Neuronal Differentiation of NT2/D1 Teratocarcinoma Cells Is Accompanied by a Loss of Lamin A/C Expression and an Increase in Lamin B1 Expression

Pierce, Tanya; Worman, Howard J.; Holy, Jon

doi:10.1006/exnr.1999.7060

Cited by 18 publications

(13 citation statements)

References 32 publications

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“…17 Second, lamin A/C expression patterns during neuronal development were found to be important for neurons. 18 Observations of transgenic LMNA-null mice gave further support to this assumption. 13,19 Currently, it is unknown how frequent mutations are in the LMNA gene among patients worldwide with axonal CMT.…”

Section: Introductionmentioning

confidence: 84%

Mutations in the LMNA gene do not cause axonal CMT in Czech patients

et al. 2009

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The LMNA gene was sequenced in 98 Czech patients from 94 unrelated families with early-onset axonal Charcot-Marie-Tooth (CMT) disease consistent with both autosomal recessive inheritance and sporadic cases. Biallelic pathogenic mutations were not found in any patient in this group. One patient carried the c.1870C4T mutation that is predicted to result in the amino-acid substitution, p. Arg624Cys, on one allele, but the second causative mutation was not detected. LMNA mutation is not likely to be associated with the disease in this family. To exclude larger deletions/duplications in the LMNA gene not detectable by sequencing, 48 patients from this group were also analyzed with multiplex ligation-dependent probe amplification. No rearrangements in the LMNA gene were detected. We conclude that mutations in the LMNA gene are absent from a large group of Czech patients with axonal autosomal recessive CMT disease. Consequently, LMNA mutation screening does not seem to be relevant for axonal CMT DNA diagnostics. A similar situation may apply to other European populations.

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Section: Introductionmentioning

confidence: 84%

Mutations in the LMNA gene do not cause axonal CMT in Czech patients

et al. 2009

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“…Lamin, actin, and actinin are associated with alterations of the cell structure itself, whereas the strong collagen expression in the last consequence extends the extracellular matrix and is a factor responsible for the tumor's mass growth. Lamin C, a component of the nuclear lamina, is reported to be altered concomitantly with differentiation or malignancy of cells‐but with contradictory reports 30,31. Actin, which is frequently used for normalization in Northern blots, seems to be upregulated in tumors.…”

Section: Discussionmentioning

confidence: 99%

“…Lamin C, a component of the nuclear lamina, is reported to be altered concomitantly with differentiation or malignancy of cells-but with contradictory reports. 30,31 Actin, which is frequently used for normalization in Northern blots, seems to be upregulated in tumors. Its cross-linker actinin is important for microfilament organization of the cytoskeleton, which ultimately leads to changes in the extracellular matrix.…”

Section: Biological Aspectsmentioning

confidence: 99%

Use of Representational Difference Analysis and cDNA Arrays for Transcriptional Profiling of Tumor Tissue

Frohme

Scharm

Delius

et al. 2000

Annals of the New York Academy of Sciences

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Representational difference analysis of cDNA (cDNA‐RDA) was used for a comparison of the global transcript level of tumor of the larynx and the corresponding normal epithelial tissue toward the end of detecting differentially expressed genes. Overall, some 130 gene fragments were identified. By sequence analysis and homology comparison, they could be put into several groups related to (potential) functions. Apart from genes whose overexpression was most likely a result of tumor growth or dedifferentiation of epithelial tissue, a lot of genes were isolated that play major roles in signal transduction pathways or apoptosis or act as oncogenes or tumor suppressor genes, in addition to new, entirely unknown genes. Moreover, some cDNAs of known genes were identified that derived from unconventional splicing activity or other transcript modifications. All identified fragments were arrayed on solid support and used for reverse Northern blot analyses. The use of preselected RDA fragments as targets in array‐based profiling experiments circumvents many of the problems encountered when dealing with large clone libraries.

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“…In fact, despite the irony that stemness genes including c-Myc [83, 104–107], Oct3/4 [108–110], and Sox2 [111–113] had already been identified in ECCs, their specific roles in self-renewal and pluripotency would not be elucidated until later [27, 114]. Meanwhile, studies showing expression of genes such as K-fgf and Hst-1 [115–117], TGFα , and LAMIN A/C [117–121] provided the framework that gene activity was sufficient and necessary to keep ECCs in the pluripotent state. Two genes linked to stemness and pluripotency are Rex1 ( Zfp42 ), encoding a zinc finger transcription factor, and Ccnd1 , encoding Cyclin D1.…”

Section: Retinoic Acid: Lessons From the Inducermentioning

confidence: 99%

Mechanisms Regulating Stemness and Differentiation in Embryonal Carcinoma Cells

Kelly

Gatie

2017

Stem Cells International

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Just over ten years have passed since the seminal Takahashi-Yamanaka paper, and while most attention nowadays is on induced, embryonic, and cancer stem cells, much of the pioneering work arose from studies with embryonal carcinoma cells (ECCs) derived from teratocarcinomas. This original work was broad in scope, but eventually led the way for us to focus on the components involved in the gene regulation of stemness and differentiation. As the name implies, ECCs are malignant in nature, yet maintain the ability to differentiate into the 3 germ layers and extraembryonic tissues, as well as behave normally when reintroduced into a healthy blastocyst. Retinoic acid signaling has been thoroughly interrogated in ECCs, especially in the F9 and P19 murine cell models, and while we have touched on this aspect, this review purposely highlights how some key transcription factors regulate pluripotency and cell stemness prior to this signaling. Another major focus is on the epigenetic regulation of ECCs and stem cells, and, towards that end, this review closes on what we see as a new frontier in combating aging and human disease, namely, how cellular metabolism shapes the epigenetic landscape and hence the pluripotency of all stem cells.

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Neuronal Differentiation of NT2/D1 Teratocarcinoma Cells Is Accompanied by a Loss of Lamin A/C Expression and an Increase in Lamin B1 Expression

Cited by 18 publications

References 32 publications

Mutations in the LMNA gene do not cause axonal CMT in Czech patients

Mutations in the LMNA gene do not cause axonal CMT in Czech patients

Use of Representational Difference Analysis and cDNA Arrays for Transcriptional Profiling of Tumor Tissue

Mechanisms Regulating Stemness and Differentiation in Embryonal Carcinoma Cells

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