scholarly journals Coming into bloom: a light-sensitive transcription factor complex tells roses when to flower

2021 ◽  
Author(s):  
Martin Balcerowicz
Keyword(s):  
Transcription Factor ◽  
Transcription Factor Complex

scholarly journals Protein kinase C-theta isoenzyme selective stimulation of the transcription factor complex AP-1 in T lymphocytes.

1996 ◽  
Vol 16 (4) ◽  
pp. 1842-1850 ◽  
Author(s):  
G Baier-Bitterlich ◽  
F Uberall ◽  
B Bauer ◽  
F Fresser ◽  
H Wachter ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcriptional Activation ◽  
Dominant Negative ◽  
Dominant Negative Mutant ◽  
Kinase C ◽  
Pkc Isoforms ◽  
Pkc Alpha ◽  
Transcriptional Complex ◽  
Induced Signal ◽  
Transcription Factor Complex

T-lymphocyte stimulation requires activation of several protein kinases, including the major phorbol ester receptor protein kinase C (PKC), ultimately leading to induction of lymphokines, such as interleukin-2 (IL-2). The revelant PKC isoforms which are involved in the activation cascades of nuclear transcription factors involved in IL-2 production have not yet been clearly defined. We have examined the potential role of two representative PKC isoforms in the induction of the IL-2 gene, i.e., PKC-alpha and PKC-theta, the latter being expressed predominantly in hematopoietic cell lines, particularly T cells. Similar to that of PKC-alpha, PKC-theta overexpression in murine EL4 thymoma cells caused a significant increase in phorbol 12-myristate 13-acetate (PMA)-induced transcriptional activation of full-length IL-2-chloramphenicol acetyltransferase (CAT) and NF-AT-CAT but not of NF-IL2A-CAT or NF-kappaB promoter-CAT reporter gene constructs. Importantly, the critical AP-1 enhancer element was differentially modulated by these two distinct PKC isoenzymes, since only PKC-theta but not PKC-alpha overexpression resulted in an approximately 2.8-fold increase in AP-1-collagenase promoter CAT expression in comparison with the vector control. Deletion of the AP-1 enhancer site in the collagenase promoter rendered it unresponsive to PKC-theta. Expression of a constitutively active mutant PKC-theta A148E (but not PKC-alpha A25E) was sufficient to induce activation of AP-1 transcription factor complex in the absence of PMA stimulation. Conversely, a catalytically inactive PKC-theta K409R (but not PKC-alpha K368R) mutant abrogated endogenous PMA-mediated activation of AP-1 transcriptional complex. Dominant negative mutant Ha-RasS17N completely inhibited the PKC-O A148E-induced signal, PKC-O. Expression of a constitutively active mutant PKC-O A148E (but not PKC-alpha A25E) was sufficient to induce activation of AP-1 transcription factor complex in the absence of PMA stimulation. Conversely, a catalytically inactive PKC-O K409R (but not PKC-alpha K368R) mutant abrogated endogenous PMA-mediated activation of AP-1 transcriptional complex. Dominant negative mutant Ha-enRasS17N completely inhibited in the PKC-O A148E-induced signal, identifying PKC-theta as a specific constituent upstream of or parallel to Ras in the signaling cascade leading to AP transcriptional activation.

scholarly journals Downregulation of c-Jun Expression by Transcription Factor C/EBPα Is Critical for Granulocytic Lineage Commitment

2002 ◽  
Vol 22 (24) ◽  
pp. 8681-8694 ◽  
Author(s):  
Janki Rangatia ◽  
Rajani Kanth Vangala ◽  
Nicolai Treiber ◽  
Pu Zhang ◽  
Hanna Radomska ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Knockout Mouse ◽  
Leucine Zipper ◽  
Fetal Liver ◽  
Mrna Level ◽  
Monocytic Differentiation ◽  
Granulocytic Differentiation ◽  
Conditional Expression ◽  
Factor C ◽  
Transcription Factor Complex

ABSTRACT The transcription factor C/EBPα is crucial for the differentiation of granulocytes. Conditional expression of C/EBPα triggers neutrophilic differentiation, and C/EBPα can block 12-O-tetradecanoylphorbol-13-acetate-induced monocytic differentiation of bipotential myeloid cells. In C/EBPα knockout mice, no mature granulocytes are present. A dramatic increase of c-Jun mRNA in C/EBPα knockout mouse fetal liver was observed. c-Jun, a component of the AP-1 transcription factor complex and a coactivator of the transcription factor PU.1, is important for monocytic differentiation. Here we report that C/EBPα downregulates c-Jun expression to drive granulocytic differentiation. An ectopic increase of C/EBPα expression decreases the c-Jun mRNA level, and the human c-Jun promoter activity is downregulated eightfold in the presence of C/EBPα. C/EBPα and c-Jun interact through their leucine zipper domains, and this interaction prevents c-Jun from binding to DNA. This results in downregulation of c-Jun's capacity to autoregulate its own promoter through the proximal AP-1 site. Overexpression of c-Jun prevents C/EBPα-induced granulocytic differentiation. Thus, we propose a model in which C/EBPα needs to downregulate c-Jun expression and transactivation capacity for promoting granulocytic differentiation.

scholarly journals Quality of TCR signaling determined by differential affinities of enhancers for the composite BATF–IRF4 transcription factor complex

2017 ◽  
Vol 18 (5) ◽  
pp. 563-572 ◽  
Author(s):  
Arifumi Iwata ◽  
Vivek Durai ◽  
Roxane Tussiwand ◽  
Carlos G Briseño ◽  
Xiaodi Wu ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Tcr Signaling ◽  
Transcription Factor Complex
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