A Human Gene (DDX10) Encoding a Putative DEAD-Box RNA Helicase at 11q22–q23

Savitsky, Kinneret; Ziv, Yael; Bar‐Shira, Anat; Gilad, Shlomit; Tagle, Danilo A.; Smith, Sherilyn; Uziel, Tamar; Sfez, Sharon; Nahmias, Joseph; Sartiel, Adam; Eddy, Roger L.; Shows, Thomas B.; Collins, Francis S.; Shiloh, Yosef; Rotman, Galit

doi:10.1006/geno.1996.0184

Cited by 55 publications

(32 citation statements)

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“…4 RNA Helicase II/Gu and putative RNA Helicase DDX10 are DEADbox superfamily members potentially involved in the modification of RNA secondary structure, important for pre-mRNA splicing, translation initiation, ribosome/spliceosome assembly, and mRNA stability. [42][43][44] Finally, SAP130, together with SAP49, -145, and -155 constitute the SF3b U2 snRNP-associated protein complex essential for spliceosome assembly, and may play a critical role at, or near, the catalytic core of the spliceosome. 45 Overexpression of these pre-mRNA processing genes may be responsible for the altered splicing patterns of the PYK2 gene observed in CML cells, of which SRPK1, RNA Helicase II/Gu, and hnRNPA2/B1 may be particularly important.…”

Section: Discussionmentioning

confidence: 99%

p210BCR/ABL-induced alteration of pre-mRNA splicing in primary human CD34+ hematopoietic progenitor cells

2004

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Chronic myelogenous leukemia (CML) is a malignancy of the human hematopoietic stem cell (HSC) caused by the p210 BCR/ABL oncoprotein. Although alternative splicing of pre-mRNA is a critical determinant of a cell's protein repertoire, it has not been associated with CML pathogenesis. We identified a BCR/ABL-dependent increase in expression of multiple genes involved in pre-mRNA splicing (eg SRPK1, RNA Helicase II/Gu, and hnRNPA2/B1) by subtractive hybridization of cDNA from p210 BCR/ABL -eGFP vs eGFP-transduced umbilical cord blood CD34 þ cells. b1-integrin signaling is important to HSC maintenance and proliferation/differentiation, and is abnormal in CML. As an example of how changes in premRNA processing might contribute to CML pathogenesis, we observed alternative splicing of a gene for a b1-integrinresponsive nonreceptor tyrosine kinase (PYK2), resulting in increased expression of full-length Pyk2 in BCR/ABL-containing cells. Treatment of p210 BCR/ABL -positive cells with the Ablspecific tyrosine kinase inhibitor STI571 reverted PYK2 splicing to a configuration more consistent with normal cells, and correlated with decreased expression of BCR/ABL-induced proteins involved in pre-mRNA processing. Whether altered PYK2 splicing contributes to CML pathogenesis remains undetermined; however, we propose that generic changes in pre-mRNA splicing as a result of p210 BCR/ABL kinase activity may contribute to CML pathogenesis.

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Section: Discussionmentioning

confidence: 99%

p210BCR/ABL-induced alteration of pre-mRNA splicing in primary human CD34+ hematopoietic progenitor cells

2004

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“…The latter gene was discovered by sequencing a PCRamplified genomic DNA fragment made with primers complementary to conserved helicase domains that are widely spaced (8). Our search of the database also revealed a human gene homolog, called DDX10 (39). This gene encodes a DEAD box protein of 875 amino acids, and the two protein sequences are 78% similar (62% identical), with highest relatedness in the DEAD box segments.…”

Section: Figmentioning

confidence: 92%

The rRNA-Processing Function of the Yeast U14 Small Nucleolar RNA Can Be Rescued by a Conserved RNA Helicase-Like Protein

Liang

Clark

Fournier

1997

Molecular and Cellular Biology

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“…The consensus region of deletion between the markers D11S2000 and D11S897 (Koreth et al, 1998) contains a number of candidate tumour suppressor genes, including ATM (AT-mutated) and possibly the DDX10 gene (James et al, 1994;Savitsky et al, 1996). To date, evidence for the involvement of ATM in many of these sporadic malignancies is equivocal (discussed further below) and the role of DDX10 in malignancy is speculative (Laake et al, 1997), indicating that further investigation is required to localize the putative tumour suppressor at 11q22-q23.1.…”

Section: Introductionmentioning

confidence: 99%