ELF a β-spectrin is a neuronal precursor cell marker in developing mammalian brain; structure and organization of the elf/β-G spectrin gene

Katuri, Varalakshmi; Iqbal, Sohail; Narayan, Tina; Wang, Zhili; Lu, Robert; Mishra, Lopa; Mishra, Bibhuti

doi:10.1038/sj.onc.1205548

Cited by 23 publications

(25 citation statements)

References 84 publications

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“…Recent observations from this lab suggest that ELF3, a novel b-spectrin, is important for brain development from an early stage (Tang et al, 2002). Its striking localization to the axon hillock and axonal projection is consistent with its known involvement in axonal guidance as well as cell polarization (Dubreuil et al, 2000;Hammarlund et al, 2000;Moorthy et al, 2000).…”

Section: Tgf-b and Elf (A B-spectrin)mentioning

confidence: 74%

“…Spectrin levels are elevated after gastrulation suggesting a role in cell fate determination (Moon and McMahon, 1987). ELF has been found to be a neuronal precursor cell marker in the developing mammalian brain (Tang et al, 2002). ELF is expressed in cell bodies as well as dendrites and initial axon segments, and in this sense is unique in its expression pattern from spectrin G and brain spectrin (Goodman et al, 1995).…”

Section: Tgf-b and Elf (A B-spectrin)mentioning

confidence: 99%

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TGF-β, Neuronal Stem Cells and Glioblastoma

Golestaneh

Mishra

2005

Oncogene

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Transforming growth factor beta (TGF-b) signaling leads to a number of biological end points involving cell growth, differentiation, and morphogenesis. Typically, the cellular effect accompanies an induction of mesodermal cell fate and inhibition of neural cell differentiation. However, during pathological conditions, these defined effects of TGF-b can be reversed; for example, the growthinhibitory effect is replaced with its tumor promoting ability. A multitude of factors and cross-signaling pathways have been reported to be involved in modulating the dual effects of TGF-b. In this review, we focus on the potential role of TGF-b signal transduction during development of neural progenitor cells and its relation to glioblastoma development from neural stem cells.

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Section: Tgf-b and Elf (A B-spectrin)mentioning

confidence: 74%

Section: Tgf-b and Elf (A B-spectrin)mentioning

confidence: 99%

TGF-β, Neuronal Stem Cells and Glioblastoma

Golestaneh

Mishra

2005

Oncogene

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“…Generation of elf þ /À mice and analysis Generation of elf þ /À knockout in mice has been described previously (Tang et al, 2002). The presence of genetic mutation was monitored by use of the PCR as described previously (Tang et al, 2002).…”

Section: Methodsmentioning

confidence: 99%

“…The presence of genetic mutation was monitored by use of the PCR as described previously (Tang et al, 2002). Double homozygous elf mutants were embryonic lethal.…”

Section: Methodsmentioning

confidence: 99%

Disruption of transforming growth factor-β signaling through β-spectrin ELF leads to hepatocellular cancer through cyclin D1 activation

et al. 2007

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Transforming growth factor-b (TGF-b) signaling members, TGF-b receptor type II (TBRII), Smad2, Smad4 and Smad adaptor, embryonic liver fodrin (ELF), are prominent tumor suppressors in gastrointestinal cancers. Here, we show that 40% of elf þ /À mice spontaneously develop hepatocellular cancer (HCC) with markedly increased cyclin D1, cyclin-dependent kinase 4 (Cdk4), c-Myc and MDM2 expression. Reduced ELF but not TBRII, or Smad4 was observed in 8 of 9 human HCCs (Po0.017). ELF and TBRII are also markedly decreased in human HCC cell lines SNU-398 and SNU-475. Restoration of ELF and TBRII in SNU-398 cells markedly decreases cyclin D1 as well as hyperphosphorylated-retinoblastoma (hyperphosphorylated-pRb). Thus, we show that TGF-b signaling and Smad adaptor ELF suppress human hepatocarcinogenesis, potentially through cyclin D1 deregulation. Loss of ELF could serve as a primary event in progression toward a fully transformed phenotype and could hold promise for new therapeutic approaches in human HCCs.

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“…Beta II spectrin (βII) is found in cell bodies as well as axons ( e.g. [15]). Furthermore, βI spectrin is absent from Purkinje cell dendrites [16].…”

Section: Introductionmentioning

confidence: 99%

Non-erythroid beta spectrin interacting proteins and their effects on spectrin tetramerization

Sevinc

Fung

2011

Cellular and Molecular Biology Letters

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With yeast two-hybrid methods, we used a C-terminal fragment (residues 1697-2145) of non-erythroid beta spectrin (βII-C), including the region involved in the association with alpha spectrin to form tetramers, as the bait to screen a human brain cDNA library to identify proteins interacting with βII-C. We applied stringent selection steps to eliminate false positives and identified 17 proteins that interacted with βII-C (IPβII-C s). The proteins include a fragment (residues 38-284) of “THAP domain containing, apoptosis associated protein 3, isoform CRA g”, “glioma tumor suppressor candidate region gene 2” (residues 1-478), a fragment (residues 74-442) of septin 8 isoform c, a fragment (residues 704-953) of “coatomer protein complex, subunit beta 1, a fragment (residues 146-614) of zinc-finger protein 251, and a fragment (residues 284-435) of syntaxin binding protein 1. We used yeast three-hybrid system to determine the effects of these βII-C interacting proteins as well as of 7 proteins previously identified to interact with the tetramerization region of non-erythroid alpha spectrin (IPαII-N s) [1] on spectrin tetramer formation. The results showed that 3 IPβII-C s were able to bind βII-C even in the presence of αII-N, and 4 IPαII-N s were able to bind αII-N in the presence of βII-C. We also found that the syntaxin binding protein 1 fragment abolished αII-N and βII-C interaction, suggesting that this protein may inhibit or regulate non-erythroid spectrin tetramer formation.

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ELF a β-spectrin is a neuronal precursor cell marker in developing mammalian brain; structure and organization of the elf/β-G spectrin gene

Cited by 23 publications

References 84 publications

TGF-β, Neuronal Stem Cells and Glioblastoma

TGF-β, Neuronal Stem Cells and Glioblastoma

Disruption of transforming growth factor-β signaling through β-spectrin ELF leads to hepatocellular cancer through cyclin D1 activation

Non-erythroid beta spectrin interacting proteins and their effects on spectrin tetramerization

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