ST7-OT3

Last update 08 May 2025

Basic Info

Synonyms

NCRNA00026, ST7 overlapping transcript 3, ST7-OT3

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Introduction-

100 Clinical Results associated with ST7-OT3

100 Translational Medicine associated with ST7-OT3

0 Patents (Medical) associated with ST7-OT3

Literatures (Medical) associated with ST7-OT3

01 Jan 2006·HEREDITAS

Genetic Analysis of Two Extremely Segregation Distorted　Popula-tions in Rice (Oryza sativa L.)

Article

Author: Zeng, Da-Li ; Tang, Ding ; Zhang, Guang-Heng ; Guo, Long-Biao ; Qian, Qian ; Cheng, Zhu-Kuan

Segregation distortion is a quite common phenomenon in living species and thought to be a potent evolutional force. The main reasons of distorted segregation ratios are responsible for the selection of gametes or sporophytes. In this study, two extreme segregation distortions from the progenies of lmi x 02428 and d6 x 93-11 were identified. The segregation ratio of molecular markers tightly linked with LMI and D6 genes were analyzed and skew segregation were found in the markers tested which were indicated by significant deviation from the expected Mendelian segregation ratio(1:2:1). The segregation distorted regions were detected between molecular markers ST8 and ST8-2 near the centromere of chromosome 8, and ST7-1 and ST7-3 near telomere of chromosome 7, respectively. Meanwhile, the results indicated that segregation distortion had related with the different crossed combinations.

01 Sep 2002·GenomicsQ3 · BIOLOGY

The RAY1/ST7 Tumor-Suppressor Locus on Chromosome 7q31 Represents a Complex Multi-transcript System

Q3 · BIOLOGY

Article

Author: Stephen W. Scherer ; Sandy Thevarkunnel ; John B. Vincent ; Megha Patel ; Joseph Cheung ; Debbie Kolozsvari ; Erwin Petek

We recently identified a novel gene, RAY1 (FAM4A1), which spans a translocation breakpoint at 7q31 in a patient with autism. This gene has more recently been reported to be a suppressor of tumorigenicity, ST7, although controversy surrounds this observation because subsequent reports have failed to corroborate these findings. Our further analysis of this locus reveals that it is composed of a multigene system that includes two noncoding sense strand genes (ST7OT3 and ST7OT4) that overlap with many alternative forms of the coding RAY1/ST7 transcript, and two noncoding genes on the antisense strand (ST7OT1 and ST7OT2). RAY1/ST7 was determined to have at least three different 5' exons with alternative start codons, one of which seems to be used almost exclusively in the brain. We have also identified a third alternative 3' end of RAY1/ST7 that uses exons from ST7OT3. ST7OT3 spans from intron 10 to exon 14 of RAY1/ST7 and includes several exons. ST7OT4 has at least seven exons and is transcribed on the sense strand between RAY1/ST7 exon 1 and a tropomyosin-like sequence, TPM3L2. ST7OT1 overlaps with the RAY1/ST7 exon 1 and promoter. ST7OT2 spans from RAY1/ST7 intron 9 to intron 1, and has multiple isoforms. We screened the exons of RAY1/ST7 and ST7OT1-3 for sequence variants in 90 unrelated autism probands and identified several rare variants, including a Ile361Val substitution. Although these variants were not observed in a control population, it is unclear whether they contribute to the autistic phenotype. We postulate that the apparent noncoding genes at the RAY1/ST7 locus may be regulatory RNAs. The RAY1/ST7 may generate at least 18 possible isoforms, with many more arising if other sense-strand exons from ST7OT3 and ST7 OT4 are used in a selective and possibly tissue-specific manner.

01 Jun 1992·Journal of Biological ChemistryQ2 · BIOLOGY

Characterization of beta-125I-endorphin cross-linked proteins in NG108-15 cell membranes. A 25-kilodalton protein with properties of delta-opioid-binding site.

Q2 · BIOLOGY

Article

Author: Ko, Jane L. ; Loh, Horace H. ; Lee, Nancy M.

Cross-linking of beta-125I-endorphin to NG108-15 cell membranes labeled bands with molecular masses of 55, 35, and 25 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. We applied several criteria to evaluate the relevance of these cross-linked bands to delta-opioid receptors, including selectivity, stereospecificity, affinity, G-protein coupling, down-regulation, and correlation with opioid receptor level in different well-characterized cell lines. Only the 25 kDa protein adequately fulfilled all these criteria. Thus, cross-linking to the 25-kDa band was selectively inhibited by ligands with delta-opioid affinity, but not by mu-opioid, kappa-opioid, or optically inactive opioid ligands or by non-opioid ligands. Based on inhibition of cross-linking, we calculated an affinity of [D-Ala2,D-Leu5]enkephalin binding to the 25-kDa and (Kd = 6 nM) that is similar to that reported for [D-Ala2,D-Leu5]enkephalin binding to NG108-15 membranes; this affinity decreased approximately 10-fold in the presence of Na+/guanyl-5'-yl imidodiphosphate. Chronic agonist treatment of NG108-15 cells reduced cross-linking to the 25-kDa band, but not to others, in a manner parallel to down-regulation of opioid receptors. Finally, the amount of the 25-kDa band was roughly proportional to the level of opioid receptors present in N18TG2, NS20Y, ST7-3, and ST8-4 cells. The 25-kDa band was absent in PC12h, NIH3T3, and C6BU1 cells as well as in liver, all of which had no detectable opioid binding.

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ST7-OT3

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