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NPTX1 is down-regulated in colon cancer. In addition, NPTX1 inhibits the proliferation of colon cancer cells via decreasing cyclin A2 (show CCNA2 Antibodies) and CDK2 (show CDK2 Antibodies).
NPTX1 was significantly associated with bipolar disorder.
findings suggest that lower NARP (show NPTX2 Antibodies) mRNA expression contributes to lower excitatory drive onto parvalbumin (show PVALB Antibodies) interneurons in schizophrenia.
These results suggest that NPTX1 hypermethylation and consequent mRNA changes might be an important molecular mechanism in lung cancer.
Taken together, these results demonstrate that NP1 gene is a target of as hypoxia inducible factor-1 alpha (show HIF1A Antibodies) and it regulates NP1 expression by binding to hypoxia responsive elements in its promoter region.
Long acting progestin contraceptive-enhanced NPTX1 secretion and reactive oxygen species generation in endometrial stromal cells impair endometrial endothelial cells survival resulting in a loss in vascular integrity.
NPTX1 binds and inhibits TDGF1, and reduces both Nodal and BMP signaling.
Neuronal pentraxin 1 transgene is a key factor for the synapse loss, the neurite damage, and the apoptotic neuronal death evoked by amyloid-beta protein, which regulates NP1 expression.
The purpose of the present study was to assess the toxic effect of taipoxin in SCLC-cell lines and to determine if toxicity correlates to NPR (show NPTXR Antibodies) and NP1 and NP2 (show NPTX2 Antibodies) expression levels.
Neuronal pentraxin 1 accumulates on the postsynaptic terminal forming functional synapses.
work highlights a potential role for synaptic proteins, such as NP1 and glutamate (show GRIN1 Antibodies) receptors in lysosomal storage diseases.
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
NPTX1 is a member of the neuronal pentraxin gene family. Neuronal pentraxin 1 is similar to the rat NP1 gene which encodes a binding protein for the snake venom toxin taipoxin. Human NPTX1 mRNA is exclusively localized to the nervous system.
47 kDa taipoxin-binding protein
, neuronal pentraxin 1
, neuronal pentraxin-1
, neuronal pentraxin I
, neuronal pentraxin 1 L homeolog