
Pan-AKT inhibitor | AZD5363 | 1143532-39-1 | Moligand™, ≥98% | Suitable for global inhibition of AKT1/2/3 | |
Akt1 translocation inhibitor | CAY10567 | 32387-96-5 | Moligand™, ≥98% | Suitable for studies on Akt1 membrane translocation | |
AKT2 inhibitor | CCT128930 | 885499-61-6 | ≥98% | Suitable for AKT2-specific inhibition studies | |
Akt1/2/3 inhibitor | GDC-0068 | 1001264-89-6 | Moligand™, ≥98% | Suitable for inhibition studies across all AKT isoforms | |
Pan-Akt kinase inhibitor | GSK-690693 | 937174-76-0 | Moligand™, ≥98% | Suitable for global inhibition studies of the AKT pathway | |
AKT inhibitor | INCB-047775 | 1430056-54-4 | ≥97% | Suitable for AKT inhibition studies | |
Akt allosteric inhibitor | Miransertib | 1313881-70-7 | Moligand™, ≥98% | Suitable for allosteric inhibition studies of AKT | |
PDK1/Akt/Flt dual-pathway inhibitor | PDK1/Akt/Flt Dual Pathway inhibitor | 331253-86-2 | Moligand™ | Suitable for studies on PDK1-coupled upstream regulation of AKT | |
AKT inhibitor | PF-AKT400 | 1004990-28-6 | ≥98% | Suitable for AKT inhibition studies | |
AKT inhibitor | PF-AKT400 | 1004990-28-6 | 10mM in DMSO | Suitable for AKT inhibition experiments | |
Dual Akt and PDK1 inhibitor | PHT-427 | 1191951-57-1 | Moligand™, ≥98% | Suitable for studies on the PI3K/PDK1/AKT axis | |
PI3K/AKT inhibitor | PI3K/AKT-IN-1 |
| ≥99% | Suitable for inhibition studies of the PI3K-AKT axis | |
PI3K/AKT inhibitor | PI3K/AKT-IN-1 |
| 10mM in DMSO | Suitable for inhibition experiments of the PI3K-AKT axis | |
PI3K/AKT inhibitor | PI3K/AKT-IN-2 | 2684412-41-5 | ≥98% | Suitable for inhibition studies of the PI3K-AKT axis | |
PI3K/AKT inhibitor | PI3K/AKT-IN-2 | 2684412-41-5 | Moligand™, 10 mM in DMSO | Suitable for inhibition experiments of the PI3K-AKT axis | |
PI3K/Akt/CREB activator | PI3K/Akt/CREB activator 1 | 2708177-73-3 | 10mM in DMSO | Suitable for PI3K-AKT activation studies | |
PI3K/Akt/CREB activator | PI3K/Akt/CREB activator 1 | 2708177-73-3 | ≥99% | Suitable for PI3K-AKT activation studies | |
PI3K/Akt/mTOR inhibitor | PI3K/Akt/mTOR-IN-2 | 2757804-89-8 | ≥99% | Suitable for combined inhibition studies of the PI3K-AKT-mTOR axis | |
PI3K/Akt/mTOR inhibitor | PI3K/Akt/mTOR-IN-2 | 2757804-89-8 | 10mM in DMSO | Suitable for combined inhibition experiments of the PI3K-AKT-mTOR axis | |
Akt inhibitor | Perifosine (KRX-0401) | 157716-52-4 | Moligand™, ≥99% | Suitable for AKT inhibition and membrane localization interference studies | |
Akt activator | SC79 | 305834-79-1 | ≥98% | Suitable for AKT pathway activation studies | |
Specific Akt inhibitor | SH-5 | 701976-54-7 | ≥98% | Suitable for AKT-specific inhibition studies | |
PI3K/Akt activator | YS-49 | 132836-42-1 | ≥98% | Suitable for activation studies of the PI3K-AKT axis |
Table 5. Antibody, Recombinant Protein, and Readout Product Table for the AKT Pathway
Product type | Catalog No. | Name | Grade and Purity | Suitable research direction/use |
p-AKT antibody | AKT(phospho S473) Antibody | Validated, ExactAb™, See COA | Suitable for detection of AKT Ser473 phosphorylation, a core readout of AKT activation | |
AKT1 antibody | AKT1 Mouse mAb | ExactAb™, Validated, Carrier Free, 1.0mg/mL | Suitable for AKT1 protein detection | |
AKT2 antibody | AKT2 Mouse mAb | Animal Free,Carrier Free,ExactAb™,Azide Free,Validated,PBS Only,≥95%(SDS-PAGE),0.5 mg/mL | Suitable for AKT2 protein detection | |
Pan-AKT1/2/3 antibody | Recombinant AKT1/AKT2/AKT3 Antibody | Recombinant,ExactAb™,Validated,See COA | Suitable for total AKT protein detection | |
AKT1 recombinant protein | Recombinant Human AKT1 Protein | Carrier Free,His Tag,≥70%(SDS-PAGE),See COA | Suitable for AKT1 enzymology and functional studies | |
AKT1 recombinant protein | Recombinant Human AKT1 Protein | Carrier Free,His Tag,≥70%(SDS-PAGE),See COA | Suitable for AKT1 enzymology and functional studies | |
AKT2 recombinant protein | Recombinant Human AKT2 Protein | Carrier Free,His Tag,≥80%(SDS-PAGE) | Suitable for AKT2 enzymology and functional studies | |
AKT3 recombinant protein | Recombinant Human AKT3 Protein | Carrier Free,His Tag,≥80%(SDS-PAGE),See COA | Suitable for AKT3 enzymology and functional studies | |
AKT substrate peptide | AKTide-2T TFA | ≥98% | Suitable for AKT kinase activity assays | |
Akt substrate peptide | Akt/SKG Substrate Peptide TFA | ≥98% | Suitable for AKT substrate phosphorylation assays | |
AKT protein ELISA | Human AKT Protein (AKT) ELISA Kit | BioReagent | Suitable for quantitative detection of total human AKT protein | |
p-AKT ELISA | Human Phosphorylated AKT Protein (p-AKT) ELISA Kit | BioReagent | Suitable for quantitative detection of human p-AKT | |
AKT2 ELISA | Human Protein Kinase B Beta (PKBb/AKT2) ELISA Kit | BioReagent | Suitable for quantitative detection of human AKT2 | |
AKT protein ELISA | Rat AKT Protein (AKT) ELISA Kit | BioReagent | Suitable for quantitative detection of total rat AKT protein | |
AKT1 ELISA | Mouse Protein Kinase B Alpha (AKT1) ELISA Kit | BioReagent | Suitable for quantitative detection of mouse AKT1 | |
AKT protein ELISA | Mouse AKT Protein (AKT) ELISA Kit | BioReagent | Suitable for quantitative detection of total mouse AKT protein | |
p-AKT ELISA | Mouse Phosphorylated AKT Protein (p-AKT) ELISA Kit | BioReagent | Suitable for quantitative detection of mouse p-AKT |
Table 6. Gene Intervention and Knockout Validation Product Table for the AKT Pathway
Product type | Catalog No. | Name | Grade and Purity | Suitable research direction/use |
siRNA | AKT1 Human Pre-designed siRNA Set A |
| Suitable for AKT1 gene silencing studies | |
siRNA | AKT2 Human Pre-designed siRNA Set A |
| Suitable for AKT2 gene silencing studies | |
siRNA | AKT3 Human Pre-designed siRNA Set A |
| Suitable for AKT3 gene silencing studies | |
siRNA | Akt1 Mouse Pre-designed siRNA Set A |
| Suitable for mouse Akt1 gene silencing studies | |
siRNA | Akt1 Rat Pre-designed siRNA Set A |
| Suitable for rat Akt1 gene silencing studies | |
siRNA | Akt2 Mouse Pre-designed siRNA Set A |
| Suitable for mouse Akt2 gene silencing studies | |
siRNA | Akt2 Rat Pre-designed siRNA Set A |
| Suitable for rat Akt2 gene silencing studies | |
siRNA | Akt3 Mouse Pre-designed siRNA Set A |
| Suitable for mouse Akt3 gene silencing studies | |
siRNA | Akt3 Rat Pre-designed siRNA Set A |
| Suitable for rat Akt3 gene silencing studies | |
Knockout validation lysate | pLenti-AKT1-sgRNA |
| Suitable for AKT1 knockout validation and protein detection controls | |
Knockout validation lysate | pLenti-AKT1-sgRNA |
| Suitable for AKT1 knockout validation and RNA detection controls | |
Knockout validation lysate | pLenti-AKT2-sgRNA |
| Suitable for AKT2 knockout validation and protein detection controls | |
Knockout validation lysate | pLenti-AKT2-sgRNA |
| Suitable for AKT2 knockout validation and RNA detection controls | |
Knockout validation lysate | pLenti-AKT3-sgRNA |
| Suitable for AKT3 knockout validation and protein detection controls | |
Knockout validation lysate | pLenti-AKT3-sgRNA |
| Suitable for AKT3 knockout validation and RNA detection controls | |
Recombinant AKT1 antibody | Recombinant AKT1 Antibody | KD Validation | Suitable for AKT1 protein detection and knockdown validation | |
Recombinant AKT1 antibody | Recombinant AKT1 Antibody | KO Validation | Suitable for AKT1 protein detection and knockout validation |
The core significance of the AKT pathway lies in its ability to integrate receptor stimulation, lipid signaling, protein kinase cascades, and metabolic regulation into a unified cellular adaptation program. Its biological relevance is not limited to promoting survival, but extends to determining the overall state transitions of cells in growth, metabolism, stress, and disease contexts.
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