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NPTX1 is a member of the neuronal pentraxin gene family. Additionally we are shipping Neuronal Pentraxin 1 Kits (14) and Neuronal Pentraxin 1 Proteins (9) and many more products for this protein.
Showing 10 out of 134 products:
Human Polyclonal NPX1 Primary Antibody for EIA, IHC (p) - ABIN359508
Hossain, Russell, OBrien, Laterra: Neuronal pentraxin 1: a novel mediator of hypoxic-ischemic injury in neonatal brain. in The Journal of neuroscience : the official journal of the Society for Neuroscience 2004
Show all 2 references for ABIN359508
Human Polyclonal NPX1 Primary Antibody for EIA, IHC (p) - ABIN359507
Schlimgen, Helms, Vogel, Perin: Neuronal pentraxin, a secreted protein with homology to acute phase proteins of the immune system. in Neuron 1995
Show all 2 references for ABIN359507
Results demonstrate a novel mechanism of neuronal death and predict that inhibition of NP1 expression is a promising strategy to prevent hypoxic-ischemic injury in immature brain
results demonstrate that extracellular release of NP1 promote hypoxic-ischemic neuronal death possibly via surface clustering with GluR1 (show GRIA1 Antibodies) at synaptic sites and that NP1, not its family member NP2 (show NRP2 Antibodies), is involved in the neuronal death mechanisms
Genetic deletion of NP1 prevents hypoxic-ischemic neuronal death by reducing synaptic clustering of GluR1 (show GRIA1 Antibodies).
These findings suggest that Narp (show NPTX2 Antibodies) in the mPFC mediates the extinction of morphine conditioned place preference.
our findings demonstrate a novel mechanism by which NP1 regulates mitochondria-driven hippocampal cell death
NP1 facilitates the accumulation of BCL2-associated X protein (BAX (show BAX Antibodies)) in mitochondria and regulates mitochondrial dynamics during apoptosis in mouse cerebellar granule neurons in culture.
Neuronal pentraxin 1 induction in hypoxic-ischemic neuronal death is regulated via a glycogen synthase kinase-3alpha/beta dependent mechanism
data indicate that the loss of NP1/2 disrupts several aspects of retinogeniculate development including the initial establishment of AMPAR transmission and the subsequent elimination of inappropriate circuit connections
The Id3 (show ID3 Antibodies) and NP1 genes become transcriptionally active after MyoD (show MYOD1 Antibodies) induction in undifferentiated myoblasts. This is a stable, heritable event that does not need continued MyoD (show MYOD1 Antibodies) activity & is not subject to negative regulation by activated H-Ras (show HRAS Antibodies) G12V.
Neuronal pentraxin 1 and 2 are necessary for early synaptic refinements in mammalian retina and dorsal lateral geniculate nucleus. May exert their effects through mechanisms paralleling known role of short pentraxins outside the CNS. (Pentraxin 1 (show CRP Antibodies) and 2)
NRP-1 (show NELL1 Antibodies) was found to be overexpressed in gastric cancer (GC) tissues, and its expression correlates with the clinical staging, tumor differentiation and pathological types of gastric cancer.
Both placental NRP1 and VEGF were expressed at lower levels in women with pre-eclampsia and homocysteine-treated mice, which may contribute to endothelial damage.
NRP1 (show NELL1 Antibodies) was targeted by miR130a and miR130b at the binding site of chromosome 10: 334668643466870, which was involved in the axon guidance signaling pathway.
Semaphorin-3a (show SEMA3A Antibodies), neuropilin-1 (show NRP1 Antibodies) and plexin-A1 (show PLXNA1 Antibodies) are axonal guidance molecules that have been recently implicated in regulating bone metabolism.
neuropilin-1 (show NRP1 Antibodies) is regulated in the oral epithelium and is selectively up-regulated during epithelial dysplasia
NRP1 (show NELL1 Antibodies) over-expression in miR (show MLXIP Antibodies)-365 expressing cells could rescue invasion and growth defects of miR (show MLXIP Antibodies)-365. In addition, miR (show MLXIP Antibodies)-365 expression inversely correlated with NRP1 (show NELL1 Antibodies) protein levels in malignant melanoma
VEGF (show VEGFA Antibodies)/NRP (show NAP1L1 Antibodies)-1axis promotes progression of breast cancer via enhancement of epithelial-mesenchymal transition and activation of NF-kappaB (show NFKB1 Antibodies) and beta-catenin (show CTNNB1 Antibodies).
Data show that binding of pleiotrophin (PTN (show PTN Antibodies)) to neuropilin-1 (NRP-1 (show NRP1 Antibodies)) stimulated the internalization and recycling of NRP-1 (show NELL1 Antibodies) at the cell surface.
Study found significant down-regulation of placental NRP-1 (show NELL1 Antibodies) expression in fetal growth restriction pregnancies complicated with absent end-diastolic flow in the umbilical artery.
PDE4D (show PDE4D Antibodies) interacts directly with Neuropilins, positive regulators of Hedgehog (show SHH Antibodies) signal transduction pathway.
This gene encodes one of two neuropilins, which contain specific protein domains which allow them to participate in several different types of signaling pathways that control cell migration. Neuropilins contain a large N-terminal extracellular domain, made up of complement-binding, coagulation factor V/VIII, and meprin domains. These proteins also contains a short membrane-spanning domain and a small cytoplasmic domain. Neuropilins bind many ligands and various types of co-receptors\; they affect cell survival, migration, and attraction. Some of the ligands and co-receptors bound by neuropilins are vascular endothelial growth factor (VEGF) and semaphorin family members. Several alternatively spliced transcript variants that encode different protein isoforms have been described for this gene.
neuronal pentraxin 1
, neuronal pentraxin I
, neuronal pentraxin-1
, 47 kDa taipoxin-binding protein
, transmembrane receptor
, vascular endothelial cell growth factor 165 receptor