High impact information on Ranbp1

• The purified soluble 23 kDa Ran binding protein RanBP1 does not activate RanGTPase, but increases GTP hydrolysis induced by the RanGTPase-activating protein RanGAP1 by an order of magnitude [1].
• We report that Tax directly binds Ran and Ran-binding protein-1, locates to centrosomes/spindle poles, and causes supernumerary centrosomes [2].
• Abnormal centrosome amplification in cells through the targeting of Ran-binding protein-1 by the human T cell leukemia virus type-1 Tax oncoprotein [2].
• Two E2F sites control growth-regulated and cell cycle-regulated transcription of the Htf9-a/RanBP1 gene through functionally distinct mechanisms [3].
• The murine Htf9-a/RanBP1 and Htf9-c genes are divergently transcribed from a shared TATA-less promoter [4].

Biological context of Ranbp1

• These results link the control of Htf9-a/RanBP-1 expression to the cell cycle progression [5].
• We have investigated whether expression of the Htf9-a/RanBP-1 gene is linked to cell proliferation [5].
• Expression of the Htf9-a/RanBP-1 transcript appeared to be dependent on the proliferating state of the cells and peaked in S phase [5].
• We have identified a promoter region required for Htf9-a cell cycle-dependent expression and for responsiveness to cell cycle regulators [5].
• Interactions with single-stranded and double-stranded DNA-binding factors and alternative promoter conformation upon transcriptional activation of the Htf9-a/RanBP1 and Htf9-c genes [4].

References