Disease relevance of heph

• Statistically significant PTB overexpression was seen in all glioma grades, with the highest increase in grade IV tumors [1].

High impact information on heph

• These proteins repress certain exons in early myoblasts, but upon differentiation of mature myotubes PTB/nPTB expression is reduced, leading to increased inclusion of their target exons [2].
• During differentiation of C2C12 myoblasts, nPTB protein but not mRNA expression is strongly reduced, concurrent with the up-regulation of miR-133 and the induction of splicing for several PTB-repressed exons [2].
• Most importantly, a signal from the somatic sex-determination pathway that is dependent on the male-specific isoform of the doublesex protein (DSX(M)) regulates PTB, providing evidence for the necessity of soma-germline communication in the differentiation of the male germline [3].
• Specifically, loss of dmPTB affects spermatid differentiation, resulting in the accumulation of cysts with elongated spermatids without producing fully separated motile sperms [3].
• Since Notch is a well-known inducer of glial cell fate, we determined whether overexpression of PTB in glial cell tumors provides a selective growth advantage by inhibiting activated Notch (Notch1IC)-mediated differentiation [1].

Biological context of heph

• These data indicate that PTB regulates gene expression in specific tissue lineages during development [4].
• Here, we investigate the expression of PTB during Drosophila embryogenesis using in situ hybridization assays [4].
• Additionally, PTB interacts with elements that mediate 3-prime end processing of nascent transcripts (Mol. Cell. Biol., 19 (1999) 78) and is required for the expression of viral mRNAs that contain an internal ribosome binding site (RNA, 5 (1999) 344; RNA, 1 (1995) 924) [4].

Anatomical context of heph

• Polypyrimidine tract binding protein (PTB) is expressed in developing mammalian astrocytes, absent in mature adult astrocytes, and aberrantly elevated in gliomas [1].

References