WTIP Antibody – Rabbit Polyclonal

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. Ref.2 Ref.4 Ref.5 Ref.6

Subunit structure: Forms homodimers

By similarity. Interacts with CD2AP and WT1. Interacts (via LIM domains) with SNAI1 (via SNAG domain), SNAI2/SLUG (via SNAG domain) and SCRT1 (via SNAG domain)

By similarity. Interacts with EIF4E, AGO1, AGO2, DCP2, DDX6, LATS1, LATS2, SAV1, EGLN2/PHD1 and EGLN3/PHD3. Interacts (via LIM domains) with isoform 1 and isoform 3 of VHL. Interacts with ROR2

By similarity. Following treatment with bacterial lipopolysaccharide (LPS), forms a complex with MAPK8IP3 and dynein intermediate chain

By similarity. Ref.2 Ref.4 Ref.6

Subcellular location: Cell junction › adherens junction. Nucleus

By similarity. 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. Ref.3 Ref.4

Sequence similarities: Belongs to the zyxin/ajuba family.Contains 3 LIM zinc-binding domains.