High impact information on TAX1BP3

• The CLIP-170-like protein tip1p and the microtubule-bundling protein ase1p are required for this asymmetric regulation of microtubule dynamics, indicating contributions of factors both at microtubule plus ends and within the microtubule bundle [1].
• Transient expression experiments with a reporter construct including the c-Fos serum response element (SRE) showed that coexpression of TIP-1 with the constitutively active RhoA.V14 mutant and human rhotekin caused a strong activation of the SRE [2].
• The localization of HsMad1 to nuclear pore complexes suggests an alternate, non-mitotic role for the Mad1/Tax interaction in the viral transformation of cells [3].
• We addressed the specificity and function of Tax interaction with members of the NF-kappa B/I kappa B alpha family by using EMSA, protein affinity chromatography, protein-protein crosslinking and co-immunoprecipitation assays [4].
• The deduced amino acid sequence of TIP1 revealed that the enzyme contains 299 amino acids (34 kDa) and shares homologies to a variety of other extradiol dioxygenases [5].

Anatomical context of TAX1BP3

• A mutation disrupting Tax interaction with CREB-binding protein, CBP, did not affect lymphocyte immortalization by the infectious molecular clone [6].

Associations of TAX1BP3 with chemical compounds

• Based on the similar catechol moieties in PAH and steroid intermediates, together with its inducibility by testosterone, it is conceivable that TIP1 functions as a steroid extradiol dioxygenase to convert steroidal secocatechols into the disecoandrostanes [5].

References