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NISCH encodes a nonadrenergic imidazoline-1 receptor protein that localizes to the cytosol and anchors to the inner layer of the plasma membrane. Additionally we are shipping Nischarin Antibodies (22) and Nischarin Kits (8) and many more products for this protein.
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results indicate that Nisch is an important AMPK (show PRKAA1 Proteins) inhibitor and a critical regulator of energy homeostasis, including lipid and glucose metabolism.
We identified a significant genetic interaction between Nisch and Itga5 (show ITGA5 Proteins); mice heterozygous for Itga5 (show ITGA5 Proteins)-null and homozygous for edison mutations display a significantly increased penetrance and severity of chronic otitis media.
Nischarin inhibits neurite outgrowth by blocking PAK1 (show PAK1 Proteins) activation in neurons.
Data from studies using various receptor antagonists/agonists suggest that imidazoline receptors (Nisch I-1), alpha2-adrenoceptors, and endothelin-A receptors are involved in body temperature regulation in mice.
Data suggest that both IR1 and IR2 (imidazoline receptor 2) play roles in acquisition of behavioral responses in alcoholism; activation of IR1 and IR2 may serve as molecular targets in prevention (and possibly treatment) of alcoholism.
Activation of I-1 R may activate FXR (show NR1H4 Proteins) to lower plasma lipids, suggesting I-1 R as a new target for the treatment of hyperlipidemia.
guanidine increases glucose uptake via an activation of imidazoline I2 receptor through AMPK (show PRKAA1 Proteins) activation in skeletal muscle cell.
Nisch regulates cell movement by inhibiting PAK.
Data suggest that nischarin, in addition to regulating the p21-activated kinase (PAK) strand of Rac1 signaling, can also regulate other links in the web of Rac1 signaling pathways.
Nischarin may serve as the functional I1-receptor
In the prefrontal cortex of long-term opiate/cocaine abusers, IRAS content was increased when compared to matched controls.
IRAS is a new mu opioid receptor (show OPRM1 Proteins) interacting protein (show RIPK1 Proteins) that regulates agonist-induced trafficking of mu opioid receptor (show OPRM1 Proteins).
Data found that NISCH was significantly downregulated in ovarian neoplasm through its promotor silencing with hypermethylation and its expression was correlated with poor prognosis.
Nischarin expression may therefore be used as a marker to predict the invasiveness and metastasis of primary breast cancer
Tobacco smoke induces methylation changes in the NISCH gene promoter before any detectable cancer.
unctional interaction between LKB1 (show STK11 Proteins) and Nischarin to inhibit cell migration and breast tumor progression
Imidazoline receptor 1 gene plays a role in the development of cardiac hypertrophy and ventirular remodeling.
Nischarin reduces alpha5 integrin expression leading to reduction of FAK (show PTK2 Proteins) phosphorylation and Rac (show AKT1 Proteins) GTP (show AK3 Proteins) loading, which in turn reduces tumor growth. NISCH also regulates PAK and LIMK (show LIMK1 Proteins) signaling.
Insulin receptor substrate 4 (show IRS4 Proteins) associates with the protein IRAS (IRAS protein)
I(1)-receptors can abrogate the primary signaling cascade activated by NGF (show NGFB Proteins), most likely by increasing levels of a specific phosphatase to return dually phosphorylated ERK (show EPHB2 Proteins) to its unphosphorylated state.
This gene encodes a nonadrenergic imidazoline-1 receptor protein that localizes to the cytosol and anchors to the inner layer of the plasma membrane. The orthologous mouse protein has been shown to influence cytoskeletal organization and cell migration by binding to alpha-5-beta-1 integrin. In humans, this protein has been shown to bind to the adapter insulin receptor substrate 4 (IRS4) to mediate translocation of alpha-5 integrin from the cell membrane to endosomes. Expression of this protein was reduced in human breast cancers while its overexpression reduced tumor growth and metastasis\; possibly by limiting the expression of alpha-5 integrin. In human cardiac tissue, this gene was found to affect cell growth and death while in neural tissue it affected neuronal growth and differentiation. Alternative splicing results in multiple transcript variants encoding differerent isoforms. Some isoforms lack the expected C-terminal domains of a functional imidazoline receptor.
, imidazoline receptor 1
, imidazoline receptor I-1-like protein
, imidazoline-1 receptor
, I-1 receptor candidate protein
, imidazoline receptor I-1
, I1R candidate protein
, imidazoline receptor antisera selected