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Human PEBP1 Protein expressed in Wheat germ - ABIN1314624
Scholler, Gross, Garvik, Wells, Liu, Loch, Ramirez, McIntosh, Lampe, Urban: Use of cancer-specific yeast-secreted in vivo biotinylated recombinant antibodies for serum biomarker discovery. in Journal of translational medicine 2008
overexpression of RKIP inhibited prostate cancer cell proliferation, migration and invasion
isruption of the TROY/RKIP interaction using the TAT-TROY (234-371 aa) protein reduced the glioma development in xenografted mice. This suggests the TROY/RKIP interaction is a potential target for therapy of gliomas.
Loss of RKIP is associated with myeloid sarcoma.
Low RKIP Expression is associated with asthma.
our studies demonstrate how KRAS inhibits the tumor suppressor RKIP, thus offering novel justification for targeting RKIP as a strategy to overcome KRAS-induced tumor metastasis and chemoresistance in PDAC.
RKIP expression in gastrointestinal stromal tumors is associated with tumor size, NIH risk grade, and mucosal invasion, and low or no expression of RKIP predicts a high malignancy potential.
Octreotide may weaken invasion and metastasis through the upregulation of PEBP1. Octreotide may reduce the risk of recurrence and metastasis after surgery for liver cancer.
Knockdown of RKIP increased phosphorylated ERK and thus suppressed sorafenib-mediated cell death.
Baseline urinary RKIP, evaluated in an independent cohort of 56 Clear cell Renal Cell Carcinoma patients and 28 healthy subjects, successfully distinguished both groups and, most importantly, a cut-off value of 10 ng/mg/g Pr/uCr enabled a highly accurate prediction of Cancer-specific survival and Progression-free survival.
we found that the RKIP expression was decreased significantly in HBV infected tumor tissues compared to normal adjacent tissues, suggesting the reduction or absence of RKIP expression was closely related to liver carcinogenesis.
downregulation of RKIP plays an important role in the breast neoplastic progression and correlates with poor prognosis in patients with breast carcinoma (BC). Aberrant RKIP methylation is one of the mechanisms that lead to downregulation of RKIP in BC.
can act as a negative mediator in autophagy through stimulation of the AKT-MTORC1 pathway and direct interaction with LC3.
PEBP1, a scaffold protein inhibitor of protein kinase cascades, complexes with two 15LO isoforms, 15LO1 and 15LO2, and changes their substrate competence to generate hydroperoxy-phosphatidylethanolamines (PE). Inadequate reduction of hydroperoxy-PE due to insufficiency or dysfunction of a selenoperoxidase, GPX4, leads to ferroptosis.
miR-23a as a negative regulator of RKIP expression in AML.
Knockdown of RKIP promotes LX-2 cell proliferation.
RKIP contributes to colitis development by promoting inflammation and mediating intestinal epithelial cell apoptosis.
The study demonstrates that miR-543 promotes the proliferation and metastasis of prostate cancer via targeting RKIP.
RKIP inhibitors locostatin reduces extracellular matrix production as well as the migration and proliferation of myometrial and leiomyoma cells.
RKIP has a role in suppressing proliferation and metastasis of breast cancer cell lines through up-regulation of miR-185 targeting HMGA2
positive p-Ser153 RKIP expression is a favorable prognostic factor and affects clinical response to radiotherapy in nasopharyngeal carcinoma
PEBP1 mRNA levels are associated with male fertility.
NMR structure of the N- and C-terminal protein fragments [PEBP]
data suggest that phosphatidylethanolamine-binding protein (PEBP) and hippocampal cholinergic neurostimulating peptide (HCNP), the N-terminal fragment of the secreted PEBP, might be considered as new endocrine factors involved in cardiac physiology [PEBP]
The investigation of PEBP binding properties towards morphine and morphine analogs, is reported.
these findings indicate that RKIP functions as an essential modulator of the IL-17R-Act1 axis in IL-17R signaling, which promotes IL-17-induced inflammation and autoimmune neuroinflammation
Under conditions of Nnt-dependent enhanced myocardial oxidative stress, RKIP plays a maladaptive role for fibrotic myocardial remodeling by suppressing the Nrf2-related beneficial effects.
Results suggested that RKIP may inhibit the TNF-alpha-induced expression of adhesion molecules in MOVACs through inactivation of the NF-kappaB pathway.
findings report that RKIP preferentially regulates the TLR3-mediated immune response in macrophages; phosphorylation of RKIP serine 109 is required for RKIP to promote TLR3-mediated signaling and inflammation
The authors report that Raf kinase inhibitory protein (RKIP) is essential for TBK1 activation and type I interferon production triggered by viral infection.
RKIP knockdown promotes ERK1 and PPAR gamma activation during adipogenesis.
this study shows that didymin ameliorates hepatic injury through up-regulating RKIP expression
overexpression of RKIP attenuated microglia inflammation through inhibiting the NF-kappaB signaling pathway in erythrocyte lysis-treated BV2 cells.
Overexpression of RKIP inhibits retinal ganglion cells apoptosis and promotes axonal regeneration after optic nerve crush.
RKIP overexpression increases cardiac contractility mediated by the beta1-adrenoceptor. RKIP deficiency exaggerates pressure overload-induced cardiac failure. RKIP is upregulated in heart failure.
In syngeneic mammary tumors, RKIP regulates tumor-associated macrophage recruitment by blocking HMGA2, resulting in reduced expression of numerous macrophage chemotactic factors, including CCL5..
These findings suggest that in addition to its known metastasis suppressor activity, RKIP may promote tumor progression through enhancing tumor initiation.
Epigenetic Pebp1 inactivation may affect activation of ERK, and it could impair spermatogenesis of mice.
The concomitant depletion of RKIP can rescue the compromised ERK activation and cell proliferation through a Raf-1-dependent mechanism.
RKIP is necessary for the exaggerated production of IFN-gamma from Systemic inflammatory response syndrome splenocytes.
Protein kinase C-dependent regulation of raf kinase inhibitory protein leads to MAP kinase activation that is required for long-term synaptic depression.
Raf-1 kinase inhibitory protein (RKIP) mediates ethanol-induced sensitization of secretagogue signaling in pancreatic acinar cells
Rkip prevents cilia formation and is associated with Cep290-mediated photoreceptor degeneration.
CG18594 was not expressed in embryos whatever the developmental stage, was detected in all larval tissues tested, and was only found in ovaries and gut of adult Drosophila.
transgenic flies overexpressing the protein are highly protected against bacterial infection
The protein encoded by this gene is a platelet-derived growth factor that belongs to the CXC chemokine family. This growth factor is a potent chemoattractant and activator of neutrophils. It has been shown to stimulate various cellular processes including DNA synthesis, mitosis, glycolysis, intracellular cAMP accumulation, prostaglandin E2 secretion, and synthesis of hyaluronic acid and sulfated glycosaminoglycan. It also stimulates the formation and secretion of plasminogen activator by synovial cells.
Raf kinase inhibitory protein
, hippocampal cholinergic neurostimulating peptide
, neuropolypeptide h3
, phosphatidylethanolamine-binding protein 1
, prostatic binding protein
, prostatic-binding protein
, raf kinase inhibitor protein
, phosphatidylethanolamine binding protein 1
, basic cytosolic 21 kDa protein
, Raf-1 inhibitor protein
, Raf-1 kinase inhibitor protein
, 23 kDa morphine-binding protein
, Raf kinase inhibitor protein
, phosphatidylethanolamine-binding protein
, Phosphatidylethanolamine-binding protein 1