ZNF16 (HZF1) promotes erythropoiesis and megakaryocytopoiesis via regulation of the c-KIT gene

2014 ◽  
Vol 458 (1) ◽  
pp. 171-183 ◽  
Author(s):  
Jing Chen ◽  
Xiao-Bo Li ◽  
Rui Su ◽  
Li Song ◽  
Fang Wang ◽  
...  
Keyword(s):  
Progenitor Cells ◽  
Target Gene ◽  
Megakaryocytic Differentiation ◽  
Kit Gene ◽  
Direct Target Gene ◽  
Direct Target

The present study demonstrated that ZNF16 (HZF1) plays an important role in erythroid and megakaryocytic differentiation of human haematopoietic stem/progenitor cells, identified and validated c-KIT as a direct target gene of ZNF16, and demonstrated that ZNF16 functions via its regulation on the c-Kit/c-Raf/MEK/ERK/c-Jun/HEY1/GATA1 cascade.

scholarly journals Identification ofTDRD1as a direct target gene ofERGin primary prostate cancer

2013 ◽  
Vol 133 (2) ◽  
pp. 335-345 ◽  
Author(s):  
Joost L. Boormans ◽  
Hanneke Korsten ◽  
Angelique J.C. Ziel-van der Made ◽  
Geert J.L.H. van Leenders ◽  
Carola V. de Vos ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Target Gene ◽  
Primary Prostate Cancer ◽  
Direct Target Gene ◽  
Direct Target

scholarly journals The Receptor Tyrosine Kinase EphA2 Is a Direct Target Gene of Hypermethylated in Cancer 1 (HIC1)

2011 ◽  
Vol 287 (8) ◽  
pp. 5366-5378 ◽  
Author(s):  
Bénédicte Foveau ◽  
Gaylor Boulay ◽  
Sébastien Pinte ◽  
Capucine Van Rechem ◽  
Brian R. Rood ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Target Gene ◽  
Direct Target Gene ◽  
Direct Target

scholarly journals Scavenger Chemokine (CXC Motif) Receptor 7 (CXCR7) Is a Direct Target Gene ofHIC1(Hypermethylated in Cancer 1)

2009 ◽  
Vol 284 (31) ◽  
pp. 20927-20935 ◽  
Author(s):  
Capucine Van Rechem ◽  
Brian R. Rood ◽  
Majid Touka ◽  
Sébastien Pinte ◽  
Mathias Jenal ◽  
...  
Keyword(s):  
Target Gene ◽  
Direct Target Gene ◽  
Direct Target

scholarly journals Combinatorial effect of miR-486-5p & miR-22-3p mimics thrombopoietin's impact on hematopoietic stem & progenitor cells

2020 ◽  
Author(s):  
Chen-Yuan Kao ◽  
Jinlin Jiang ◽  
ELEFTHERIOS TERRY PAPOUTSAKIS
Keyword(s):  
Progenitor Cells ◽  
Single Molecule ◽  
Kinase Inhibitors ◽  
Negative Regulator ◽  
Hematopoietic Stem ◽  
Megakaryocytic Differentiation ◽  
Peripheral Blood Cd34 ◽  
Mtor Phosphorylation ◽  
Direct Target ◽  
Differentiation And Proliferation

Megakaryocytes shed and release submicron size microparticles (MkMPs), the most abundant microparticle in circulation. We have previously reported that MkMPs target peripheral-blood CD34+ hematopoietic stem/progenitor cells (HSPCs) to induce megakaryocytic differentiation and proliferation, and that small RNAs delivered to HSPCs via MkMPs play an important role in the development of this phenotype. Here, using single-molecule real-time (SMRT) RNA sequencing (RNAseq), we identify the top seven most abundant microRNAs (miRs) in MkMPs as potential candidates in mediating the effect of MkMPs on HSPCs. Using miR mimics, we demonstrate that among the seven most abundant miRs, two, miR-486-5p and miR-22-3p, are able to drive the Mk differentiation of HSPCs in the absence of thrombopoietin (TPO). The effect of these two miRs is comparable to the TPO- or MkMP-induced megakaryocytic differentiation of HSPCs, thus suggesting that these two miRs are responsible for this MkMP-induced phenotype. To probe the signaling through which MkMPs might enable this phenotype, we used kinase inhibitors of potential signaling pathways engaged in megakaryocytic differentiation. Our data suggest that MkMP-induced Mk differentiation of HSPCs is enabled through JNK and PI3K/Akt/mTOR signaling. Our data show that MkMPs activate Akt and mTOR phosphorylation. Furthermore, MkMPs downregulate PTEN expression, a direct target of miR-486-5p and a negative regulator of PI3K/Akt signaling, via JNK signaling. Taken together, our data provide a mechanistic understanding of the biological effect of MkMPs in inducing megakaryocytic differentiation of HSPCs, which, as was previously suggested, is a phenotype of potential physiological significance in stress megakaryopoiesis.

scholarly journals YTHDF2, a protein repressed by miR-145, regulates proliferation, apoptosis and migration in ovarian cancer cells

2020 ◽  
Author(s):  
Jie Li ◽  
Lei Wu ◽  
Meili Pei ◽  
Yun Zhang
Keyword(s):  
Ovarian Cancer ◽  
Feedback Loop ◽  
Target Gene ◽  
Epigenetic Modification ◽  
Ovarian Cancer Cells ◽  
Direct Target Gene ◽  
Direct Target ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract RNA methylation can reverse the methylation modification at RNA level, which is a kind of extremely important epigenetic modification. YTHDF2, as a reader of m6A modification, the function and mechanisms of in epithelial ovarian cancer(EOC) have not been elucidated so far. In this study, we demonstrated that YTHDF2 was significantly upregulated in EOC tissues compared with normal ovarian tissues, further function studies confirmed that YTHDF2 significantly promoted the proliferation and migration of EOC cell lines, and reduced the global mRNA m6A levels. Next, we found that the expression levels of miR-145 and YTHDF2 were inversely correlated in ovarian cancer tissues and cells, and YTHDF2 is the direct target gene of miR-145. Interestingly, there was a crucial crosstalk between miR-145 and YTHDF2 via a double-negative feedback loop. Overexpression of YTHDF2 rescues miR-145-induced reduction of proliferation and migration in EOC cells. To conclude, YTHDF2 and miR-145, as two crucial m6A regulators, are involved in the progression of EOC by indirectly modulating m6A levels. In view of these promising results, YTHDF2 and miR-145 may provide new insights into the carcinogenesis and new potential therapeutic targets for EOC.

scholarly journals SEMA6D, Negatively Regulated by miR-7, Contributing to Chondrocyte Catabolic and Anabolic Activities via p38 Signaling Pathway

2020 ◽  
Author(s):  
Xindie Zhou ◽  
Yi Zhang ◽  
Junjie Zhang ◽  
Zhicheng Yang ◽  
Haoyu Yang ◽  
...  
Keyword(s):  
Target Gene ◽  
Regulatory Mechanism ◽  
Regulatory Factor ◽  
Regulatory Relation ◽  
Direct Target Gene ◽  
Direct Target ◽  
Novel Therapeutic ◽  
P38 Pathway

Abstract Background: MiR-7 has been recognized as a promoting factor of osteoarthritis (OA), but the specific down-stream pathway of miR-7 still remains unknown. Further investigation of the molecular regulatory mechanism of miR-7 might help develop a novel therapeutic method for OA.Results: Here we revealed that Semaphorin 6D (SEMA6D) was a direct target gene of miR-7, of which presented a negatively regulatory relation in vitro and in vivo. Lucubration of SEMA6D suggested that SEMA6D is validated to promote the anabolic metabolism and reduce the catabolism of chondrocytes via inhibiting the activation of p38 pathway.Conclusions: Present research illustrated that SEMA6D is a negatively regulatory factor of miR-7 and a pivotal mediator of the catabolism and anabolism of chondrocytes. SEMA6D exerts its function via inhibiting the activation of p38 pathway.

Clinical significance of serum miR-101-3p expression in patients with neonatal sepsis

2021 ◽  
Author(s):  
Juan Zhang ◽  
Xinwei Xu ◽  
Min Wang
Keyword(s):  
Neonatal Sepsis ◽  
Target Gene ◽  
Operating Characteristic ◽  
Characteristic Curve ◽  
Quantitative Real Time Pcr ◽  
Tnf Α ◽  
Direct Target Gene ◽  
Direct Target ◽  
Operating Characteristic Curve

Aim: This study aimed to evaluate the levels and functions of miR-101-3p in neonatal sepsis (NS). Materials & methods: Quantitative real-time PCR was conducted to investigate the expression of miR-101-3p and the receiver operating characteristic curve was applied to manifest its diagnostic effects. Results: MiR-101-3p was increased in the NS patients and the dysregulation of miR-101-3p was associated with levels of procalcitonin, CRP, IL-8 and TNF-α. The combination of miR-101-3p and procalcitonin could function as a promising indicator in distinguishing NS patients. The silenced miR-101-3p reversed the increased levels of TNF-α and IL-8 caused by lipopolysaccharide in vitro. DUSP1 was identified as a direct target gene of miR-101-3p in NS. Conclusion: The abundance of miR-101-3p facilitated the inflammation in NS by targeting DUSP1.

scholarly journals Transglutaminase 2 Is a Direct Target Gene of YAP/TAZ—Letter

2017 ◽  
Vol 77 (17) ◽  
pp. 4734-4735 ◽  
Author(s):  
Chen-Ying Liu ◽  
Ajaybabu V. Pobbati ◽  
Zhenyu Huang ◽  
Long Cui ◽  
Wanjin Hong
Keyword(s):  
Target Gene ◽  
Transglutaminase 2 ◽  
Direct Target Gene ◽  
Direct Target
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