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The antibody against NISCH was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 500-700 of human NISCH (NP_009115.2) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, ELISA.
The antibody against NISCH was raised in Rabbit using the recombinant fusion protein containing a sequence corresponding to amino acids 500-700 of human NISCH (NP_009115.2) as the immunogen. The polyclonal antibody exists as a isotype IgG, by affinity purification. This antibody has been validated on WB, ELISA.
| Cat.No | ADA-01081A | Clonality | Polyclonal |
|---|---|---|---|
| Host Species | Rabbit | Target Name | NISCH |
| Target Synonyms | I-1; IR1; IRAS; hIRAS; NISCH | Form | Liquid |
| Species Reactivity | Human, Mouse | Isotype | IgG |
| Storage Buffer | 50% Glycerol, PBS with 0.02% sodium azide, pH7.3. | Purification Method | Affinity purification |
| Positive Samples | BT-474, Jurkat, Mouse brain | Application | ELISA, WB |
| Immunogen Description | Recombinant fusion protein containing a sequence corresponding to amino acids 500-700 of human NISCH (NP_009115.2). | Target Species | Human |
|---|---|---|---|
| Uniprot ID | Q9Y2I1 | Immunogen Sequence |
Uniprot Id
Q9Y2I1
Target Species
Human
Target Name
NISCH
Target Full Name
Nischarin
Target Function
Acts either as the functional imidazoline-1 receptor (I1R) candidate or as a membrane-associated mediator of the I1R signaling. Binds numerous imidazoline ligands that induces initiation of cell-signaling cascades triggering to cell survival, growth and migration. Its activation by the agonist rilmenidine induces an increase in phosphorylation of mitogen-activated protein kinases MAPK1 and MAPK3 in rostral ventrolateral medulla (RVLM) neurons that exhibited rilmenidine-evoked hypotension. Blocking its activation with efaroxan abolished rilmenidine-induced mitogen-activated protein kinase phosphorylation in RVLM neurons. Acts as a modulator of Rac-regulated signal transduction pathways. Suppresses Rac1-stimulated cell migration by interacting with PAK1 and inhibiting its kinase activity. Also blocks Pak-independent Rac signaling by interacting with RAC1 and inhibiting Rac1-stimulated NF-kB response element and cyclin D1 promoter activation. Inhibits also LIMK1 kinase activity by reducing LIMK1 'Tyr-508' phosphorylation. Inhibits Rac-induced cell migration and invasion in breast and colon epithelial cells. Inhibits lamellipodia formation, when overexpressed. Plays a role in protection against apoptosis. Involved in association with IRS4 in the enhancement of insulin activation of MAPK1 and MAPK3. When overexpressed, induces a redistribution of cell surface ITGA5 integrin to intracellular endosomal structures.
Target Subcellular Location
Cell membrane. Cytoplasm. Early endosome. Recycling endosome.
Target Tissue Specificity
Isoform 1, isoform 3 and isoform 4 are expressed in brain. Isoform 1 is expressed in endocrine tissues.
Target Synonyms
NISCH; IRAS; KIAA0975; Nischarin; Imidazoline receptor 1; I-1; IR1; Imidazoline receptor antisera-selected protein; hIRAS; Imidazoline-1 receptor; I1R; Imidazoline-1 receptor candidate protein; I-1 receptor candidate protein; I1R candidate protein
Target Background
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.
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