scholarly journals Enhancer variants reveal a conserved transcription factor network governed by PU.1 during osteoclast differentiation

Bone Research ◽  
2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Heather A. Carey ◽  
Blake E. Hildreth ◽  
Jennifer A. Geisler ◽  
Mara C. Nickel ◽  
Jennifer Cabrera ◽  
...  
2007 ◽  
Vol 8 (1) ◽  
pp. 17 ◽  
Author(s):  
Ricardo Saban ◽  
Cindy Simpson ◽  
Carole A Davis ◽  
Igor Dozmorov ◽  
Julie Maier ◽  
...  

2012 ◽  
Vol 142 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Ilaria Laudadio ◽  
Isabelle Manfroid ◽  
Younes Achouri ◽  
Dominic Schmidt ◽  
Michael D. Wilson ◽  
...  

2005 ◽  
Vol 201 (8) ◽  
pp. 1197-1203 ◽  
Author(s):  
Kazu Kikuchi ◽  
Anne Y. Lai ◽  
Chia-Lin Hsu ◽  
Motonari Kondo

Cytokine receptor signals have been suggested to stimulate cell differentiation during hemato/lymphopoiesis. Such action, however, has not been clearly demonstrated. Here, we show that adult B cell development in IL-7−/− and IL-7Rα2/− mice is arrested at the pre–pro-B cell stage due to insufficient expression of the B cell–specific transcription factor EBF and its target genes, which form a transcription factor network in determining B lineage specification. EBF expression is restored in IL-7−/− pre–pro-B cells upon IL-7 stimulation or in IL-7Rα−/− pre–pro-B cells by activation of STAT5, a major signaling molecule downstream of the IL-7R signaling pathway. Furthermore, enforced EBF expression partially rescues B cell development in IL-7Rα−/− mice. Thus, IL-7 receptor signaling is a participant in the formation of the transcription factor network during B lymphopoiesis by up-regulating EBF, allowing stage transition from the pre–pro-B to further maturational stages.


2005 ◽  
Vol 129 (3) ◽  
pp. 360-365
Author(s):  
Rolando Y. Ramos ◽  
Helen M. Haupt ◽  
Peter A. Kanetsky ◽  
Rakesh Donthineni-Rao ◽  
Carmen Arenas-Elliott ◽  
...  

Abstract Context.—Osteoclast-like giant cells (GCs) in giant cell tumors (GCTs) are thought to derive from a monocyte-macrophage lineage. Microphthalmia transcription factor (MITF) is necessary for osteoclast gene expression and tartrate-resistant acid phosphatase (TRAP) activation; c-Kit plays a role in regulation of MITF. Objective.—To gain insight into the differentiation of GCTs of bone (GCTBs) and GCTs tendon sheath (GCTTSs) by investigating immunohistochemical staining for c-Kit, MITF, TRAP, and HAM-56 in the GCs and stroma. Design.—Immunoreactivity for CD117 (c-Kit), MITF, TRAP, and HAM-56 was studied in 35 GCTBs, 15 GCTTSs, and 5 foreign-body GC controls. Results.—Across tumors, MITF and TRAP but not c-Kit were generally expressed in GCs; TRAP was variably expressed in stromal cells. The MITF was expressed more consistently in stromal cells of GCTTSs than GCTBs (P < .001). The GCTBs showed more intense MITF stromal (P < .001) and TRAP GC staining (P = .04) than GCTTSs. HAM-56 staining by stromal cells was associated with MITF stromal staining (r2 = 0.6, P < .001). Conclusions.—Results suggest that MITF and TRAP are expressed during osteoclast differentiation and that a proportion of mononuclear cells in GCTs express the macrophage marker HAM-56. Both GCTBs and GCTTSs show similar patterns of immunohistochemical expression.


Author(s):  
Harikrishna Nakshatri ◽  
Sunil Badve

Breast cancer is a heterogeneous disease and classification is important for clinical management. At least five subtypes can be identified based on unique gene expression patterns; this subtype classification is distinct from the histopathological classification. The transcription factor network(s) required for the specific gene expression signature in each of these subtypes is currently being elucidated. The transcription factor network composed of the oestrogen (estrogen) receptor α (ERα), FOXA1 and GATA3 may control the gene expression pattern in luminal subtype A breast cancers. Breast cancers that are dependent on this network correspond to well-differentiated and hormone-therapy-responsive tumours with good prognosis. In this review, we discuss the interplay between these transcription factors with a particular emphasis on FOXA1 structure and function, and its ability to control ERα function. Additionally, we discuss modulators of FOXA1 function, ERα–FOXA1–GATA3 downstream targets, and potential therapeutic agents that may increase differentiation through FOXA1.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Zoe E. Gillespie ◽  
Chenxuan Wang ◽  
Flaviu Vadan ◽  
Topaza Y. Yu ◽  
Juan Ausió ◽  
...  

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