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The protein encoded by Prok1 induces proliferation, migration, and fenestration (the formation of membrane discontinuities) in capillary endothelial cells derived from endocrine glands.
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important role for PK-1 in luteal function by acting as a mitogen and survival factor in corpus luteum derived endothelial cells
PROK1, acting via PROKR1 (Montrer PROKR1 Anticorps), may be involved in the recruitment of monocytes to regressing CL
EG-VEGF/PK1 and Bv8/PK2 (Montrer PROK2 Anticorps) thus represent new regulatory peptides acting as autocrine mitogens for endocrine cells
The VEGF (Montrer VEGFA Anticorps)/sVEGF-R1 ratio in follicular fluid on the day of oocyte retrieval in women undergoing IVF (Montrer SCN5A Anticorps) procedure, regardless of the type of stimulation protocol, might predict the risk of developing ovarian hyperstimulation syndrome (OHSS). To the best of our knowledge this is the first paper in the literature to show interplay among VEGF (Montrer VEGFA Anticorps), EG-VEGF and sVEGF-R1 and the correlation between their concentration and OHSS risk.
These findings demonstrate a novel function of primary cilia in controlling EG-VEGF-regulated trophoblast invasion and reveal the underlying molecular mechanism.
miR (Montrer MLXIP Anticorps)-346 and miR (Montrer MLXIP Anticorps)-582-3p regulate EG-VEGF-induced trophoblast invasion through repressing MMP 2 (Montrer MMP2 Anticorps) and MMP 9 (Montrer MMP9 Anticorps), and may become novel diagnostic biomarkers or therapeutic targets for EG-VEGF-related obstetric disorders. (c) 2016 BioFactors, 43(2):210-219, 2017.
Each follicular fluid (FF) was individually aspirated and FF/serum EG-VEGF, inhibin-a (Montrer INHA Anticorps), and FF IGF-1 (Montrer IGF1 Anticorps) levels were evaluated. The pregnant group was characterized by increased numbers of WVFs (p = 0.044), a WVE (p = 0.022), and increased levels of FF IGF-1 (Montrer IGF1 Anticorps) (p = 0.001) and serum EG-VEGF (p = 0.03).
Results show the biological effects of PROK1-V67I on cell functions are similar to those of wild type, and the common variant of V67I may act as a modifier in the PROK1-PROKR system through down-regulation of PROK1 expression.
Data suggest that prokineticins (PROK1 and PROK2 (Montrer PROK2 Anticorps)) and prokineticin receptors (PROKR1 (Montrer PROKR1 Anticorps) and PROKR2 (Montrer PROKR2 Anticorps)) act as main regulators of physiological functions of ovary, uterus, placenta, and testis. [REVIEW]
EG-VEGF and its receptor PKR1 (Montrer PROKR1 Anticorps) might play a role in the pathogenesis of adrenocortical tumors and could serve as prognostic markers for this rare malignant disease.
The prognosis was poorer in colorectal cancers that expressed both PROK1 and VEGF (Montrer VEGFA Anticorps) relative to the cases that expressed only 1 protein, and the expression of both proteins was found to be an independent prognostic factor.
PROK1 levels in follicular fluid and fertilization culture media could constitute new predictive noninvasive markers of successful embryo implantation in conventional in vitro fertilization-embryo transfer
Simultaneous targeting of both angiogenic growth factors (VEGF (Montrer VEGFA Anticorps)/PROK1) may prove more useful in colorectal cancer
EG-VEGF is a new mediator of PPARgamma (Montrer PPARG Anticorps) effects during pregnancy and bring new insights into the fine mechanism of trophoblast invasion.
Bv8 (Montrer PROK2 Anticorps) and EG-VEGF, along with other factors such as VEGF-A (Montrer VEGFA Anticorps), may maintain the integrity and also regulate proliferation of the blood vessels in the testis
This is the first report demonstrating that Prok-1 acts as a gut (Montrer GUSB Anticorps) mucosa/mesenchyme-derived factor and maintains proliferation and differentiation of enteric neural crest cells.
EG-VEGF was mainly localised in the labyrinth in mouse placenta. It may have direct effect on both endothelial & trophoblastic cells & is likely to play an important role in mouse placentation.
Prokineticin-1 (Prok-1) works coordinately with glial cell line-derived neurotrophic factor (GDNF) to mediate proliferation and differentiation of enteric neural crest cells.
The protein encoded by this gene induces proliferation, migration, and fenestration (the formation of membrane discontinuities) in capillary endothelial cells derived from endocrine glands. It has little or no effect on a variety of other endothelial and non-endothelial cell types. Its expression is restricted to the steroidogenic glands (ovary, testis, adrenal, and placenta), is induced by hypoxia, and often complementary to the expression of vascular endothelial growth factor (VEGF), suggesting that these molecules function in a coordinated manner.
, black mamba toxin-related protein
, endocrine-gland-derived vascular endothelial growth factor