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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 (zeige CCNA2 Antikörper) and CDK2 (zeige CDK2 Antikörper).
NPTX1 was significantly associated with bipolar disorder.
findings suggest that lower NARP (zeige NPTX2 Antikörper) mRNA expression contributes to lower excitatory drive onto parvalbumin (zeige PVALB Antikörper) 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 (zeige HIF1A Antikörper) 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 (zeige NPTXR Antikörper) and NP1 and NP2 (zeige NPTX2 Antikörper) 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 (zeige GRIN1 Antikörper) 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 (zeige GRIA1 Antikörper) at synaptic sites and that NP1, not its family member NP2 (zeige NRP2 Antikörper), is involved in the neuronal death mechanisms
Genetic deletion of NP1 prevents hypoxic-ischemic neuronal death by reducing synaptic clustering of GluR1 (zeige GRIA1 Antikörper).
These findings suggest that Narp (zeige NPTX2 Antikörper) 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 (zeige BAX Antikörper)) 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