BTG2 is a member of the BTG/Tob family. It plays an important role in cellular differentiation and cancer. It is a direct transcriptional target of p53 and has been shown to be a major effector of suppression of Ras-induced transformation by p53 []. BTG2 has been shown to function as a transcription cofactor []. BTG2 is also found to interact directly with the first RRM domain of the poly(A)-binding protein PABPC1 and promoted mRNA poly(A) tail shortening []. In mice, its overexpression during neurogenesis led to microcephaly, while its deletion triggered impaired neuronal differentiation [].The BTG/Tob family members contain an conserved N-terminal domain, known as APRO domain (AntiPROliferative) or BTG domain. In mammals, six family members have been identified: BTG1, BTG2/PC3/Tis21, BTG3/ANA, BTG4/PC3B, Tob1/Tob and Tob2. They interact with CAF1, a subunit of the CCR4-NOT complex. They display antiproliferative properties as their ectopic expression in a variety of cell lines reduced cell proliferation [].
This entry represents a conserved domain found in the N-terminal of the BTG family members (also known as anti-proliferative proteins). In mammals, BTG family comprises six proteins: BTG1, BTG2/PC3/Tis21, BTG3/ANA, BTG4/PC3B, Tob1/Tob and Tob2. They regulate cell cycle progression in a variety of cell types [].These proteins have from 158 to 363 amino acid residues, that are highly similar and include 3 conserved cysteine residues. BTG2 seems to have asignal sequence; while the other proteins may lack such a domain.
This entry represents a conserved domain found in the N-terminal of the BTG family members (also known as anti-proliferative proteins). In mammals, BTG family comprises six proteins: BTG1, BTG2/PC3/Tis21, BTG3/ANA, BTG4/PC3B, Tob1/Tob and Tob2. They regulate cell cycle progression in a variety of cell types [].These proteins have from 158 to 363 amino acid residues, that are highly similar and include 3 conserved cysteine residues. BTG2 seems to have asignal sequence; while the other proteins may lack such a domain.
