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A-L Hillje M A S Pavlou E Beckmann M M A Worlitzer L Bahnassawy L Lewejohann T Palm J C Schwamborn 《Cell death & disease》2013,4(12):e976
In the adult mammalian brain, neural stem cells in the subventricular zone continuously generate new neurons for the olfactory bulb. Cell fate commitment in these adult neural stem cells is regulated by cell fate-determining proteins. Here, we show that the cell fate-determinant TRIM32 is upregulated during differentiation of adult neural stem cells into olfactory bulb neurons. We further demonstrate that TRIM32 is necessary for the correct induction of neuronal differentiation in these cells. In the absence of TRIM32, neuroblasts differentiate slower and show gene expression profiles that are characteristic of immature cells. Interestingly, TRIM32 deficiency induces more neural progenitor cell proliferation and less cell death. Both effects accumulate in an overproduction of adult-generated olfactory bulb neurons of TRIM32 knockout mice. These results highlight the function of the cell fate-determinant TRIM32 for a balanced activity of the adult neurogenesis process. 相似文献
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Thomas Palm Kathrin Hemmer Julia Winter Inga B. Fricke Katsiaryna Tarbashevich Fereshteh Sadeghi Shakib Ina-Maria Rudolph Anna-Lena Hillje Paola De Luca Lamia'a Bahnassawy Rabea Madel Thomas Viel Adriana De Siervi Andreas H. Jacobs Sven Diederichs Jens C. Schwamborn 《Nucleic acids research》2013,41(6):3699-3712
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Heike Meiselbach Nico Vogel Georg Langlhofer Sabine Stangl Barbara Schleyer Lamia'a Bahnassawy Heinrich Sticht Hans-Georg Breitinger Cord-Michael Becker Carmen Villmann 《The Journal of biological chemistry》2014,289(42):29135-29147
Cys loop receptors are pentameric arrangements of independent subunits that assemble into functional ion channels. Each subunit shows a domain architecture. Functional ion channels can be reconstituted even from independent, nonfunctional subunit domains, as shown previously for GlyRα1 receptors. Here, we demonstrate that this reconstitution is not restricted to α1 but can be transferred to other members of the Cys loop receptor family. A nonfunctional GlyR subunit, truncated at the intracellular TM3–4 loop by a premature stop codon, can be complemented by co-expression of the missing tail portion of the receptor. Compared with α1 subunits, rescue by domain complementation was less efficient when GlyRα3 or the GABAA/C subunit ρ1 was used. If truncation disrupted an alternative splicing cassette within the intracellular TM3–4 loop of α3 subunits, which also regulates receptor desensitization, functional rescue was not possible. When α3 receptors were restored by complementation using domains with and without the spliced insert, no difference in desensitization was found. In contrast, desensitization properties could even be transferred between α1/α3 receptor chimeras harboring or lacking the α3 splice cassette proving that functional rescue depends on the integrity of the alternative splicing cassette in α3. Thus, an intact α3 splicing cassette in the TM3–4 loop environment is indispensable for functional rescue, and the quality of receptor restoration can be assessed from desensitization properties. 相似文献
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