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Friday, July 17, 2020 | History

1 edition of Alternative TrkA Splicing and Neuroblastoma found in the catalog.

Alternative TrkA Splicing and Neuroblastoma

by Antonietta R. Farina

  • 19 Want to read
  • 26 Currently reading

Published by INTECH Open Access Publisher .
Written in English


Edition Notes

En.

ContributionsAlberto Gulino, author, Andrew R. Mackay, author, Lucia Cappabianca, author, Marzia Ragone, author, Natalia Di Ianni, author, Pierdomenico Ruggeri, author, Stefania Merolle, author
The Physical Object
Pagination1 online resource
ID Numbers
Open LibraryOL27085527M
ISBN 109533070161
ISBN 109789533070162
OCLC/WorldCa884202620

TrkAIII is a developmentally regulated alternative splice variant of the NGF receptor tropomyosin-related kinase TrkA that is expressed by advanced stage human neuroblastomas (NBs), characterised by exon skipping and exon 9 omission, and exhibits oncogenic activity in NB models [ 1 – 5 ].   Keywords: KIT, TrkA (tropomyosin receptor kinase), neuroblastoma, acute myeloid leukemia, alternative splicing, SCF (stem cell factor), NGF (nerve growth factor), oncogenic signature Citation: Lebedev TD, Vagapova ER, Popenko VI, Leonova OG, Spirin PV and Prassolov VS () Two Receptors, Two Isoforms, Two Cancers: Comprehensive Analysis of.

As a consequence, GA has been developed for future chemotherapeutic use in several tumour types including neuroblastoma (NB). Alternative splicing of the neurotrophin receptor tyrosine kinase TrkA may have a pivotal function in regulating NB behaviour, with reports suggesting that tumour-suppressing signals from TrkA may be converted to. mers that ¯ank an alternative splicing site at position , Book. Jan ; CURR TOP MICROBIOL Investigate the role of TrkA and TrkB in neuroblastoma behavior .

Introduction. Alternative splicing of mRNA is a highly conserved process that is subject to both genetic regulation and heritability ().Some of these regulatory systems act in cis within the primary sequence of the pre-mRNA transcript, whereas others act in trans via genetically distant factors recruited to the splice site ().Alternative splicing may be particularly important to cancer, as the. Lucia Cappabianca's 37 research works with citations and 3, reads, including: Hypoxia-induced alternative splicing: the 11th Hallmark of Cancer.


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Alternative TrkA Splicing and Neuroblastoma by Antonietta R. Farina Download PDF EPUB FB2

Alternative TrkA Splicing and Neuroblastoma extracellular domain N-glycosylation and/or fo lding (Watson et al., ; Rajagopal et al., ). TrkA oncogenes The first TrkA oncogene was identified in colon cancer as a novel constitutively active cytoplasmic chimera bearing tropomyosin substitution of the TrkA extracellular domain.

Alternative TrkA Splicing and Neuroblastoma. By Antonietta R. Farina, Lucia Cappabianca, Pierdomenico Ruggeri, Natalia Di Ianni, Marzia Ragone, Stefania Merolle, Alberto Gulino and Andrew R. Mackay. Submitted: February 23rd Reviewed: July Cited by: 4. PDF | On Feb 8,Antonietta R.

Farina and others published Alternative TrkA Splicing and Neuroblastoma | Find, read and cite all the research you need on ResearchGate. We identify a novel alternative TrkA splice variant, TrkAIII, with deletion of exons 6, 7, and 9 and functional extracellular IG-C1 and N-glycosylation domains, that exhibits expression restricted to undifferentiated early neural progenitors, human neuroblastomas (NBs), and a subset of other neural crest-derived by: Summary We identify a novel alternative TrkA splice variant, TrkAIII, with deletion of exons 6, 7, and 9 and functional extracellular IG-C1 and N-glycosylation domains, that exhibits expression restricted to undifferentiated early neural progenitors, human neuroblastomas (NBs), and a subset of other neural crest-derived tumors.

Introduction. Alternative splicing of mRNA is a highly conserved process that is subject to both genetic regulation and heritability ().Some of these regulatory systems act in cis within the primary sequence of the pre-mRNA transcript, while others act in trans via genetically distant factors recruited to the splice site ().Alternative splicing may be particularly important to cancer, as the.

In cancer cells, hypoxia promotes alternative TrkAIII splicing in KCNR, SK-N-BE, SH-SY5Y and Neuro 2 neuroblastoma, Jurkat T cell leukaemia, PC12 pheochromocytoma and TT medullary thyroid cancer cells and is constitutively predominant in U glioblastoma cells, suggesting that physiological alternative TrkAIII splicing is conserved and.

We identify a novel alternative TrkA splice variant, TrkAIII, with deletion of exons 6, 7, and 9 and functional extracellular IG-C1 and N-glycosylation domains, that exhibits expression restricted to undifferentiated early neural progenitors, human neuroblastomas (NBs), and a subset of other neural crest-derived tumors.

Isoforms of the Trk Receptors. TrkA, TrkB, and TrkC have distinct isoforms that affect the function of the receptors. The major isoform of TrkA (TrkA-II) expressed in most nonneuronal cells is aa, whereas the neuronal TrkA isoform (TrkA-I) lacks exon 9 ( aa) (Fig.

2A) ().Exon 9 encodes 6 aa in the extracellular domain near the transmembrane region in TrkA and does not alter the reading. Andrew Mackay and colleagues have identified an alternative splicing mechanism that causes neuroblastoma cells to switch from expressing a growth-inhibiting form of the receptor tyrosine kinase.

Keywords: TrkAIII, Alternative splicing, Neuroblastoma, Oncogenic signaling, Unfolded protein response, Warburg effect, Hallmarks of cancer, Therapeutic approaches Background The neurotrophin receptor tropomyosin-related kinase A (TrkA) regulates responses to the neurotrophins NGF and NT3 in a wide variety of normal tissues and is.

In this short review, the authors integrate this novel information into a modified concept that places alternative TrkA splicing as a potential pivotal regulator of neuroblastoma behavior and identifies the TrkAIII alternative splice variant as a potential biomarker of patient prognosis and novel therapeutic target.

© Future Medicine Ltd. As a consequence, GA has been developed for future chemotherapeutic use in several tumour types including neuroblastoma (NB). Alternative splicing of the neurotrophin receptor tyrosine kinase TrkA.

6. Alternative TrkA Splicing and Neuroblastoma. By Antonietta R. Farina, Lucia Cappabianca, Pierdomenico Ruggeri, Natalia Di Ianni, Marzia Ragone, Stefania Merolle, Alberto Gulino and Andrew R. Mackay. Open access peer-reviewed. Sympathetic Neurotransmitters in Neuroblastoma – Between Physiology and Pathology.

The TrkA gene, which is organised into 17 exons (Greco et al., ), exhibits alternative splicing and is expressed as TrkAI or TrkAII variants exhibiting differential exon 9 use (Barker et al., ), TrkA L0 or L1 variants exhibiting differential exons 1, 2 and 3 usage (Dubus et al., ) and the recently described TrkAIII variant, which.

Alternative TrkAIII splicing of the neurotrophin receptor gene TrkA in neuroblastoma (NB) is characterised by exon skipping, associates with advanced stage metastatic disease and post.

BACKGROUND. This study was conducted to investigate the prognostic significance and biologic relevance of trkA expression levels in peripheral neuroblastic tumors (pNTs) (i.e., neuroblastoma, ganglioneuroblastoma, and ganglioneuroma).

METHODS. Levels of trkA expression from a total of pNTs were determined by quantitative polymerase chain reaction analysis with. Tacconelli A, Farina AR, Cappabianca L, Desantis G, Tessitore A, Vetuschi A et al. TrkA alternative splicing: a regulated tumor-promoting switch in human neuroblastoma.

Cancer Cell ; 6: – Neuroblastoma, the most common and deadly solid tumor in children, exhibits heterogeneous clinical behavior, from spontaneous regression to relentless progression.

Current evidence suggests that the TRK family of neurotrophin receptors plays a critical role in these diverse behaviors. Neuroblastomas expressing TrkA are biologically favorable and prone to spontaneous regression or. Alternative splicing and whole gene expression changes in neuroblastoma To compare global splicing and transcription regulation in high stage neuroblastoma, we derived whole gene expression signatures by pairwise comparison of gene-level transcript cluster signals.

Human neuroblastoma cell lines frequently express the TRK-A proto-oncogene and bind nerve growth factor (NGF) but do not differentiate when exposed to NGF. Transient transfection of an exogenous TRK-A gene into SH-SY5Y and LA-N-5 neuroblastoma cells restored the ability of these tumor cells to differentiate with NGF.

Stable TRK-A-transfected SH-SY5Y cell clones were isolated, and they.In neuroblastomas, alternative splicing of the NTRK1/TrkA receptor has already been reported to have an impact on tumour aggressiveness (Tacconelli et al, ), suggesting that the phenomenon of.

In neuroblastomas, alternative splicing of the NTRK1 /TrkA receptor has already been reported to have an impact on tumour aggressiveness (Tacconelli et al, ), suggesting that the phenomenon of differential transcripts use has a major impact on neuroblastoma biology.