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anti-Mouse (Murine) Neuregulin 1 Antikörper:
anti-Human Neuregulin 1 Antikörper:
anti-Rat (Rattus) Neuregulin 1 Antikörper:
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Human Polyclonal Neuregulin 1 Primary Antibody für WB - ABIN516692
Nordqvist, Kårehed, Hambiliki, Wånggren, Stavreus-Evers, Akerud: The presence of histidine-rich glycoprotein in the female reproductive tract and in embryos. in Reproductive sciences (Thousand Oaks, Calif.) 2010
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Monoclonal Neuregulin 1 Primary Antibody für ELISA, WB - ABIN533792
Talmage: Mechanisms of neuregulin action. in Novartis Foundation symposium 2008
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Human Polyclonal Neuregulin 1 Primary Antibody für IHC (p), ELISA - ABIN545729
Ritch, Carroll, Sontheimer: Neuregulin-1 enhances motility and migration of human astrocytic glioma cells. in The Journal of biological chemistry 2003
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Human Polyclonal Neuregulin 1 Primary Antibody für FACS, IHC (p) - ABIN390160
Vermeer, Einwalter, Moninger, Rokhlina, Kern, Zabner, Welsh: Segregation of receptor and ligand regulates activation of epithelial growth factor receptor. in Nature 2003
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Human Polyclonal Neuregulin 1 Primary Antibody für WB - ABIN3043580
Wang, Zhou, Ding, Zhu, Jiang, Fu, Wang, Hu, Ge: Qiliqiangxin improves cardiac function and attenuates cardiac remodeling in rats with experimental myocardial infarction. in International journal of clinical and experimental pathology 2015
Schwann cells induce the expression of Neuregulin-1 type I (NRG1-I), a paracrine growth factor, in various chronic demyelinating diseases. Genetic disruption of Schwann cell-derived NRG1 signalling in a mouse model of Charcot-Marie-Tooth Disease 1A (CMT1A), suppresses hypermyelination and the formation of onion bulbs.
Study shows altered hippocampal gene expression and structure in transgenic mice overexpressing neuregulin 1 (Nrg1) type I.
genetically ablating muscle dihydropyridine receptor (DHPR) beta1 subunit (Cacnb1) or ryanodine receptor 1 (Ryr1) also rescued muscle denervation and neuromuscular synapse loss in CRD-Nrg1-/-mice
The results of this study demonstrated that Nrg1 deficiency moderates the effects of prenatal stress on adult behaviour, but it does so in a complex, domain-specific fashion.
Our results identify a key role for NRG1/ErbB signalling in the regulation of hippocampal mGluRI-dependent synaptic and cognitive functions, whose alteration might contribute to the pathogenesis of different brain diseases.
NOTCH1 signalling promotes extracellular matrix (ECM) degradation during the formation of endocardial projections that are critical for individualization of trabecular units, whereas NRG1 promotes myocardial ECM synthesis, which is necessary for trabecular rearrangement and growth.
Overexpression of neuregulin 1 alpha suppressed Nuclear forkhead box protein O1 (FoxO1) and its downstream targets, PEPCK and G6Pase in liver and isolated hepatocytes.
Study shows that within endoplasmic reticulum-related subsurface cistern, sigma-1 receptors, Kv2.1 and neuregulin-1 are clustered in highly specific, non-overlapping, microdomains, whereas ErbB2 and ErbB4 are present in the adjacent presynaptic compartment. This organization may define highly ordered and spatially restricted sites for different signal-transduction pathways.
It plays a role in non-amyloidogenic processing.
Result suggest the potential for a paracrine signalling network whereby basal cells secrete neuregulin 1 (Nrg1), which acts on luminal cells via Erbb3 and Erbb4 receptors.
In the ovary of 6-month-old gcNrg1KO mice, follicular development was blocked in bilayer secondary follicles and heterogeneous cells accumulated in ovarian stroma.
We show here that cleavage-stimuli-induced specific ICD-modifications cause structural substrate changes that enhance ectodomain sensitivity of neuregulin-1 (NRG1; epidermal-growth-factor) or CD44 (receptor-tyrosine-kinase (RTK) co-receptor) to chymotrypsin/trypsin or soluble ADAM.
Compromised neuregulin function from birth might lead to schizophrenia-relevant behavioral changes in adulthood.
Study found that the expression level of the neuregulin-1 (NRG1) protein was increased in the medial prefrontal cortex of fear-conditioned mice and manipulation of NRG1 activity in the prelimbic cortex affected fear-conditioning behaviors.
The manipulation of NRG1/ErbB4 signaling in the present study revealed that NRG1/ErbB4 activity in the hippocampus is critical for learning and memory.
Nrg1-I intramuscular injection enhanced muscle reinnervation by collateral sprouting
These results collectively suggest that sustained activation of Wnt/beta-catenin signaling in endothelial cells might be a cause of heart failure through suppressing neuregulin-ErbB signaling.
These results suggest that the neuropsin-NRG1 signaling system has a role in pathological processes underlying temporal lobe epilepsy by regulating the activity of parvalbumin-expressing interneurons, and that neuropsin regulates E/I balance and gamma oscillations through NRG1-ErbB4 signaling toward parvalbumin-expressing interneurons.
we show that the antifibrotic effect of neuregulin-1 is at least partially mediated through anti-inflammatory activity, linked to receptor tyrosine-protein kinase erbB-4 activation in macrophages
Results show that at ventral hippocampus-nucleus accumbens synapses, presynaptic type III Nrg1 bidirectional signaling controls the establishment of ventral hippocampus-nucleus accumbens glutamatergic synapses. Type III Nrg1 back-signaling contributes to functional synaptic vesicle clustering and neurotransmitter vesicle release.
Results showed a significant association between Hirschsprung's Disease (HSCR) risk and neuregulin 1 (NTRG1) single nucleotide polymorphism rs7835688 in all genetic models [Meta-analysis].
Strong evidence for association was observed for the nonsynonymous single-nucleotide polymorphism RS10503929 within the neuregulin 1 gene and the minor allele C was associated with an increased risk of Sudden cardiac death in patients with Schizophrenia (Review).
Schwann cells induce the expression of Neuregulin-1 type I (NRG1-I), a paracrine growth factor, in various chronic demyelinating diseases.
This study demonstrates that stimulation of macrophages by tumor cell NRG1 can enhance transendothelial migration and intravasation. We also demonstrate that this effect is due to induction of macrophage JAG1, an important ligand of the Notch signaling pathway.
Findings primarily have been suggested involvement of NRG1 in etiology of Autism spectrum disorder. Also correlation of NRG1 mRNA level with EF deficiencies could shed lights on EF mechanisms and may suggest targeted treatments to improve particular executive functions.
There is a potential relationship between serum NRG and improved LVEF, indicating the need to investigate the utility of NRG in predicting HF outcomes, including LVEF maintenance.
Low NRG1 expression is associated with progression of breast cancer.
NRG1 mRNA levels were significantly higher in individuals with poor functional outcome, than individuals with good functional outcome in psychosis patients.
Enhanced ERBB4 phosphorylation could mediate NRG1 effects on mitochondrial function through signalling pathways
In Autism Spectrum Disorder patients, the NRG1 levels were found to be statistically significantly high compared to the healthy control group.
COMT-GG and NRG1-AA genotypes aid the transcranial direct current stimulation-induced improvement in auditory verbal hallucinations in schizophrenia patients.
The neuregulin1 was observed to be cleaved, adding to the 3 known NS3/4A cleavage targets. It showed that NS3/4A triggers an increase in neuregulin1 mRNA levels in HCV infected cells.
These results support the association between genetic variation of RET and NRG1 and susceptibility to Hirschsprung disease in the Chinese population.
Results found that NRG1, a potential prognostic marker is highly expressed in papillary thyroid cancer (PTC). Also, further data demonstrate that NRG1 activates the antioxidant pathway by upregulating the expression of antioxidant enzymes through NRF2, thus modulating redox homeostasis in PTC.
Mesenchymal stem cell-drived paclitaxel resistance in ErbB2/ErbB3-coexpressing breast cancer cells could be attributed to upregulation of Survivin via paracrine effect of NRG-1/ErbB3/PI-3K/Akt signaling, as either specific knockdown expression of ErbB3, or blocking of downstream PI-3K/Akt signaling, or specific inhibition of Survivin can completely reverse this effect.
The data suggest a role for transcriptional regulation of NRG1 in the predisposition to papillary thyroid carcinoma.
NRG1rs3924999 and NRG1 rs6994992 are associated with change of temperament scores in a clinical sample of subjects with major depression (MDD), who received selective serotonin reuptake inhibitor treatment.
NRG1 is a potential prognostic and therapeutic biomarker in gastric cancer patients
Study found that the protein levels of NRG1 and ErbB4 were significantly increased in the temporal cortex of patients with symptomatic epilepsy. Also, NRG1-ErbB4 signaling suppresses GluN2B phosphorylation by Src inhibition. GluN2B is closely related to synaptic activity and its regulation by the NRG1-ErbB4-Src signaling axis highlights the importance of NRG1-ErbB4 signaling in symptomatic epilepsy pathology.
Levels of NRG1 type III expression in peripheral blood mononuclear cells were positively correlated with impairments in social interaction in children with autism spectrum disorder.
Data suggest that epidermal growth factor receptor B [ErbB] isoforms and their ligands (epidermal growth factor [EGF], amphiregulin [AREG], and neuregulin-1 [NRG1]) are expressed in uteroplacental tissues in mid- and late-phases of pregnancy.
Cloning of a novel isoform of NRG1 (IgNRG1beta2) containing an immunoglobulin-like domain which is probably essential for efficient interaction with ErbB receptors.
The present research focused on morphological distribution of Nrg1 and its receptors, ErbB2 and ErbB4, in main gastrointestinal tissues of the non-human primate rhesus monkey.
Loss of zinc finger protein multitype 1 (Zfpm1) activity resulted in over-activation of Neuregulin-ErbB signaling and abnormally elevated cardiomyocyte proliferation.
we observed the activation of Notch signaling in cardiomyocytes adjacent to those undergoing apical constriction, and we showed that this activation is positively regulated by Neuregulin signaling.
these results suggest that Nrg1 is not the primary effector of trabeculation and/or that other EGF-like ligand(s) activates the ErbB2/ErbB4 pathway, either through functioning as the primary ligand or acting in a redundant manner. Overall, our work provides an example of cross-species differences in EGF family member requirements for an evolutionary conserved process.
Notch1 activation induces expression of ephrin b2a (efnb2a) and neuregulin 1 (nrg1) in the endocardium to promote trabeculation and forced Notch activation in the absence of cardiac contraction rescues efnb2a and nrg1 expression
These findings identify Nrg1 as a potent, induced mitogen for the endogenous adult heart regeneration program.
These results demonstrate that Nrg1 type III is an essential signal that controls Schwann cell migration to ensure that these glia are present in the correct numbers and positions in developing nerves.
ErbB3 signaling is required for normal migration of trunk, but not cranial, neural crest cells
Disc1 and nrg1 function in controlling development of oligodendrocytes and neurones from olig2-expressing precursor cells.
NRG1 and PI3K functionally interact with ErbB2 and ErbB3 during regeneration
The protein encoded by this gene was originally identified as a 44-kD glycoprotein that interacts with the NEU/ERBB2 receptor tyrosine kinase to increase its phosphorylation on tyrosine residues. This protein is a signaling protein that mediates cell-cell interactions and plays critical roles in the growth and development of multiple organ systems. It is known that an extraordinary variety of different isoforms are produced from this gene through alternative promoter usage and splicing. These isoforms are tissue-specifically expressed and differ significantly in their structure, and thereby these isoforms are classified into types I, II, III, IV, V and VI. The gene dysregulation has been linked to diseases such as cancer, schizophrenia and bipolar disorder (BPD).
, pro-neuregulin-1, membrane-bound isoform
, type I neuregulin 1
, type III neuregulin 1
, neuregulin 1
, glial growth factor
, heregulin, alpha (45kD, ERBB2 p185-activator)
, neu differentiation factor
, neuregulin 1 type IV beta 1a
, neuregulin 1 type IV beta 3
, sensory and motor neuron derived factor
, neuregulin 1 type III beta 3
, membrane-bound isoform
, neuregulin 1 alpha isoform