scholarly journals A Zinc Finger Transcription Factor, αA-Crystallin Binding Protein 1, Is a Negative Regulator of the Chondrocyte-Specific Enhancer of the α1(II) Collagen Gene

2006 ◽  
Vol 26 (13) ◽  
pp. 5202-5202 ◽  
Author(s):  
Kazuhiro Tanaka ◽  
Yoshihiro Matsumoto ◽  
Fumihiko Nakatani ◽  
Yukihide Iwamoto ◽  
Yoshihiko Yamada
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Binding Protein ◽  
Negative Regulator ◽  
Collagen Gene ◽  
Zinc Finger Transcription Factor

ZAT11, a zinc finger transcription factor, is a negative regulator of nickel ion tolerance in Arabidopsis

2014 ◽  
Vol 33 (12) ◽  
pp. 2015-2021 ◽  
Author(s):  
Xiao-Min Liu ◽  
Jonguk An ◽  
Hay Ju Han ◽  
Sun Ho Kim ◽  
Chae Oh Lim ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Zinc Finger ◽  
Negative Regulator ◽  
Nickel Ion ◽  
Zinc Finger Transcription Factor

scholarly journals Zinc finger transcription factor zDC is a negative regulator required to prevent activation of classical dendritic cells in the steady state

2012 ◽  
Vol 209 (9) ◽  
pp. 1583-1593 ◽  
Author(s):  
Matthew M. Meredith ◽  
Kang Liu ◽  
Alice O. Kamphorst ◽  
Juliana Idoyaga ◽  
Arito Yamane ◽  
...  
Keyword(s):  
Dendritic Cells ◽  
Transcription Factor ◽  
Steady State ◽  
Zinc Finger ◽  
Immune Cell ◽  
Negative Regulator ◽  
Binding Motif ◽  
Zinc Finger Transcription Factor ◽  
Mhc Molecules ◽  
Activation Pathways

Classical dendritic cells (cDCs) process and present antigens to T cells. Under steady-state conditions, antigen presentation by cDCs induces tolerance. In contrast, during infection or inflammation, cDCs become activated, express higher levels of cell surface MHC molecules, and induce strong adaptive immune responses. We recently identified a cDC-restricted zinc finger transcription factor, zDC (also known as Zbtb46 or Btbd4), that is not expressed by other immune cell populations, including plasmacytoid DCs, monocytes, or macrophages. We define the zDC consensus DNA binding motif and the genes regulated by zDC using chromatin immunoprecipitation and deep sequencing. By deleting zDC from the mouse genome, we show that zDC is primarily a negative regulator of cDC gene expression. zDC deficiency alters the cDC subset composition in the spleen in favor of CD8+ DCs, up-regulates activation pathways in steady-state cDCs, including elevated MHC II expression, and enhances cDC production of vascular endothelial growth factor leading to increased vascularization of skin-draining lymph nodes. Consistent with these observations, zDC protein expression is rapidly down-regulated after TLR stimulation. Thus, zDC is a TLR-responsive, cDC-specific transcriptional repressor that is in part responsible for preventing cDC maturation in the steady state.

scholarly journals A Zinc Finger Transcription Factor, αA-Crystallin Binding Protein 1, Is a Negative Regulator of the Chondrocyte-Specific Enhancer of the α1(II) Collagen Gene

2000 ◽  
Vol 20 (12) ◽  
pp. 4428-4435 ◽  
Author(s):  
Kazuhiro Tanaka ◽  
Yoshihiro Matsumoto ◽  
Fumihiko Nakatani ◽  
Yukihide Iwamoto ◽  
Yoshihiko Yamada
Keyword(s):  
Zinc Finger ◽  
Binding Protein ◽  
Screening Method ◽  
Limb Bud ◽  
Negative Regulator ◽  
Cdna Expression Library ◽  
Collagen Gene ◽  
Specific Expression ◽  
Enhancer Activity ◽  
Enhancer Element

ABSTRACT Transcription of the type II collagen gene (Col2a1) is regulated by multiple cis-acting sites. The enhancer element, which is located in the first intron, is necessary for high-level and cartilage-specific expression of Col2a1. A mouse limb bud cDNA expression library was screened by theSaccharomyces cerevisiae one-hybrid screening method to identify protein factors bound to the enhancer. A zinc finger protein, αA-crystallin binding protein 1 (CRYBP1), which had been reported to bind to the mouse αA-crystallin gene promoter, was isolated. We herein demonstrate that CRYBP1 is involved in the negative regulation of Col2a1 enhancer activity. CRYBP1 mRNA expression was downregulated during chondrocyte differentiation in vitro. In situ hybridization analysis of developing mouse cartilage showed that CRYBP1 mRNA was also downregulated during mesenchymal condensation and that CRYBP1 mRNA was highly expressed by hypertrophic chondrocytes, but at very low levels by resting and proliferating chondrocytes. Expression of recombinant CRYBP1 in a transfected rat chondrosarcoma cell line inhibitedCol2a1 enhancer activity. Electrophoretic mobility shift assays showed that CRYBP1 bound a specific sequence within theCol2a1 enhancer and inhibited the binding of Sox9, an activator for Col2a1, to the enhancer. Cotransfection of CRYBP1 with Sox9 into BALB/c 3T3 cells inhibited activation of theCol2a1 enhancer by Sox9. These results suggest a novel mechanism that negatively regulates cartilage-specific expression ofCol2a1.

Characterization of the human suppressor of fused, a negative regulator of the zinc-finger transcription factor Gli

1999 ◽  
Vol 112 (23) ◽  
pp. 4437-4448 ◽  
Author(s):  
D.M. Stone ◽  
M. Murone ◽  
S. Luoh ◽  
W. Ye ◽  
M.P. Armanini ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Amino Acid ◽  
Zinc Finger ◽  
Hedgehog Signaling ◽  
Adaptor Protein ◽  
Negative Regulator ◽  
Calculated Molecular Mass ◽  
Zinc Finger Transcription Factor ◽  
Suppressor Of Fused ◽  
Sequence Identity

Drosophila Suppressor of fused (Su(fu)) encodes a novel 468-amino-acid cytoplasmic protein which, by genetic analysis, functions as a negative regulator of the Hedgehog segment polarity pathway. Here we describe the primary structure, tissue distribution, biochemical and functional analyses of a human Su(fu) (hSu(fu)). Two alternatively spliced isoforms of hSu(fu) were identified, predicting proteins of 433 and 484 amino acids, with a calculated molecular mass of 48 and 54 kDa, respectively. The two proteins differ only by the inclusion or exclusion of a 52-amino-acid extension at the carboxy terminus. Both isoforms were expressed in multiple embryonic and adult tissues, and exhibited a developmental profile consistent with a role in Hedgehog signaling. The hSu(fu) contains a high-scoring PEST-domain, and exhibits an overall 37% sequence identity (63% similarity) with the Drosophila protein and 97% sequence identity with the mouse Su(fu). The hSu(fu) locus mapped to chromosome 10q24-q25, a region which is deleted in glioblastomas, prostate cancer, malignant melanoma and endometrial cancer. HSu(fu) was found to repress activity of the zinc-finger transcription factor Gli, which mediates Hedgehog signaling in vertebrates, and to physically interact with Gli, Gli2 and Gli3 as well as with Slimb, an F-box containing protein which, in the fly, suppresses the Hedgehog response, in part by stimulating the degradation of the fly Gli homologue. Coexpression of Slimb with Su(fu) potentiated the Su(fu)-mediated repression of Gli. Taken together, our data provide biochemical and functional evidence for the hypothesis that Su(fu) is a key negative regulator in the vertebrate Hedgehog signaling pathway. The data further suggest that Su(fu) can act by binding to Gli and inhibiting Gli-mediated transactivation as well as by serving as an adaptor protein, which links Gli to the Slimb-dependent proteasomal degradation pathway.

scholarly journals The apple C2H2-type zinc finger transcription factor MdZAT10 positively regulates JA-induced leaf senescence by interacting with MdBT2

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Kuo Yang ◽  
Jian-Ping An ◽  
Chong-Yang Li ◽  
Xue-Na Shen ◽  
Ya-Jing Liu ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
Transcription Factor ◽  
Liquid Chromatography ◽  
Zinc Finger ◽  
Leaf Senescence ◽  
Transcriptional Activity ◽  
Molecular Mechanisms ◽  
Liquid Chromatography Mass Spectrometry ◽  
Zinc Finger Transcription Factor ◽  
Insight Into

AbstractJasmonic acid (JA) plays an important role in regulating leaf senescence. However, the molecular mechanisms of leaf senescence in apple (Malus domestica) remain elusive. In this study, we found that MdZAT10, a C2H2-type zinc finger transcription factor (TF) in apple, markedly accelerates leaf senescence and increases the expression of senescence-related genes. To explore how MdZAT10 promotes leaf senescence, we carried out liquid chromatography/mass spectrometry screening. We found that MdABI5 physically interacts with MdZAT10. MdABI5, an important positive regulator of leaf senescence, significantly accelerated leaf senescence in apple. MdZAT10 was found to enhance the transcriptional activity of MdABI5 for MdNYC1 and MdNYE1, thus accelerating leaf senescence. In addition, we found that MdZAT10 expression was induced by methyl jasmonate (MeJA), which accelerated JA-induced leaf senescence. We also found that the JA-responsive protein MdBT2 directly interacts with MdZAT10 and reduces its protein stability through ubiquitination and degradation, thereby delaying MdZAT10-mediated leaf senescence. Taken together, our results provide new insight into the mechanisms by which MdZAT10 positively regulates JA-induced leaf senescence in apple.

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