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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. Zusätzlich bieten wir Ihnen Nischarin Antikörper (22) und Nischarin Kits (8) und viele weitere Produktgruppen zu diesem Protein an.
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results indicate that Nisch is an important AMPK (zeige PRKAA1 Proteine) inhibitor and a critical regulator of energy homeostasis, including lipid and glucose metabolism.
We identified a significant genetic interaction between Nisch and Itga5 (zeige ITGA5 Proteine); mice heterozygous for Itga5 (zeige ITGA5 Proteine)-null and homozygous for edison mutations display a significantly increased penetrance and severity of chronic otitis media.
Nischarin inhibits neurite outgrowth by blocking PAK1 (zeige PAK1 Proteine) 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 (zeige NR1H4 Proteine) 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 (zeige PRKAA1 Proteine) 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
IRAS is a new mu opioid receptor (zeige OPRM1 Proteine) interacting protein (zeige RIPK1 Proteine) that regulates agonist-induced trafficking of mu opioid receptor (zeige OPRM1 Proteine).
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 (zeige STK11 Proteine) 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 (zeige PTK2 Proteine) phosphorylation and Rac (zeige AKT1 Proteine) GTP (zeige AK3 Proteine) loading, which in turn reduces tumor growth. NISCH also regulates PAK and LIMK (zeige LIMK1 Proteine) signaling.
Insulin receptor substrate 4 (zeige IRS4 Proteine) associates with the protein IRAS (IRAS protein)
I(1)-receptors can abrogate the primary signaling cascade activated by NGF (zeige NGFB Proteine), most likely by increasing levels of a specific phosphatase to return dually phosphorylated ERK (zeige EPHB2 Proteine) to its unphosphorylated state.
hIRAS expression in PC12 cells resulted in protection against apoptosis
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