Application Methods: Immunofluorescence (Immunocytochemistry), Immunohistochemistry (Paraffin), Immunoprecipitation, Western Blotting
Background: Wilms' Tumor 1 (WT1) is a transcription factor named from Wilms' Tumor 1, an embryonal malignancy of the kidneys that is caused by mutations in the WT1 gene (1). It is highly important in development, particularly of the genitourinary system, and mutations and dysregulation of expression of WT1 result in a variety of syndromes affecting the genitourinal system and other tissues (2-5).WT1 has a myriad of biological functions and a host of interacting partners and target genes (6). It can behave as a transcriptional activator, or a repressor, and can act as an oncogene or a tumor suppressor (7). It exerts influence over the epigenetic landscape, and also has post translational influence of gene expression through RNA interactions (8). The diverse biological roles of WT1 have been attributed to the existence of multiple isoforms and post translation modifications of the protein (9).
Application Methods: Flow Cytometry, Immunofluorescence (Immunocytochemistry), Western Blotting
Background: Bcl-2 exerts a survival function in response to a wide range of apoptotic stimuli through inhibition of mitochondrial cytochrome c release (1). It has been implicated in modulating mitochondrial calcium homeostasis and proton flux (2). Several phosphorylation sites have been identified within Bcl-2 including Thr56, Ser70, Thr74, and Ser87 (3). It has been suggested that these phosphorylation sites may be targets of the ASK1/MKK7/JNK1 pathway and that phosphorylation of Bcl-2 may be a marker for mitotic events (4,5). Mutation of Bcl-2 at Thr56 or Ser87 inhibits its anti-apoptotic activity during glucocorticoid-induced apoptosis of T lymphocytes (6). Interleukin-3 and JNK-induced Bcl-2 phosphorylation at Ser70 may be required for its enhanced anti-apoptotic functions (7).
|Human, Monkey, Mouse, Rat|
Application Methods: Chromatin IP, Immunofluorescence (Immunocytochemistry), Immunoprecipitation, Western Blotting
Background: TAZ is a transcriptional co-activator with a PDZ-binding motif that is regulated by its interaction with 14-3-3 proteins (1). TAZ shares homology with the WW domain of Yes-associated protein (YAP) (1). TAZ is proposed to modulate the switch between proliferation and differentiation of mesenchymal stem cells (MSC) via interaction with transcription factors Runx2 and PPARγ. This process is critical to normal tissue development and the prevention of tumor formation. Due to its role in determination of MSC fate, TAZ may have clinical relevance to several human diseases caused by an imbalance of MSC differentiation (2,3). TAZ is negatively regulated via phosphorylation by LATS1/2, core kinases in the Hippo signaling pathway that controls stem cell development, tissue growth and tumor development (4).