Rabbit Recombinant Monoclonal PTEN antibody - conjugated to HRP. Suitable for WB and reacts with Human samples.
pH: 7.4
Preservative: 0.1% Proclin 300 Solution
Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
WB | |
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Human | Tested |
Mouse | Predicted |
Rat | Predicted |
Species | Dilution info | Notes |
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Species Human | Dilution info 1/5000 | Notes - |
Species | Dilution info | Notes |
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Species Mouse, Rat | Dilution info - | Notes - |
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Dual-specificity protein phosphatase, dephosphorylating tyrosine-, serine- and threonine-phosphorylated proteins (PubMed:9187108, PubMed:9256433, PubMed:9616126). Also functions as a lipid phosphatase, removing the phosphate in the D3 position of the inositol ring of PtdIns(3,4,5)P3/phosphatidylinositol 3,4,5-trisphosphate, PtdIns(3,4)P2/phosphatidylinositol 3,4-diphosphate and PtdIns3P/phosphatidylinositol 3-phosphate with a preference for PtdIns(3,4,5)P3 (PubMed:16824732, PubMed:26504226, PubMed:9593664, PubMed:9811831). Furthermore, this enzyme can also act as a cytosolic inositol 3-phosphatase acting on Ins(1,3,4,5,6)P5/inositol 1,3,4,5,6 pentakisphosphate and possibly Ins(1,3,4,5)P4/1D-myo-inositol 1,3,4,5-tetrakisphosphate (PubMed:11418101, PubMed:15979280). Antagonizes the PI3K-AKT/PKB signaling pathway by dephosphorylating phosphoinositides and thereby modulating cell cycle progression and cell survival (PubMed:31492966, PubMed:37279284). The unphosphorylated form cooperates with MAGI2 to suppress AKT1 activation (PubMed:11707428). In motile cells, suppresses the formation of lateral pseudopods and thereby promotes cell polarization and directed movement (PubMed:22279049). Dephosphorylates tyrosine-phosphorylated focal adhesion kinase and inhibits cell migration and integrin-mediated cell spreading and focal adhesion formation (PubMed:22279049). Required for growth factor-induced epithelial cell migration; growth factor stimulation induces PTEN phosphorylation which changes its binding preference from the p85 regulatory subunit of the PI3K kinase complex to DLC1 and results in translocation of the PTEN-DLC1 complex to the posterior of migrating cells to promote RHOA activation (PubMed:26166433). Meanwhile, TNS3 switches binding preference from DLC1 to p85 and the TNS3-p85 complex translocates to the leading edge of migrating cells to activate RAC1 activation (PubMed:26166433). Plays a role as a key modulator of the AKT-mTOR signaling pathway controlling the tempo of the process of newborn neurons integration during adult neurogenesis, including correct neuron positioning, dendritic development and synapse formation (By similarity). Involved in the regulation of synaptic function in excitatory hippocampal synapses. Recruited to the postsynaptic membrane upon NMDA receptor activation, is required for the modulation of synaptic activity during plasticity. Enhancement of lipid phosphatase activity is able to drive depression of AMPA receptor-mediated synaptic responses, activity required for NMDA receptor-dependent long-term depression (LTD) (By similarity). May be a negative regulator of insulin signaling and glucose metabolism in adipose tissue. The nuclear monoubiquitinated form possesses greater apoptotic potential, whereas the cytoplasmic nonubiquitinated form induces less tumor suppressive ability (PubMed:10468583, PubMed:18716620). Isoform alpha. Functional kinase, like isoform 1 it antagonizes the PI3K-AKT/PKB signaling pathway. Plays a role in mitochondrial energetic metabolism by promoting COX activity and ATP production, via collaboration with isoform 1 in increasing protein levels of PINK1.
MMAC1, TEP1, PTEN, Inositol polyphosphate 3-phosphatase, Mutated in multiple advanced cancers 1, Phosphatase and tensin homolog
Rabbit Recombinant Monoclonal PTEN antibody - conjugated to HRP. Suitable for WB and reacts with Human samples.
pH: 7.4
Preservative: 0.1% Proclin 300 Solution
Constituents: PBS, 30% Glycerol (glycerin, glycerine), 1% BSA
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMAb® patents.
The PTEN protein also known as phosphatase and tensin homolog is a phosphatase enzyme with a molecular mass of approximately 47 kDa. It acts mechanically by removing phosphate groups from phosphatidylinositol (345)-trisphosphate (PIP3) converting it to phosphatidylinositol (45)-bisphosphate. PTEN is ubiquitously expressed in various tissues with pronounced presence in the brain lung kidney and testis. This enzyme is an important regulator of cellular functions through its impact on signaling pathways.
PTEN plays important roles in cellular processes like apoptosis cell proliferation and migration. It negatively regulates the PI3K/AKT signaling pathway critical for cell survival and growth. PTEN is not part of a larger protein complex but interacts with various other proteins modulating its activity. It maintains cellular homeostasis by balancing growth-promoting signals with cell cycle arrest and apoptotic pathways.
PTEN is an important component in the PI3K/AKT and mTOR signaling pathways. These pathways regulate cell growth metabolism and survival and are interlinked with insulin signaling and cancer progression. PTEN's function directly interacts with proteins such as AKT and mTOR serving as a checkpoint that ensures controlled cellular proliferation. This positions PTEN as a tumor suppressor inhibiting uncontrolled cell growth via modulation of these pathways.
PTEN mutations or deletions are strongly associated with various types of cancers including breast and prostate cancer. PTEN interaction with the PI3K/AKT pathway influences cancer development often through loss-of-function mutations leading to unrestrained cellular growth. Beyond cancer PTEN mutations also relate to neurological disorders like Autism Spectrum Disorder where it affects signaling pathways involving proteins like mTOR. Understanding PTEN's role aids in unravelling the mechanistic underpinnings of these diseases paving the way for targeted therapeutic interventions.
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ab202358 was shown to specifically react with PTEN in wild-type HAP1 cells as signal was lost in PTEN knockout cells. Wild-type and PTEN knockout samples were subjected to SDS-PAGE. ab202358 and Alexa Fluor® 680 Anti-GAPDH antibody [mAbcam 9484] - Loading Control ab184095 (Mouse monoclonal [mAbcam 9484] to GAPDH - Loading Control (Alexa Fluor® 680) loading control) were incubated overnight at 4°C at 1/5000 dilution and 1/1000 dilution respectively. The loading control was imaged using the Licor Odyssey CLx prior to blots being developed with ECL technique.
All lanes: Western blot - HRP Anti-PTEN antibody [EPR9941-2] (ab202358) at 1/5000 dilution
Lane 1: Wild-type HAP1 whole cell lysate at 20 µg
Lane 2: PTEN knockout HAP1 whole cell lysate at 20 µg
Predicted band size: 47 kDa
Observed band size: 47 kDa
Exposure time: 16min
This blot was produced using a 4-12% Bis-tris gel under the MOPS buffer system. The gel was run at 200V for 50 minutes before being transferred onto a Nitrocellulose membrane at 30V for 70 minutes. The membrane was then blocked for an hour using 2% Bovine Serum Albumin before being incubated with ab202358 overnight at 4°C. Antibody binding was visualised using ECL development solution ECL Substrate Kit (High Sensitivity) ab133406.
All lanes: Western blot - HRP Anti-PTEN antibody [EPR9941-2] (ab202358) at 1/5000 dilution
Lane 1: HeLa (Human epithelial carcinoma cell line) Whole Cell Lysate at 10 µg
Lane 2: MCF7 (Human breast adenocarcinoma cell line) Whole Cell Lysate at 10 µg
Lane 3: HEK293 (Human embryonic kidney cell line) Whole Cell Lysate at 10 µg
Developed using the ECL technique.
Performed under reducing conditions.
Predicted band size: 47 kDa
Observed band size: 50 kDa
Exposure time: 20s
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