Beta globin gene inhibition by antisense RNA transcripts

Xu, Li‐Yan; Ferry, A E; Monteiro, Carlos Augusto; Pace, Betty S.

doi:10.1038/sj.gt.3301106

Cited by 9 publications

(2 citation statements)

References 24 publications

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“…The newly constructed antisense TRE construct carries both ampicillin and hygromycin resistance genes for selection in Escherichia coli and in mammalian cells, respectively. The subsequent transcription of antisense RNA downregulates the endogenous expression of the complement transcript (20,27,39).…”

Section: Methodsmentioning

confidence: 99%

Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression

Helms¹,

Fejes-Tóth²,

Náray-Fejes-Tóth³

2003

American Journal of Physiology-Renal Physiology

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To study the role of serum and glucocorticoid-inducible kinase-1 (SGK1) in mammalian cells, we compared Na(+) transport rates in wild-type (WT) M1 cortical collecting duct cells with M1 populations stably expressing human full-length SGK1, NH(2)-terminal truncated (DeltaN-60) SGK1, "kinase-dead" (K127M) SGK1, and cells that have downregulated levels of SGK1 mRNA (antisense SGK1). Basal rates of transepithelial Na(+) transport were highest in full-length SGK1 populations, compared among the above populations. Dexamethasone treatment increased Na(+) transport in WT and full-length SGK1 cells 2.7- and 2-fold, respectively. Modest stimulation of Na(+) absorption was detected after dexamethasone treatment in DeltaN-60 SGK1 populations. However, DeltaN-60 SGK1 transport rates remained substantially lower than WT values. Importantly, a combination of high insulin, dexamethasone, and serum failed to significantly stimulate Na(+) transport in antisense or K127M SGK1 cells. Additionally, expression of antisense SGK1 significantly decreased transepithelial resistance values. Overall, we concluded that SGK1 is a critical component in corticosteroid-regulated Na(+) transport in mammalian cortical collecting duct cells. Furthermore, our data suggest that the NH(2) terminus of SGK1 may contain a Phox homology-like domain that may be necessary for effective Na(+) transport.

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Section: Methodsmentioning

confidence: 99%

Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression

Helms¹,

Fejes-Tóth²,

Náray-Fejes-Tóth³

2003

American Journal of Physiology-Renal Physiology

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“…pBD-MS2, pMS2, pMS2-IRE, pMS2-TAR, pAD-IRP, and pAD-Tat were generously provided by Dr. M. Wenkins. pZeo␤AS expressing the full-length human ␤-globin in a reverse orientation has been described elsewhere (34). The full-length Tip110 cDNA was obtained as described under "Results."…”

Section: Cell Lines and Cellmentioning

confidence: 99%

HIV-1 Tat Protein-mediated Transactivation of the HIV-1 Long Terminal Repeat Promoter Is Potentiated by a Novel Nuclear Tat-interacting Protein of110 kDa, Tip110

Liu¹,

Li²,

Kim³

et al. 2002

Journal of Biological Chemistry

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Moreover, digital fluorescence microscopic imaging revealed that Tip110 was expressed exclusively in the nucleus, and within a nuclear speckle structure that has recently been described for human cyclin T and CDK9, two critical components for Tat transactivation function on HIV-1 long terminal repeat promoter. Taken together, these data demonstrate that Tip110 regulates Tat transactivation activity through direct interaction, and suggest that Tip110 is an important cellular factor for HIV-1 gene expression and viral replication.

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Inhibition of Sickle Hemoglobin Polymerization as a Basis for Therapeutic Approaches to Sickle‐Cell Anemia

Noguchi

Schechter

Haley³

et al. 2003

Burger's Medicinal Chemistry and Drug Discovery

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This chapter reviews current understanding of the molecular and cellular basis of the pathophysiology of sickle‐cell anemia, with emphasis on the biophysics of the intracellular polymerization of sickle hemogobin. Factors that modify the severity of the disease manifestations, primarily by altering polymerization tendency, are discussed. This framework is used to present an overview of the major rational approaches to the therapy of sickle‐cell anemia based on inhibiting polymerization with agents that affect either the hemoglobin molecule or the sickle erythrocyte. Discussion of agents that may decrease vascular entrapment of sickle erythrocytes is also presented. Detailed review of the most important current approaches to therapy—pharmacologically elevating fetal hemoglobin—focuses primarily on hydroxyurea, the only drug currently FDA approved for treating sickle‐cell anemia. A brief discussion of other approaches, including stem cell transplantation and gene therapy, concludes the chapter.

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Beta globin gene inhibition by antisense RNA transcripts

Cited by 9 publications

References 24 publications

Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression

Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression

HIV-1 Tat Protein-mediated Transactivation of the HIV-1 Long Terminal Repeat Promoter Is Potentiated by a Novel Nuclear Tat-interacting Protein of110 kDa, Tip110

Inhibition of Sickle Hemoglobin Polymerization as a Basis for Therapeutic Approaches to Sickle‐Cell Anemia

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Beta globin gene inhibition by antisense RNA transcripts

Cited by 9 publications

References 24 publications

Hormone-regulated transepithelial Na+transport in mammalian CCD cells requires SGK1 expression

Hormone-regulated transepithelial Na+transport in mammalian CCD cells requires SGK1 expression

HIV-1 Tat Protein-mediated Transactivation of the HIV-1 Long Terminal Repeat Promoter Is Potentiated by a Novel Nuclear Tat-interacting Protein of110 kDa, Tip110

Inhibition of Sickle Hemoglobin Polymerization as a Basis for Therapeutic Approaches to Sickle‐Cell Anemia

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Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression

Hormone-regulated transepithelial Na⁺transport in mammalian CCD cells requires SGK1 expression