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Rabbit anti-Human NISCH Polyclonal Antibody

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.

ADA-01081A

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.

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Specifications


Cat.No ADA-01081A ClonalityPolyclonal
Host SpeciesRabbitTarget NameNISCH
Target SynonymsI-1; IR1; IRAS; hIRAS; NISCHFormLiquid
Species ReactivityHuman, MouseIsotypeIgG
Storage Buffer50% Glycerol, PBS with 0.02% sodium azide, pH7.3.Purification MethodAffinity purification
Positive SamplesBT-474, Jurkat, Mouse brainApplicationELISA, WB

Immunogen Information


Immunogen DescriptionRecombinant fusion protein containing a sequence corresponding to amino acids 500-700 of human NISCH (NP_009115.2).Target SpeciesHuman
Uniprot IDQ9Y2I1Immunogen Sequence
Background Information
  • 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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