|Application ||IHC-P, WB, IF, E|
|Calculated MW||45124 Da|
|Antigen Region||243-271 aa|
|Other Names||Wilms tumor protein 1-interacting protein, WT1-interacting protein, WTIP|
|Target/Specificity||This WTIP antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 243-271 amino acids of human WTIP.|
|Format||Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification.|
|Storage||Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles.|
|Precautions||WTIP Antibody (C-term) is for research use only and not for use in diagnostic or therapeutic procedures.|
|Function||Adapter or scaffold protein which participates in the assembly of numerous protein complexes and is involved in several cellular processes such as cell fate determination, cytoskeletal organization, repression of gene transcription, cell-cell adhesion, cell differentiation, proliferation and migration. Positively regulates microRNA (miRNA)-mediated gene silencing. Negatively regulates Hippo signaling pathway and antagonizes phosphorylation of YAP1. Acts as a transcriptional corepressor for SNAI1 and SNAI2/SLUG-dependent repression of E-cadherin transcription. Acts as a hypoxic regulator by bridging an association between the prolyl hydroxylases and VHL enabling efficient degradation of HIF1A. In podocytes, may play a role in the regulation of actin dynamics and/or foot process cytoarchitecture (By similarity). In the course of podocyte injury, shuttles into the nucleus and acts as a transcription regulator that represses WT1-dependent transcription regulation, thereby translating changes in slit diaphragm structure into altered gene expression and a less differentiated phenotype. Involved in the organization of the basal body (By similarity). Involved in cilia growth and positioning (By similarity).|
|Cellular Location||Cell junction, adherens junction. Nucleus. Cytoplasm, P-body. Note=Following podocyte injury, caused by treatment with LPS, puromycin aminonucleoside, ultraviolet or hydrogen peroxide, translocates from sites of cell- cell contacts into the cytosol and nucleus. The shift from cell contacts to intracellular plaques starts as early as 1 hour after LPS stimulation and intranuclear localization begins 3 hours after LPS treatment. Maximal nuclear localization is achieved 6 hours after LPS treatment. Nuclear translocation requires dynein motor activity and intact microtubule network (By similarity). Returns to cell-cell contacts 24 hours after LPS stimulation. In the presence of ROR2, localizes to the plasma membrane (By similarity).|
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Provided below are standard protocols that you may find useful for product applications.
WTIP may monitor slit diaphragm protein assembly, a specialized adherens junction characteristic of podocytes. In case of podocyte injury, it shuttles into the nucleus and acts as a transcription regulator that represses WT1-dependent transcription regulation, thereby translating changes in slit diaphragm structure into altered gene expression and a less differentiated phenotype (By similarity).
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