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Anatomy of the Respiratory Neural Network
Published in Susmita Chowdhuri, M Safwan Badr, James A Rowley, Control of Breathing during Sleep, 2022
Christopher A Del Negro, Christopher G Wilson
Central chemosensor neurons are situated at ventral and medial margins of the VII nucleus. Those pFV chemosensors are derived from Atoh1 (a.k.a., Math1) and Egr2 (a.k.a., Krox20) expressing progenitor cells (142, 143), and they express the transcription factor Phox2b throughout development into adulthood (144–146). Phox2b expression has proved to be a convenient marker to identify pFV neurons anatomically and a tool to manipulate them experimentally and thus probe their functions. pFV neurons are excitatory (glutamatergic) rather than inhibitory (Figures 1.6A–D).
Resistance Mechanisms of Tumor Cells
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
In the hematopoietic system, other proteins are also able to exhibit these features. The EGR1 transcription factor (as well as EGR2 or EGR3) allows stem cells to go into homeostasis or dormancy to maintain them (Min et al., 2008; reviewed in Kühn et al., 2016). EGR1 has initially identified as activator of p21 and as gatekeeper of the TP53 (Krones-Herzig et al., 2003). Cells (over)expressing EGR1 protein can potentially escape treatment, and are presumably one of the reasons for relapses. A dormant cell needs only to switch back from this dormant state to the normal growth program. Recently, it has been shown that CDK4 but mainly overexpressed CDK6 (under certain stress conditions) re-activates dormant stem cells and causes tumor cell formation (Scheicher et al., 2015). Similarly, other factors have been described, such as HOXB4 (an OCT4 and GATA2 downstream target gene; Huang et al., 2016), which is capable of inducing sufficient amounts of the RUNX1 transcription factor to maintain hematopoietic stem cells (Teichweyde et al., 2017).
Ewing Sarcoma
Published in Dongyou Liu, Tumors and Cancers, 2017
Ewing sarcoma is shown to contain chromosomal translocation of EWS-ETS t(11;22) (q24;q12) (in 85% of cases), EWS-ERG t(21;22)(q22;q12) (in 10% of cases), EWS-ETV t(7;22)(p22;q12) and t(17;22)(q12;q12), and EWS-FEV t(2;22)(q35;q12), as well as TLS-ERG t(16;21)(p11;q22) and TLS-FEV t(2;16)(q35;p11). In addition, patients often harbor the Ewing sarcoma susceptibility gene (EGR2), located within the chromosome 10 susceptibility locus (10q21.3), which is regulated by the EWSR1 (Ewing sarcoma breakpoint region 1 of the TET family on chromosome 22)-FLI1 (friend leukemia insertion of the ETS family on chromosome 11) fusion oncogene via a GGAA microsatellite. Additional numerical and structural aberrations in Ewing sarcoma include gains of chromosomes 2, 5, 8, 9, 12, and 15; the nonreciprocal translocation t(1;16)(q12;q11.2); deletions on the short arm of chromosome 6; and trisomy 20. Further, STAG2 mutations are observed in 15%–20% of the cases, CDKN2A deletions in 12%–22% of cases, TP53 mutations in 6%–7% of cases, and intrachromosomal X-fusion in 4% of cases, leading to altered BCOR (encoding the BCL6 corepressor) and CCNB3 (encoding the testis-specific cyclin B3). In contrast, small, round, blue cell tumors of bone and soft tissue do not have rearrangements of the EWSR1 gene [2].
Transgenic rice seeds expressing altered peptide ligands against the M3 muscarinic acetylcholine receptor suppress experimental sialadenitis-like Sjögren’s syndrome
Published in Modern Rheumatology, 2020
Hanae Kudo, Hiroto Tsuboi, Hiromitsu Asashima, Hiroyuki Takahashi, Yuko Ono, Saori Abe, Fumika Honda, Yuya Kondo, Yuhya Wakasa, Fumio Takaiwa, Makoto Takano, Minoru Matsui, Isao Matsumoto, Takayuki Sumida
The third possible pathway is induction of anergy. We have previously shown that intravenous administration of N1-APL7 repressed MIS via upregulation of Egr2 expression in CLN CD4+ T cells and elevation of anergy-related molecules in CD4+ T cells [14]. By contrast, we detected lower expression of Egr2 in the MLNs of the N1-APL7-rice-treated group than in those of the N1 group. Anderson et al. [33] revealed that Egr2 is induced after TCR stimulation by the antigen peptide in vivo. N1-APL7 has a substitution of amino acid residues at TCR contact sites; therefore, the mechanism of TCR stimulation could be altered to reduce TCR stimulation following less Egr2 expression. We speculate that the discrepancy in the results was caused by the difference in the administration route of APL. Oral administration of APL transgenic rice seems to affect the intestinal immune response, and N1-APL7 might upregulate Treg cells.
Long noncoding RNA (lncRNA): a target in neuropathic pain
Published in Expert Opinion on Therapeutic Targets, 2019
Shaogen Wu, Jamie Bono, Yuan-Xiang Tao
The demyelination of peripheral sensory fibers after injury participates in neuropathic pain [50]. An antisense lncRNA, which is transcribed for the opposite strand of the proximal promoter of Egr2, was discovered by Martinez-Moreno et al. in both mouse and rat sciatic nerves [51]. After peripheral nerve injury, the expression of Egr2 AS RNA is increased and affects the expression of Egr2 mRNA via an epigenetic mechanism [51]. Ectopic expression of Egr2 AS RNA in mouse DRG cultures inhibits the expression of Egr2 mRNA and attenuates myelination of Schwann cells [51]. This work sheds light on the investigation of lncRNAs in peripheral nerves. A microarray-based analysis revealed that a large number of lncRNAs are differentially expressed in the distal segment of the sciatic nerve at different time points following injury [52]. The ectopic expression of the lncRNA, NONMMUG014387, promotes the proliferation of mouse Schwann cells [52]. Yao et al. analyzed the microarray data of lncRNAs in rat DRG after sciatic nerve injury and reported the expressional change of a down-regulated lncRNA, uc.217, in regenerative DRG neuronal outgrowth. Knock-down of uc.217 expression could significantly promote neurite outgrowth in cultured DRG neurons [53]. These studies show the regulatory function of plasticity in peripheral nerves by lncRNAs. Nevertheless, it is still obscure if lncRNAs play a role in neuropathic pain genesis.