PRODUCT CODE: EM40507

AKT1 Mouse Monoclonal Antibody [D9-9-C9] (EM40507)

Applications

  • WB

  • ICC

  • IHC-P

  • FC

REACTIVITY

  • Human

  • Mouse

Western blot analysis of Akt1 on different cell lysates using anti-Akt1 antibody at 1/2000 dilution.<br />
Positive control:   <br />
Lane 1: HepG2             <br />
Lane 2: MCF-7 <br />
Lane 3: Hela
  • Western blot analysis of Akt1 on different cell lysates using anti-Akt1 antibody at 1/2000 dilution.<br />
Positive control:   <br />
Lane 1: HepG2             <br />
Lane 2: MCF-7 <br />
Lane 3: Hela
  • ICC staining Akt1 in Hela cells (red). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
  • ICC staining Akt1 in HepG2 cells (red). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
  • ICC staining Akt1 in MCF-7 cells (red). Cells were fixed in paraformaldehyde, permeabilised with 0.25% Triton X100/PBS.
  • Immunohistochemical analysis of paraffin-embedded human breast carcinoma tissue using anti-Akt1 antibody. Counter stained with hematoxylin.
  • Flow cytometric analysis of Hela cells with Akt1 antibody at 1/100 dilution (blue) compared with an unlabelled control (cells without incubation with primary antibody; red). Goat anti rabbit IgG (FITC) was used as the secondary antibody.
Western blot analysis of Akt1 on different cell lysates using anti-Akt1 antibody at 1/2000 dilution.
Positive control:
Lane 1: HepG2
Lane 2: MCF-7
Lane 3: Hela

Applications

  • WB

  • ICC

  • IHC-P

  • FC

REACTIVITY

  • Human

  • Mouse

SPECIFICATIONS

Product Type

Mouse monoclonal primary

Product Name

AKT1 Mouse Monoclonal Antibody [D9-9-C9] (EM40507)

Immunogen

Peptide

Host

Mouse

Positive Control

Hela, HepG2, MCF-7, human breast carcinoma tissue.

Conjugation

Unconjugated

Clonality

Monoclonal

Clone Number

D9-9-C9

PROPERTIES

Form

Liquid

Storage Condition

Store at +4C after thawing. Aliquot store at -20C or -80C. Avoid repeated freeze / thaw cycles.

Storage Buffer

1*PBS (pH7.4), 0.2% BSA, 40% Glycerol. Preservative: 0.05% Sodium Azide.

Concentration

2 ug/ul

PURIFICATION

Protein A purified.

MOLECULAR WEIGHT

56 kDa

Isotype

IgG2b

APPLICATION DILUTION

  • WB

  • 1:2,000

  • IHC-P

  • 1:100-1:200

  • ICC

  • 1:100-1:200

  • FC

  • 100-1:200

TARGET

UNIPROT #

PROTEIN NAME

AKT1

SYNONYMS

AKT 1 antibody; AKT antibody; AKT1 antibody; AKT1_HUMAN antibody; MGC99656 antibody; PKB antibody; PKB-ALPHA antibody; PRKBA antibody; Protein Kinase B Alpha antibody; Protein kinase B antibody; Proto-oncogene c-Akt antibody; RAC Alpha antibody; RAC antibody; RAC-alpha serine/threonine-protein kinase antibody; RAC-PK-alpha antibody

SEQUENCE SIMILARITIES

Belongs to the protein kinase superfamily. AGC Ser/Thr protein kinase family. RAC subfamily.

TISSUE SPECIFICITY

Expressed in prostate cancer and levels increase from the normal to the malignant state (at protein level). Expressed in all human cell types so far analyzed. The Tyr-176 phosphorylated form shows a significant increase in expression in breast cancers during the progressive stages i.e. normal to hyperplasia (ADH), ductal carcinoma in situ (DCIS), invasive ductal carcinoma (IDC) and lymph node metastatic (LNMM) stages.

POST-TRANSLATIONAL MODIFICATION

O-GlcNAcylation at Thr-305 and Thr-312 inhibits activating phosphorylation at Thr-308 via disrupting the interaction between AKT1 and PDPK1. O-GlcNAcylation at Ser-473 also probably interferes with phosphorylation at this site.; Phosphorylation on Thr-308, Ser-473 and Tyr-474 is required for full activity. Activated TNK2 phosphorylates it on Tyr-176 resulting in its binding to the anionic plasma membrane phospholipid PA. This phosphorylated form localizes to the cell membrane, where it is targeted by PDPK1 and PDPK2 for further phosphorylations on Thr-308 and Ser-473 leading to its activation. Ser-473 phosphorylation by mTORC2 favors Thr-308 phosphorylation by PDPK1. Phosphorylated at Thr-308 and Ser-473 by IKBKE and TBK1. Ser-473 phosphorylation is enhanced by interaction with AGAP2 isoform 2 (PIKE-A). Ser-473 phosphorylation is enhanced in focal cortical dysplasias with Taylor-type balloon cells. Ser-473 phosphorylation is enhanced by signaling through activated FLT3 (By similarity). Ser-473 is dephosphorylated by PHLPP. Dephosphorylated at Thr-308 and Ser-473 by PP2A phosphatase. The phosphorylated form of PPP2R5B is required for bridging AKT1 with PP2A phosphatase. Ser-473 is dephosphorylated by CPPED1, leading to termination of signaling.; Ubiquitinated via 'Lys-48'-linked polyubiquitination by ZNRF1, leading to its degradation by the proteasome (By similarity). Ubiquitinated; undergoes both 'Lys-48'- and 'Lys-63'-linked polyubiquitination. TRAF6-induced 'Lys-63'-linked AKT1 ubiquitination is critical for phosphorylation and activation. When ubiquitinated, it translocates to the plasma membrane, where it becomes phosphorylated. When fully phosphorylated and translocated into the nucleus, undergoes 'Lys-48'-polyubiquitination catalyzed by TTC3, leading to its degradation by the proteasome. Also ubiquitinated by TRIM13 leading to its proteasomal degradation. Phosphorylated, undergoes 'Lys-48'-linked polyubiquitination preferentially at Lys-284 catalyzed by MUL1, leading to its proteasomal degradation.; Acetylated on Lys-14 and Lys-20 by the histone acetyltransferases EP300 and KAT2B. Acetylation results in reduced phosphorylation and inhibition of activity. Deacetylated at Lys-14 and Lys-20 by SIRT1. SIRT1-mediated deacetylation relieves the inhibition.

SUBCELLULAR LOCATION

Nucleus, cytoplasm, cell membrane.

FUNCTION

The serine-threonine protein kinase AKT1 is catalytically inactive in serum-starved primary and immortalized fibroblasts. AKT1 and the related AKT2 are activated by platelet-derived growth factor. The activation is rapid and specific, and it is abrogated by mutations in the pleckstrin homology domain of AKT1. It was shown that the activation occurs through phosphatidylinositol 3-kinase. In the developing nervous system AKT is a critical mediator of growth factor-induced neuronal survival. Survival factors can suppress apoptosis in a transcription-independent manner by activating the serine/threonine kinase AKT1, which then phosphorylates and inactivates components of the apoptotic machinery. Mice lacking Akt1 display a 25% reduction in body mass, indicating that Akt1 is critical for transmitting growth-promoting signals, most likely via the igf1 receptor. Mice lacking Akt1 are also resistant to cancer: They experience considerable delay in tumor growth initiated by the large T antigen or the Neuoncogene.

CITATIONS

  • Xiao, Xiao et al.

    Biogenic nanoselenium particles activate Nrf2-ARE pathway by phosphorylating p38, ERK1/2, and AKT on IPEC-J2 cells. | Journal of Cellular Physiology [2019]

    • WB

    • The porcine jejunum epithelial (IPEC‐J2) cells

    • Citation