Retraction: Oct-3 is a maternal factor required for the first mouse embryonic division

Rosner, Mitchell H.; Santo, Ronald J. De; Heinz, Andreas; Staudt, Louis M.

doi:10.1016/0092-8674(92)90284-j

Cited by 3 publications

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“…Both resulted in developmental arrest at the onecell stage. These-for that time-rather spectacular (early days of antisense RNA) and difficult-to-explain results were later revealed as being incorrect and retracted (Rosner et al 1992). Rather a long period of silence ensued but finally, using gene targeting, the role of Oct4 in development was revealed (Nichols et al 1998).…”

Section: Oct4 and Its Role In Development And Pluripotencymentioning

confidence: 99%

Cloning v. clowning

Solter¹

2002

Genes Dev.

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Section: Oct4 and Its Role In Development And Pluripotencymentioning

confidence: 99%

Cloning v. clowning

Solter¹

2002

Genes Dev.

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“…The 1991 paper, unfortunately, turned out to be fraudulent (Rosner et al, , 1992. It was published in Cell and the authors subsequently wrote a perspective in Science, titled "Oct-3 and the beginning of mammalian development" .…”

Section: Hans This First Question Is a "Must": How Did You Become Inmentioning

confidence: 99%

Reprogramming cell fate: a scientific journey from viral enhancers to the master gene regulator Oct4 - an interview with Hans R. Schöler

Boiani¹

2010

Int. J. Dev. Biol.

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KEY WORDS: cell fate, ES cell, Oct4, pluripotency, reprogrammingTen years ago, I thought the fate of cells was sealed in the mammalian embryo at the stage of gastrulation. The prevalent view by far was that the adult body's founder tissues, known as the "germ layers" (primitive endoderm, mesoderm, primitive ectoderm) were established in the gastrula, kept separate from the primordial germ cells (PGCs), and the progeny of a given cell would be marked and never leave its germ layer of origin. This model fit reality so well that it was almost considered as a dogma. However, even a very good fit is not always correct. In fact, in the years from 1996 to 1998, the first successful nuclear transfer experiments in both sheep and mice showed that the nuclei of adult somatic cells remembered how to make all three embryonic germ layers if transplanted into an oocyte. From the year 1999 on, evidence was mounting that cells could "transdifferentiate" from one tissue to another across germ layers, often but not always by means of fusion with local cells (Bjornson et al., 1999;Ying et al., Int. J. Dev. Biol. 54: 1685-1695 (2010) 2002). These reports prompted a host of questions as to the occurrence and biological significance of these unexpected observations, to the definition of the germ layers and to the identity of the genes whose expression or silencing underlay the cell fate conversion. Since then, the term "reprogramming" has been used to summarize with one word the changes occurring when one cell takes on features that it was not supposed to have. In this context, Hans Schöler has made key contributions to the molecular understanding of reprogramming. Before moving on to the interview in which I asked Hans Schöler about the said contributions, Abbreviations used in this paper: EMBL, European Molecular Biology Laboratory; EMSA, electrophoretic mobility band shift assay; ES, embryonic stem cell; ICM, inner cell mass; ICSI, intracytoplasmic sperm injection; iPS, induced pluripotent stem cell; PGC, primordial germ cell; POU, Pit-1+Oct-1/ 2+Unc-86 family; TE, trophectoderm. M. BoianiI first put them into context by briefly reviewing the steps in the scientific career of Hans.Hans Schöler was born on January 30th 1953, in Toronto, Canada. He studied Biology in Heidelberg (Germany) (Fig. 1), where he received his diploma (1982) and his PhD (1985). After working in the industry at Boehringer Mannheim (now Roche) for two years, he returned to academia, joining the Max Planck Institute for Biophysical Chemistry in Göttingen (Germany). In 1991, Hans founded his own group at the European Molecular Biology Laboratory (EMBL) in Heidelberg, and during this time he achieved the "Habilitation" (1994) to later become professor. In 1999 he was appointed Professor of Reproduction Physiology at the "School of Veterinary Medicine" and Director of the "Center for Animal Transgenesis and Germ Cell Research" at the University of Pennsylvania (USA). In 2003, Hans returned to Germany, in Münster, where he now leads the Department for Cell an...

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Specificity of antisense oligonucleotides in vivo.

Woolf

Melton

Jennings

1992

Proc. Natl. Acad. Sci. U.S.A.

239

102

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Antisense oligonucleotides are widely used as inhibitors of gene expression in cultured cells and have been proposed as potential therapeutic agents, but it is not known to what extent they are specific for their intended target RNAs. Statistical considerations indicate that if oligonucleotides can form hybrids with mRNA molecules in vivo by means of short or imperfect regions of complementarity, then the specificity of oligonucleotides as antisense reagents will be greatly compromised. We have used Xenopus oocytes as a model system in which to investigate the potential specificity of antisense oligonucleotides in vivo. We injected perfect and partially matched antisense oligonucleotides into oocytes and measured the resulting degradation of the target RNA in each case. On the basis of the extent to which antisense oligonucleotides can cause cleavage of RNAs at imperfectly matched target sites, we conclude that in this system it is probably not possible to obtain specific cleavage of an intended target RNA without also causing at least the partial destruction of many nontargeted RNAs.

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Retraction: Oct-3 is a maternal factor required for the first mouse embryonic division

Cited by 3 publications

References 0 publications

Cloning v. clowning

Cloning v. clowning

Reprogramming cell fate: a scientific journey from viral enhancers to the master gene regulator Oct4 - an interview with Hans R. Schöler

Specificity of antisense oligonucleotides in vivo.

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