|Application ||WB, E|
|Other Accession||Q9WTR8, Q8CHE4|
|Calculated MW||184672 Da|
|Antigen Region||531-560 aa|
|Other Names||PH domain leucine-rich repeat-containing protein phosphatase 1, Pleckstrin homology domain-containing family E member 1, PH domain-containing family E member 1, Suprachiasmatic nucleus circadian oscillatory protein, hSCOP, PHLPP1, KIAA0606, PHLPP, PLEKHE1, SCOP|
|Target/Specificity||This PHLPP1 antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 531-560 amino acids from the N-terminal region of human PHLPP1.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is prepared by Saturated Ammonium Sulfate (SAS) precipitation followed by dialysis against PBS.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||PHLPP1 Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Synonyms||KIAA0606, PHLPP, PLEKHE1, SCOP|
|Function||Protein phosphatase involved in regulation of Akt and PKC signaling. Mediates dephosphorylation in the C-terminal domain hydrophobic motif of members of the AGC Ser/Thr protein kinase family; specifically acts on 'Ser-473' of AKT2 and AKT3, 'Ser-660' of PRKCB and 'Ser-657' of PRKCA (PubMed:15808505, PubMed:17386267, PubMed:18162466). Isoform 2 seems to have a major role in regulating Akt signaling in hippocampal neurons (By similarity). Akt regulates the balance between cell survival and apoptosis through a cascade that primarily alters the function of transcription factors that regulate pro- and antiapoptotic genes. Dephosphorylation of 'Ser-473' of Akt triggers apoptosis and suppression of tumor growth. Dephosphorylation of PRKCA and PRKCB leads to their destabilization and degradation (PubMed:18162466). Dephosphorylates STK4 on 'Thr-387' leading to STK4 activation and apoptosis (PubMed:20513427). Dephosphorylates RPS6KB1 and is involved in regulation of cap-dependent translation (PubMed:21986499). Inhibits cancer cell proliferation and may act as a tumor suppressor (PubMed:19079341). Dephosphorylates RAF1 inhibiting its kinase activity (PubMed:24530606). May act as a negative regulator of K-Ras signaling in membrane rafts (By similarity). Involved in the hippocampus-dependent long-term memory formation (By similarity). Involved in circadian control by regulating the consolidation of circadian periodicity after resetting (By similarity). Involved in development and function of regulatory T-cells (By similarity).|
|Cellular Location||Cytoplasm. Membrane; Peripheral membrane protein. Nucleus. Note=In colorectal cancer tissue, expression is concentrated at the lateral membrane of epithelial cells|
|Tissue Location||In colorectal cancer tissue, expression is highest in the surface epithelium of normal colonic mucosa adjacent to the cancer tissue but is largely excluded from the crypt bases. Expression is lost or significantly decreased in 78% of tested tumors (at protein level). Ubiquitously expressed in non-cancerous tissues.|
Thousands of laboratories across the world have published research that depended on the performance of antibodies from Abgent to advance their research. Check out links to articles that cite our products in major peer-reviewed journals, organized by research category.
email@example.com, and receive a free "I Love Antibodies" mug.
Provided below are standard protocols that you may find useful for product applications.
PHLPP1 is a protein phosphatase that specifically mediates dephosphorylation of 'Ser-473' of AKT1, a protein that regulates the balance between cell survival and apoptosis through a cascade that primarily alters the function of transcription factors that regulate pro- and antiapoptotic genes.
Gao,T., J. Biol. Chem. 283 (10), 6300-6311 (2008)
Brognard,J., Mol. Cell 25 (6), 917-931 (2007)
Gao,T., Mol. Cell 18 (1), 13-24 (2005)
If you have used an Abgent product and would like to share how it has performed, please click on the "Submit Review" button and provide the requested information. Our staff will examine and post your review and contact you if needed.
If you have any additional inquiries please email technical services at firstname.lastname@example.org.