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anti-Human PHLPP1 Antibodies:
anti-Mouse (Murine) PHLPP1 Antibodies:
anti-Rat (Rattus) PHLPP1 Antibodies:
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Human Polyclonal PHLPP1 Primary Antibody for ELISA, WB - ABIN544485
Gao, Furnari, Newton: PHLPP: a phosphatase that directly dephosphorylates Akt, promotes apoptosis, and suppresses tumor growth. in Molecular cell 2005
Show all 3 Pubmed References
Human Polyclonal PHLPP1 Primary Antibody for ELISA, WB - ABIN6264947
Dai, Zhang, Cheng, Yang, Chen, Liu, Wang, Yang, Jiang: RNA-binding Protein Trinucleotide repeat-containing 6A Regulates the Formation of Circular RNA 0006916, with Important Functions in Lung Cancer Cells. in Carcinogenesis 2018
PHLPP1 functions as a metastasis suppressor through its phosphatase activity, and PHLPP1 represents a novel diagnostic and therapeutic marker for metastatic melanoma.
Data suggest a tumor suppressor role of Xist in inhibiting AKT activation via regulation of non-X-chromosome gene PHLPP1 expression.
Low PHLPP expression is associated with gallbladder cancer.
nickel exposure results in DNMT3b induction and MEG3 promoter hypermethylation and expression inhibition, further reduces its binding to c-Jun and in turn increasing c-Jun inhibition of PHLPP1 transcription, leading to the Akt/p70S6K/S6 axis activation, and HIF-1alpha protein translation, as well as malignant transformation of human bronchial epithelial cells.
Data suggest that PHLPP1 plays an important role in assembly of kinetochores by counteracting RNF41-mediated SGT1 degradation. (PHLPP1 = PH domain and leucine rich repeat protein phosphatase 1; RNF41 = ring finger protein 41; SGT1 = suppressor of G2 allele of SKP1)
Studies indicate that two PHLPP isozymes, PHLPP1 and PHLPP2, were identified in a search for phosphatases that dephosphorylate Akt, and thus suppress growth factor signaling.
During LPS induced macrophage inflammatory response, PHLPP levels in macrophages are depleted through the inhibition of SP1 dependent transcriptional regulation.
results identify a novel role of PHLPP in regulating aPKC and cell polarity.
Abnormal PHLPP, FoxO3a, and RAD51 protein expressions may be involved in the development of high- and low-grade ovarian serous adenocarcinomas, suggesting common molecular pathways.
this study shows that PHLPP1 played a suppression role in inflammatory response of glioma
Increased PHLPP expression is associated with pancreatic cancer.
our results suggest that PHLPP1 plays a crucial role in sacral chordoma
high levels of PHLPP might reflect a less aggressive lung adenocarcinoma phenotype and predict better survival in patients with lung adenocarcinoma.
Results showed that PHLPP1 and PHLPP2 gene expression are down-regulated in esophageal squamous cell carcinoma. Their promotor is a target for mir-224.
Data show that both serine/threonine phosphatases PHLPP and dephosphorylated the physiological substrates of Akt1 and Akt3 with similar efficiencies.
Aberrant expression of PHLPP1 and PHLPP2 correlates with poor prognosis in patients with hypopharyngeal squamous cell carcinoma
PHLPP1, along with miR-522, promoted tumor cell growth in glioblastoma cells.
Suppression of PHLPP1 by DNA methylation contributes to melanoma development and progression.
miR-141 and its targets PHLPP1 and PHLPP2 play critical roles in NSCLC tumorigenesis
biochemical characterization of phosphatase domain of PHLPP1 and PHLPP2;PHLPP1 and PHLPP2 have similar in vitro activities and respond comparably to the presence of metallic ions; metallic ions affect structural stability of the domain;identified 3 residues likely involved in metal coordination and 2 that may be important for structural integrity
Transfection with either a mimic or an inhibitor of miR-29b-1-5p confirmed that downregulation of PHLPP1 upregulates Akt-dependent NF-kappaB signalling leading to activation of matrix metalloproteinases 2 and 9, players in the degradation of extracellular matrix during Helicobacter pylori infection.
Silencing of PHLPP1 promotes neuronal apoptosis and inhibits functional recovery after spinal cord injury.
TNF-alpha is involved in cardiac PHLPP1 upregulation during reoxygenation, which is mediated by NF-kappaB transcriptional activity
the circadian expression of SCOP in the basolateral amygdala plays a key role in generating circadian rhythmicity in the anxiety-like behavior.
Results strengthen the roles of both calpain-1 and PHLPP1 in synaptic plasticity and learning and memory, and illustrate the complexities of the interactions between multiple pathways participating in synaptic plasticity.
PHLPP1 reduced IFN-gamma-stimulated but not LPS-induced ERK1/2 phosphorylation, and inhibition of ERK1/2 abolished IFN-gamma-induced ser(727) STAT1 phosphorylation and iNOS expression.
Phlpp1 deficiency increases Akt2 activity, which diminishes FoxO1 levels and induces Fgf18 expression to stimulate chondrocyte proliferation.
enhancing Akt activity by inhibiting its PHLPP1-mediated dephosphorylation promotes processes associated with physiological hypertrophy
data are consistent with a model in which PHLPP modifies the histone code to control the transcription of RTKs.
SRPK1 overexpression is also tumorigenic because excess SRPK1 squelches PHLPP1.
PHLPP is a negative regulator of RAF1, which reduces colorectal cancer cell motility and prevents tumor progression in mice.
Histone deacetylase 3 suppression increases PH domain and leucine-rich repeat phosphatase (Phlpp)1 expression in chondrocytes to suppress Akt signaling and matrix secretion
deletion of PHLPP1 can enhance Akt activation in neurons and astrocytes, and can significantly increase cell survival and diminish infarct size
PHLPP1 has tumor suppressive activity and might represent a therapeutic or diagnostic tool for pancreatic ductal adenocarcinoma.
PHLPP as a novel tumor suppressor.
findings show that PH-domain leucine-rich-repeat protein phosphatase (PHLPP), which dephosphorylates Akt, is upregulated in Tregs, thus suppressing Akt activation
These results show that PHLPP-1 is an endogenous negative regulator of Akt activity and cell survival in the heart.
show that PHLPP1-null mice, although displaying normal circadian rhythmicity, have a drastically impaired capacity to stabilize the circadian period after light-induced resetting, producing a large phase shift after light resetting.
To determine if hippocampus-dependent memory is influenced by SCOP in vivo, a transgenic mouse strain was generated for the inducible overexpression of SCOP in the forebrain; overexpression SCOP completely blocked memory for novel objects.
This gene encodes a member of the serine/threonine phosphatase family. The encoded protein promotes apoptosis by dephosphorylating and inactivating the serine/threonine kinase Akt, and functions as a tumor suppressor in multiple types of cancer. Increased expression of this gene may also play a role in obesity and type 2 diabetes by interfering with Akt-mediated insulin signaling.
PH domain and leucine rich repeat protein phosphatase 1
, PH domain leucine-rich repeat-containing protein phosphatase 1-like
, PH domain leucine-rich repeat-containing protein phosphatase 1
, PH domain-containing family E member 1
, SCN circadian oscillatory protein
, pleckstrin homology domain containing, family E (with leucine rich repeats) member 1
, suprachiasmatic nucleus circadian oscillatory protein
, pleckstrin homology domain-containing family E member 1
, Circadian Oscillatory Protein (SCOP)
, PH domain leucine-rich repeat protein phosphatase 1
, pleckstrin homology domain-containing family E protein 1