A Hippocampal Protein Associated with Paraneoplastic Neurologic Syndrome and Small Cell Lung Carcinoma

Sakai, Koichiro; Gofuku, M.; Kitagawa, Yoko; Ogasawara, Toshiyuki; Hirose, Genjiro; Yamazaki, M.; Koh, Chang−Sung; Yanagisawa, Nobuo; Steinman, Lawrence

doi:10.1006/bbrc.1994.1358

Cited by 80 publications

(43 citation statements)

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“…Interest in this family of proteins was originally fueled by the observation that their human homologs are tumor antigens (19). There are four members of the human Elav-like family, namely, HuD, HuC, Hel-N1, and HuR (17,19,28,29). HuD, HuC, and Hel-N1 are expressed exclusively in postmitotic neurons and in specific neuroendocrine tumors (29 -32).…”

Section: Discussionmentioning

confidence: 99%

Hypoxic Stabilization of Vascular Endothelial Growth Factor mRNA by the RNA-binding Protein HuR

Levy¹,

Chung²,

Furneaux³

et al. 1998

Journal of Biological Chemistry

611

507

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Section: Discussionmentioning

confidence: 99%

Hypoxic Stabilization of Vascular Endothelial Growth Factor mRNA by the RNA-binding Protein HuR

Levy¹,

Chung²,

Furneaux³

et al. 1998

Journal of Biological Chemistry

611

507

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“…This syndrome arises in a small subset of patients when the ectopic expression of Hu proteins in certain types of cancers, typically small cell lung carcinomas (SCLCs), provokes an autoimmune attack on the nervous system. Out of the four Hu members, HuD was the first to be cloned and characterized, followed by HuC/ELAVl3, HuB/ELAVl2, and HuR/ELAVl1 (Szabo et al 1991;King et al 1994;Sakai et al 1994;Ma et al 1996). The expression of three Hu members-HuB, HuC and HuD-is predominantly restricted to neurons (nELAVs), while HuR is found in most cell types (Szabo et al 1991;King et al 1994;Good 1995;Ma et al 1996;Okano and Darnell 1997).…”

Section: The Hud Gene Mrna and Proteinmentioning

confidence: 99%

Emerging complexity of the HuD/ELAVl4 gene; implications for neuronal development, function, and dysfunction

Bronicki

Jasmin

2013

RNA

111

118

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Precise control of messenger RNA (mRNA) processing and abundance are increasingly being recognized as critical for proper spatiotemporal gene expression, particularly in neurons. These regulatory events are governed by a large number of transacting factors found in neurons, most notably RNA-binding proteins (RBPs) and micro-RNAs (miRs), which bind to specific cisacting elements or structures within mRNAs. Through this binding mechanism, trans-acting factors, particularly RBPs, control all aspects of mRNA metabolism, ranging from altering the transcription rate to mediating mRNA degradation. In this context the best-characterized neuronal RBP, the Hu/ELAVl family member HuD, is emerging as a key component in multiple regulatory processes-including pre-mRNA processing, mRNA stability, and translation-governing the fate of a substantial amount of neuronal mRNAs. Through its ability to regulate mRNA metabolism of diverse groups of functionally similar genes, HuD plays important roles in neuronal development and function. Furthermore, compelling evidence indicates supplementary roles for HuD in neuronal plasticity, in particular, recovery from axonal injury, learning and memory, and multiple neurological diseases. The purpose of this review is to provide a detailed overview of the current knowledge surrounding the expression and roles of HuD in the nervous system. Additionally, we outline the present understanding of the molecular mechanisms presiding over the localization, abundance, and function of HuD in neurons.

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“…HuD, HuC, and Hel-N1 show 82 ± 90% sequence homology (King et al, 1994;Sakai et al, 1993;Szabo et al, 1991). In addition, they show an *54% homology to the Drosophila melanogaster RNA-binding proteins Sex-lethal and ELAV (King et al, 1994;Szabo et al, 1991), which participate in alternative splicing (Baker, 1989;Koushika et al, 1996).…”

Section: Introductionmentioning

confidence: 99%

HuD, a neuronal-specific RNA-binding protein, is a putative regulator of N-myc pre-mRNA processing/stability in malignant human neuroblasts

et al. 1999

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N-myc gene copy numbers and transcription rates are similar in N (neuroblastic, tumorigenic) and S (nonneuronal, non-tumorigenic) neuroblastoma cells with chromosomally integrated ampli®ed N-myc genes. However, N cells show signi®cantly higher N-myc mRNA levels than S cells. Therefore, post-transcriptional control of N-myc gene expression must di er between these cell types. Since no di erences in N-myc mRNA half-life were found between N and S cells from two cell lines, steady-state levels of N-myc pre-mRNA processing intermediates were analysed. Results suggest that the di erences in N-myc expression arise primarily at the nuclear post-transcriptional level. The neuronal-speci®c RNA-binding Hu proteins are present in cytoplasmic and nuclear fractions of N cells and one of them, HuD, binds speci®cally to both exonic and intronic N-myc RNA sequences. In sense and antisense HuD-transfected N cells, there are coordinate changes in HuD and N-myc expression levels. Thus, we propose that HuD plays a role in the nuclear processing/stability of N-myc premRNA in N-type neuroblastoma cells.

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A Hippocampal Protein Associated with Paraneoplastic Neurologic Syndrome and Small Cell Lung Carcinoma

Cited by 80 publications

References 0 publications

Hypoxic Stabilization of Vascular Endothelial Growth Factor mRNA by the RNA-binding Protein HuR

Hypoxic Stabilization of Vascular Endothelial Growth Factor mRNA by the RNA-binding Protein HuR

Emerging complexity of the HuD/ELAVl4 gene; implications for neuronal development, function, and dysfunction

HuD, a neuronal-specific RNA-binding protein, is a putative regulator of N-myc pre-mRNA processing/stability in malignant human neuroblasts

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