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anti-Human Prokineticin Receptor 2 Anticorps:
anti-Rat (Rattus) Prokineticin Receptor 2 Anticorps:
anti-Mouse (Murine) Prokineticin Receptor 2 Anticorps:
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Mouse (Murine) Polyclonal Prokineticin Receptor 2 Primary Antibody pour ELISA, IF - ABIN375371
Ito, Noda, Yoshida, Otani, Yoshiga, Oto, Saito, Kurosaka: Prokineticin 2 antagonist, PKRA7 suppresses arthritis in mice with collagen-induced arthritis. dans BMC musculoskeletal disorders 2016
Human Polyclonal Prokineticin Receptor 2 Primary Antibody pour ELISA, WB - ABIN4239964
Monnier, Dodé, Fabre, Teixeira, Labesse, Pin, Hardelin, Rondard: PROKR2 missense mutations associated with Kallmann syndrome impair receptor signalling activity. dans Human molecular genetics 2008
Findings suggest that in vitro modeling of WT/Mutant interactions increases the resolution for identifying causal variants, uncovers novel dominant negative mutations, and provides new insights into the pathogenic mechanisms underlying heterozygous PROKR2 variants.
EG-VEGF and PROKR2 were highly expressed in colorectal primary lesions compared to positive controls. PROKR1 expression was lower and did not change in tumor specimens.
The deletion contained 17 protein coding genes including PROKR2 and BMP2, both of which are expressed during embryological development of the pituitary gland. PROKR2 mutations have been associated with hypopituitarism but a heterozygous deletion of this gene with hypopituitarism is a novel observation.
PROKR2 genetic mutation plays a role in the pathogenesis of pituitary stalk interruption syndrome.
a significant association between PKR2 rs6053283 polymorphism and Recurrent pregnancy loss (RPL) (P=0.003), whereas no association was observed between PKR1 rs4627609 polymorphism and RPL (P=0.929) in the Chinese Han population.
Data suggest that prokineticins (PROK1 and PROK2) and prokineticin receptors (PROKR1 and PROKR2) act as main regulators of physiological functions of ovary, uterus, placenta, and testis. [REVIEW]
PROKR2 may play a role in susceptibility of pituitary stalk interruption syndrome
PROKR2 expression in human fetal ovary remained unchanged throughout gestation.
EG-VEGF, BV8, and PROKR2 gene expression is approximately five, four, and two times higher in cystic fibrosis lungs compared with controls.
PKR2 protomers form type II dimers involving TMs 4 and 5, with a role for TM5 in modulation of PKR2 function.
Study corroborates the clinical relevance of the EG-VEGF system in human early pregnancy, and provides evidence for the gene-gene interactions of EG-VEGF and PROKR variants.
PK2-induced PKR2 endocytosis is GRK2- and clathrin-dependent, but beta-arrestin-independent.
Wild-type PROKR2 activates different G-protein subtypes (Gq, Gs, and Gi/o) and recruits beta-arrestins. The effects of 9 missense mutations on these 2 processes showed that some mutations affected both or only one of them.
Single PROKR2 missense allelic variants can either affect both cAMP and IP signaling pathways differently or selectively.
Prokineticin (PK)1/PKR2-signalling pathway is involved in the regulation of the functional adequate capillarization in late pregnancy
TSHZ1 is a key regulator of mammalian olfactory bulb development and function and controls the expression of PROKR2.
V331M variant confers lower risk for recurrent miscarriage
An unexpectedly large prevalence of PROKR2 mutations was found in Kallmann syndrome patients from the Maghreb.
the distal region of the IL3 region of PROKR2 may differentially influence receptor trafficking and G-protein coupling
PROKR2 signaling does not directly affect Sertoli cell function in autosomal recessive Kallmann syndrome.
The sexually dimorphic pattern of Prokr2 expression indicates differential roles in reproductive function and, potentially, in other physiological systems.
This study presents the first experimental evidence indicating a molecular interaction between anosmin 1 and PKR2. A truncated anosmin 1 protein comprising the first three domains of the protein interacts with the second extracellular loop of PKR2, involved in PK2 binding.
Data show that the prokineticins and their receptors PROK2, PKR1 and PKR2 contributes to altered sensitivity in diabetic neuropathy and its inhibition blocked both allodynia and inflammatory events underlying disease.
Studies indicate PK2 signaling is required for the maintenance of normal female estrous cycles.
We sought to clarify the role of PROKR2 in hypothalamopituitary development through analysis of Prokr2(-/-) mice.
Prokr2 is specifically expressed in the XY gonads during sex determination and fetal sexual differentiation, and knockout mice display a variable degree of compromised vasculature in the fetal testes
The functional characteristics of coronary endothelial cells depend on the expression of PKR1 and PKR2 levels and the divergent signaling pathways used by these receptors.
prokineticin 2 is expressed in neurons of the mouse suprachiasmatic nucleus
Phenotypic analysis indicated that not Pkr1(-/-)but Pkr2(-/-)mice exhibited hypoplasia of the olfactory bulb.
is an essential link for coordination of circadian behavior and physiology by the suprachiasmatic nucleus, especially in defining the onset and maintenance of circadian night
PKR2 expression was maintained over 10.5dpc with both trophoblastic and endothelial cell localisations in mice.
Important role for Prokr2 in olfactory bulb neurogenesis.
Prokineticin 2 polypeptide (Prokr2) signaling plays a role in hypothalamic regulation of energy balance, and loss of this pathway results in physiological and behavioral responses normally only detected when mice are in negative energy balance.
Cardiomyocyte PKR2 signalling leads to eccentric hypertrophy in an autocrine regulation and impaired endothelial integrity in a paracrine regulation without inducing angiogenesis.
All mutated PROKR2 except one (M323I) had decreased signalling activities.
Results describe the identity of the prokineticin receptor 2-expressing cells in the subventricular zone/rostral migratory stream/olfactory bulb pathway in adult mice.
Data show that the inflammation-induced up-regulation of PK2 was significantly less in pkr1 null mice than in WT and pkr2 null mice, demonstrating a role of PKR1 in setting PK2 levels during inflammation.
G-protein-coupled receptor for prokineticin
G protein-coupled receptor 73-like 1
, G protein-coupled receptor I5E
, G-protein coupled receptor 73-like 1
, G-protein coupled receptor I5E
, prokineticin receptor 2
, prokineticin receptor 2-like