scholarly journals A Pivotal Role of the Basic Leucine Zipper Transcription Factor bZIP53 in the Regulation of Arabidopsis Seed Maturation Gene Expression Based on Heterodimerization and Protein Complex Formation

2009 ◽  
Vol 21 (6) ◽  
pp. 1747-1761 ◽  
Author(s):  
Rosario Alonso ◽  
Luis Oñate-Sánchez ◽  
Fridtjof Weltmeier ◽  
Andrea Ehlert ◽  
Isabel Diaz ◽  
...  
2002 ◽  
Vol 169 (10) ◽  
pp. 5715-5725 ◽  
Author(s):  
Shanjin Cao ◽  
Jianguo Liu ◽  
Marta Chesi ◽  
Peter Leif Bergsagel ◽  
I-Cheng Ho ◽  
...  

Cell Systems ◽  
2018 ◽  
Vol 6 (1) ◽  
pp. 75-89.e11 ◽  
Author(s):  
Philippe Lucarelli ◽  
Marcel Schilling ◽  
Clemens Kreutz ◽  
Artyom Vlasov ◽  
Martin E. Boehm ◽  
...  

2012 ◽  
Vol 40 (2) ◽  
pp. 415-418 ◽  
Author(s):  
Marcellus Ubbink

Recent studies have provided experimental information about the initial stage of protein complex formation, the encounter complex. This stage is particularly important in the weak and transient complexes formed between electron transfer proteins and their partners. These studies are discussed and the role of the encounter complex is interpreted in terms of the specific requirements that the biological function puts on these complexes.


2013 ◽  
Vol 289 (3) ◽  
pp. 1629-1638 ◽  
Author(s):  
So-ichi Tamai ◽  
Keisuke Imaizumi ◽  
Nobuhiro Kurabayashi ◽  
Minh Dang Nguyen ◽  
Takaya Abe ◽  
...  

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the loss of motor neurons. Here we show that the basic leucine zipper transcription factor NFIL3 (also called E4BP4) confers neuroprotection in models of ALS. NFIL3 is up-regulated in primary neurons challenged with neurotoxic insults and in a mouse model of ALS. Overexpression of NFIL3 attenuates excitotoxic neuronal damage and protects neurons against neurodegeneration in a cell-based ALS model. Conversely, reduction of NFIL3 exacerbates neuronal demise in adverse conditions. Transgenic neuronal expression of NFIL3 in ALS mice delays disease onset and attenuates motor axon and neuron degeneration. These results suggest that NFIL3 plays a neuroprotective role in neurons and constitutes a potential therapeutic target for neurodegeneration.


eLife ◽  
2014 ◽  
Vol 3 ◽  
Author(s):  
Xiaofei Yu ◽  
Yuhao Wang ◽  
Mi Deng ◽  
Yun Li ◽  
Kelly A Ruhn ◽  
...  

Innate lymphoid cells (ILCs) are recently identified lymphocytes that limit infection and promote tissue repair at mucosal surfaces. However, the pathways underlying ILC development remain unclear. Here we show that the transcription factor NFIL3 directs the development of a committed bone marrow precursor that differentiates into all known ILC lineages. NFIL3 was required in the common lymphoid progenitor (CLP), and was essential for the differentiation of αLP, a bone marrow cell population that gives rise to all known ILC lineages. Clonal differentiation studies revealed that CXCR6+ cells within the αLP population differentiate into all ILC lineages but not T- and B-cells. We further show that NFIL3 governs ILC development by directly regulating expression of the transcription factor TOX. These findings establish that NFIL3 directs the differentiation of a committed ILC precursor that gives rise to all ILC lineages and provide insight into the defining role of NFIL3 in ILC development.


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