scholarly journals Inhibition of Glucocorticoid-induced Apoptosis by Targeting the Major Splice Variants ofBIMmRNA with Small Interfering RNA and Short Hairpin RNA

2004 ◽  
Vol 279 (53) ◽  
pp. 55809-55817 ◽  
Author(s):  
Marc T. Abrams ◽  
Noreen M. Robertson ◽  
Kyonggeun Yoon ◽  
Eric Wickstrom
2007 ◽  
Vol 18 (1) ◽  
pp. 74-80 ◽  
Author(s):  
Hiroyuki Mizuguchi ◽  
Naoko Funakoshi ◽  
Tetsuji Hosono ◽  
Fuminori Sakurai ◽  
Kenji Kawabata ◽  
...  

2004 ◽  
Vol 279 (40) ◽  
pp. 42230-42239 ◽  
Author(s):  
Jacek Krol ◽  
Krzysztof Sobczak ◽  
Urszula Wilczynska ◽  
Maria Drath ◽  
Anna Jasinska ◽  
...  

2006 ◽  
Vol 0 (0) ◽  
pp. 061222104941001
Author(s):  
Hiroyuki Mizuguchi ◽  
Naoko Funakoshi ◽  
Tetsuji Hosono ◽  
Fuminori Sakurai ◽  
Kenji Kawabata ◽  
...  

2017 ◽  
Vol 6 ◽  
pp. 173-182 ◽  
Author(s):  
Mitsuhiro Machitani ◽  
Fuminori Sakurai ◽  
Keisaku Wakabayashi ◽  
Kosuke Takayama ◽  
Masashi Tachibana ◽  
...  

2009 ◽  
Vol 43 (4) ◽  
pp. 157-169 ◽  
Author(s):  
Boris Thurisch ◽  
Shermi Y Liang ◽  
Nanette Sarioglu ◽  
Lutz Schomburg ◽  
Jörg Bungert ◽  
...  

Homozygous deficiency of the transcription factor Gata4 in mice causes lethality due to defects in ventral morphogenesis and heart tube formation. There is increasing evidence demonstrating that GATA4 function is also relevant for normal developed organ systems, including the heart and endocrinum. To analyze the implication of Gata4 beyond development, we generated transgenic mice expressing inducible small interfering RNA against Gata4. In longitudinal analysis, efficient suppression of Gata4 mRNA (down to 80% of wild-type levels) and protein expression in the heart was detected 38 days after induction of Gata4 short hairpin RNA. Decreased Gata4 expression was associated with reduction in the expression of known cardiac target genes, but the function of the heart remained unperturbed at 20–30% of normal Gata4 levels. Interestingly, Gata4 expression was almost abolished in the ovary and testis. This was accompanied in the testis by a significant reduction of GATA4 downstream target genes, such as the genes encoding Mullerian inhibiting substance (MIS) and steroidogenic acute regulatory (StAR) protein. By contrast, expression levels of Mis and Star were only slightly modified in the ovary, and concentrations of circulating FSH and LH were normal in female transgenic mice after induction of Gata4 short hairpin RNA. However, inhibition of Gata4 expression led to the formation of ovarian teratoma in 10% of females. Histology of the teratomas showed predominantly ectodermal and mesodermal structures. Our data demonstrate that Gata4 is critically involved in the function and integrity of the gonads in vivo.


2006 ◽  
Vol 17 (6) ◽  
pp. 2811-2823 ◽  
Author(s):  
Petra Kopp ◽  
Reiner Lammers ◽  
Martin Aepfelbacher ◽  
Günther Woehlke ◽  
Thomas Rudel ◽  
...  

Microtubules are important for the turnover of podosomes, dynamic, actin-rich adhesions implicated in migration and invasion of monocytic cells. The molecular basis for this functional dependency, however, remained unclear. Here, we show that contact by microtubule plus ends critically influences the cellular fate of podosomes in primary human macrophages. In particular, we identify the kinesin KIF1C, a member of the Kinesin-3 family, as a plus-end–enriched motor that targets regions of podosome turnover. Expression of mutation constructs or small interfering RNA-/short hairpin RNA-based depletion of KIF1C resulted in decreased podosome dynamics and ultimately in podosome deficiency. Importantly, protein interaction studies showed that KIF1C binds to nonmuscle myosin IIA via its PTPD-binding domain, thus providing an interface between the actin and tubulin cytoskeletons, which may facilitate the subcellular targeting of podosomes by microtubules. This is the first report to implicate a kinesin in podosome regulation and also the first to describe a function for KIF1C in human cells.


2007 ◽  
Vol 28 (10) ◽  
pp. 1621-1627 ◽  
Author(s):  
Xie-chuan WENG ◽  
Jian-quan ZHENG ◽  
Qing-e JIN ◽  
Xiao-yun MA

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