PHLPP1 Antibodies

PH domain leucine-rich repeat-containing protein phosphatase 1 (PHLPP1)

Mediates dephosphorylation in the C-terminal domain hydrophobic motif of all members of the AGC Ser/Thr protein kinase family; especially 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 significant role in regulating Akt signaling in hippocampal neurons (By similarity).

Akt modulates the balance between cell survival and apoptosis by means of 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 development.

Gene Information

Human
Gene Name:	PHLPP1
Uniprot:	O60346
Entrez:	23239

Family

Belongs to:
No superfamily

Alternative Names

EC 3.1.3.16; hSCOP; KIAA0606; MGC161555; PH domain and leucine rich repeat protein phosphatase 1; PH domain and leucine rich repeat protein phosphatase; PH domain leucine-rich repeat-containing protein phosphatase 1; PHLPP; pleckstrin homology domain containing, family E (with leucine rich repeats)member 1; Pleckstrin homology domain-containing family E member 1; PLEKHE1; SCN circadian oscillatory protein; SCOPPH domain-containing family E member 1; Suprachiasmatic nucleus circadian oscillatory protein

Molecular Weight

Mass (kDA):
184.672 kDA

Genomic Context

Human
Location:	18q21.33
Sequence:	18; NC_000018.10 (62715445..62980433)

Tissue Specificity

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.

Subcellular Localizations

Cytoplasm. Membrane; Peripheral membrane protein. Nucleus. In colorectal cancer tissue, expression is concentrated at the lateral membrane of epithelial cells.; [Isoform 2]: Cell membrane.

Diseases

• Malignant Neoplasms
• Neoplasms
• Prostatic Neoplasms
• Malignant Neoplasm Of Prostate
• Cell Transformation, Neoplastic
• Malignant Neoplasm Of Breast
• Malignant Tumor Of Colon
• Diabetes Mellitus
• Leukemia
• Colorectal Cancer
• Chronic Lymphocytic Leukemia
• Glioblastoma
• Lymphoid Leukemia

• Neoplasm Metastasis
• Carcinoma
• Lymphoma
• Mammary Neoplasms
• Diabetes Mellitus, Non-insulin-dependent
• Colorectal Neoplasms
• Ductal Breast Carcinoma

Interacting Proteins

• SCRIB
• Scrib
• SLC9A3R1

Pathways

• Cell Proliferation
• Cell Growth
• Translation
• Cell Death
• Circadian Rhythm
• Localization
• Cell Cycle
• Transport
• Hyperphosphorylation
• Cellular Homeostasis
• Aging

• Dna Repair
• Sensitization
• Cellular Localization
• Rna Interference
• Glucose Transport
• Oncogenesis

PTMs

• Phosphorylation

• Dephosphorylation

• Ubiquitination

Research Areas

• Cancer
• Protein Phosphatase
• Tumor Suppressors

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/PHLPP1

Boster Bio - Best Uses Of The PHLPP1 Marker

Inhibiting PHLPP-1 may be one way to keep injured heart cells alive after a heart attack. What are the potential side effects of this drug and how effective is it? Continue reading to learn more. Learn more about Boster Bio’s PHLPP1 indicator and other conditions where PHLPP1 could be an important marker. This article will provide a detailed review about Boster Bio’s PHLPP1-product.

Inhibiting PHLPP-1 could help keep injured heart cells healthy after a heart attack.

Researchers have shown that inhibiting PHLPP-1, a phosphatase found in heart cells, can help keep these cells alive after a heart attack. These findings are promising for many reasons. First, it decreases cardiac fibrillation by inhibiting PHLPP-1. It helps preserve cardiac function. It is possible to save heart cells after a heart attack by targeting certain pathways.

Researchers can identify a new target to gene therapy as the human and pig hearts have similar characteristics. Researchers used an adenovirus containing a DNA-silencingRNA that suppressed the Hippo signaling pathway to create the virus. They also observed improvements to the heart function in pig models with heart attack. It is still unclear whether this treatment will work in humans.

The results of this study showed that H9c2 cardiomyoblasts are protected against HG treatment by siRNAs. This treatment also reduced apoptosis in a cell culture model that was induced by a heart attack. The PHLPP1 -siRNA blocked the PI3K/AKT/mTOR signalsing pathway and prevented apoptosis.

Numerous studies have shown PHLPP-1 inhibits the activity and collagens in rat heart tissue. This study also showed that PHLPP1 inhibited the expression of collagens I, III, and MMP2 and MMP9 in rat heart tissue, which inhibits the development of heart disease. These findings suggest PHLPP-1 could be used to protect injured heart cells from damage after a coronary event.

This study also showed siRNAs from rat cardiac myocytes may be capable of inhibiting PHLPP-1. These cells are essential for the repair of damaged cardiac tissue. This drug has also been shown to improve the heart's overall functioning. It may also prevent arrhythmia patients from developing heart failure. However, the results may not be indicative of future treatments.

A heart attack is when blood supply to a cardiac muscle is cut off. Blood flow may be blocked by cholesterol buildup in the arteries. Myocardial inflammation, also known as myocardial blockage, can cause the heart to stop pumping blood and lead to death. A blood clot within the heart muscle can worsen the problem. The body's ability of repair the damaged heart muscle begins deteriorating within 30 minutes after a severe heart attack. The symptoms may persist for several days or weeks, or may even be life-threatening.

The animals were tolerant to the gene therapy used in this experiment. It did nothing to cause cancer or other side effects. Researchers concluded that the therapy could help patients suffering from sudden cardiac arrest or heart attacks. They cautioned that sudden cardiac arrest does not always occur from a heart attack. It is possible for heart conditions like thickened heart muscle or long QT syndrome to cause disruptions in the heart rhythm.

Possible side effects

A recent study has uncovered potential side effects associated with the PHLPP1 marker. It also showed that the PHLPP1a anti-body may not be specific enough for all tissues like the heart. Physicians should be concerned that this test is not effective in detecting low-expression types of cancers. However, the test could help us to better understand the potential role for this protein as a therapeutic target.

In a mouse model, PHLPP1 gene deletion led to increased metastasis in the presence of invasion. ApcMin mice lost this gene, which promoted tumor progression. In contrast, higher expression led to greater invasion. The function of Runx2, which is a transcription factor that promotes growth and cell invasion, is also influenced by the PHLPP1 gene. Mammary carcinogenesis can be linked to the Akt pathway. In addition, a deregulation of this pathway can increase the risk of metastasis.

Cre-deficient mice that are PHLPP1-mutant have lower levels of PHLPP1 in their blood. Similarly, Cre-deficient mice have a lower level of neuronal differentiation than Cre+ littermates. Although some experiments have reported variations in molecular weight, the results of this study are not yet conclusive. This study is still ongoing. However, it has provided us a useful marker of neuronal differentiation.

The PHLPP1 markers are a great tool for diagnosing metastatic disease. They can also predict lung cancer risk. The PHLPP gene can be found in nearly 20% of lung tumors. It is inversely linked with Survivin. It inhibits cell apoptosis, promotes cell proliferation and is involved in AKT activity. We recommend reading our most recent study to learn more about this cancer gene.

The brain has many functions for the PHLPP1 gene. Mice with low levels of PHLPP1 have delayed phase transitions and a large phase delay after the light is turned off. The regulation and plasticity of neuronal cells may be affected through the PHLPP1 genetic. The PHLPP1 genetic marker can also cause side effects. Here are some examples. It's important that you remember that this research was only preliminary. You should consult with a doctor before going under any tests or undergoing any surgery.

There are many methods to test the PHLPP1 protein, but immunohistochemistry is still the best. Cosmo antibody is an IHC reagent that has been proven to be superior for PHLPP1a/b. We tested the antibody for its ability in brain tissues to detect PHLPP1a/b. It produced a strong fluorescent signal when it was used in cultured neural cells. It did not co-localize to the astrocyte marker GFAP.

The PHLPP1 gene regulates cellular homeostasis. Studies have shown that PHLPP expression is linked to many pathologies, including cancer. This gene is also linked to many cellular functions and may be useful in diagnosing insulin resistance. These proteins have many roles within the body, including the regulation of the epigenome. Read on to find out if PHLPP can be used as a biomarker for lung carcinoma.

Efficacy

PHLPP1 is a biomarker that is highly selective, but it isn't clear if this marker can be used to identify Parkinson's drug candidates. In fact, studies show that PHLPP1 is a weak inhibitor of Parkinson's disease, which is not surprising. The marker isn't specific enough to distinguish between Parkinson's drug types. PHLPP1 and several other members make up the PP2C clan.

Although it does not predict Parkinson's disease, PHLPP1 is useful in helping to reset the circadian time in rodents and humans. PHLPP1/ mice showed delayed phase shifts after long-light exposures compared to wild type controls. This suggests that PHLPP1 contributes in some way to SCN neuronalplasticity.

A recent study revealed that patients with high expression of PHLPP1 had improved survival during an E. coli infection. PHLPP1 was detected in 69.3% BMDMs and was associated with patients' clinicopathologic characteristics. The results of this study are encouraging, even though it is not clear how PHLPP1 works. It is possible to detect cancer earlier by using the PHLPP1 genetic.

PaCa cells are inactivated when they receive exogenous H2O2. Growth factors can be inhibited if inhibitors of the PHLPP1 gene decrease phosphatase activation. The ability to inhibit pHLPP1 activity has been shown to be as strong as seventy-five percent. This is the highest level of activity found in PaCa cells.

This gene is highly expressed on orthotopic mouse models for paCa. In addition, it has been shown to play a tumor-suppressive role in the disease. PHLPP1 may be used as a target gene for future therapeutic approaches, or as a diagnostic tool in PDAC. It is also possible to use a lentiviral marker to detect PHLPP1 in a cell line expressing PHLPP1.

PHLPP1 could be used as an important biomarker in the treatment of lung cancer patients. PHLPP1 gene expression is associated with higher survival rates and better responses to EGFR-TKI treatments. The gene is a useful prognostic indicator for lung cancer. PHLPP1 can be used as a biomarker to help target therapies. There are many benefits. This marker is a biomarker that you should research carefully. This marker might be the most promising.

The SCN's PHLPP1 gene was discovered to be expressed in a circadian way. PHLPP1 expression is highest during subjective night. Its role in the circadian cycle is unclear, but it is likely to be a central factor in this complex phenomenon. The PHLPP1 gene is a key player in this process. The PHLPP1 gene may play a critical role in circadian regulation of sleep and wakefulness in humans.