Expression of mouse <i>igf2</i> mRNA‐binding protein 3 and its implications for the developing central nervous system

Mori, Hiroshi; Sakakibara, Shin-ichi; Imai, Toshio; Nakamura, Yuki; Iijima, Takahiro; Suzuki, Akira; Yuasa, Y.; Takeda, M.; Okano, Hideyuki

doi:10.1002/jnr.1060

Cited by 55 publications

(53 citation statements)

References 18 publications

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“…Although the fetal expression is prominent, data indicating that the proteins are also present in mature tissues have been accumulating (Mori et al 2001, Gu et al 2004. Adding to the previous data, we found that IMP1 mRNA was present in adult human kidneys, prostate, testis and ovaries, and IMP3 mRNA was found in brain, testis and ovaries, whereas IMP2 mRNA was more widespread but at low levels of expression.…”

Section: Discussionsupporting

confidence: 56%

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Expression of IGF-II mRNA-binding proteins (IMPs) in gonads and testicular cancer

Hammer¹,

Hansen²,

Byskov³

et al. 2005

Reproduction

129

118

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Insulin-like growth factor-II mRNA-binding proteins 1, 2 and 3 (IMP1, IMP2 and IMP3) belong to a family of RNA-binding proteins implicated in mRNA localization, turnover and translational control. We examined their expression pattern during development of murine and human testis and ovaries. In the mouse, IMPs were expressed in male and female gonadal cells at embryonic day 12.5 (E12.5). From E16.5, IMP1 and IMP3 became restricted to the developing germ cells, whereas IMP2 expression persisted in the interstitial cells. In mature mouse and human ovaries, IMP1, IMP2 and IMP3 were detected in resting and growing oocytes and in the granulosa cells. In testis, IMP1 and IMP3 were found mainly in the spermatogonia, whereas IMP2 was expressed in the immature Leydig cells. Moreover, all three IMPs were detected in human semen. The developmental expression pattern of IMP1 and IMP3 in the human testis prompted us to examine their possible involvement in testicular neoplasia. IMPs were detected primarily in germ-cell neoplasms, including preinvasive testicular carcinoma in situ, classical and spermatocytic seminoma, and nonseminomas, with particularly high expression in undifferentiated embryonal carcinoma. The relative expression of IMP1, IMP2 and IMP3 varied among tumor types and only IMP1 was detected in all carcinoma in situ cells. Thus IMPs, and in particular IMP1, may be useful auxiliary markers of testicular neoplasia. Reproduction (2005) 130 203-212

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Section: Discussionsupporting

confidence: 56%

“…Near the end of mouse embryogenesis IMP1 and IMP3 expression have almost disappeared (Mueller-Pillasch et al 1999. IMP1, IMP2 and IMP3 expression have, in general, not been reported in adult tissues, with a notable exception of the testis, where both IMP1 and IMP3 mRNAs have been described (Mori et al 2001, Wang et al 2003.…”

Section: Introductionmentioning

confidence: 96%

Expression of IGF-II mRNA-binding proteins (IMPs) in gonads and testicular cancer

Hammer¹,

Hansen²,

Byskov³

et al. 2005

Reproduction

129

118

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“…The early increase in Igf2 mRNA parallels the increase in neurons: both occur prior to the time at which let-7 levels normally rise, and both require the two conserved RNA-binding domains of LIN28. Igf2 has a documented role in the formation of neural tumors and promotes neurogenesis (Corcoran et al, 2008;Mori et al, 2001;Sim et al, 2006). Thus, the importance of Igf2 in neurogenesis is consistent with it being involved in the increase in neurons observed with constitutive LIN28.…”

Section: Research Articlementioning

confidence: 57%

LIN28 alters cell fate succession and acts independently of the let-7 microRNA during neurogliogenesis in vitro

et al. 2010

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SUMMARYLIN28 is an RNA-binding protein that is expressed in many developing tissues. It can block let-7 (Mirlet7) microRNA processing and help promote pluripotency. We have observed LIN28 expression in the developing mouse neural tube, colocalizing with SOX2, suggesting a role in neural development. To better understand its normal developmental function, we investigated LIN28 activity during neurogliogenesis in vitro, where the succession of neuronal to glial cell fates occurs as it does in vivo. LIN28 expression was high in undifferentiated cells, and was downregulated rapidly upon differentiation. Constitutive LIN28 expression caused a complete block of gliogenesis and an increase in neurogenesis. LIN28 expression was compatible with neuronal differentiation and did not increase proliferation. LIN28 caused significant changes in gene expression prior to any effect on let-7, notably on Igf2. Furthermore, a mutant LIN28 that permitted let-7 accumulation was still able to completely block gliogenesis. Thus, at least two biological activities of LIN28 are genetically separable and might involve distinct mechanisms. LIN28 can differentially promote and inhibit specific fates and does not function exclusively by blocking let-7 family microRNAs. Importantly, the role of LIN28 in cell fate succession in vertebrate cells is analogous to its activity as a developmental timing regulator in C. elegans.

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“…In this way, they are involved in the temporal and spatial control of gene expression at the level of mRNA rather than at the level of gene transcription. The three mammalian VICKZ proteins (IMP1/CRD-BP, IMP2, and IMP3/KOC) are primarily expressed during embryonic development, and their expression is generally not detected in adult tissues, with the exception of placenta and testes (1)(2)(3)(4). In contrast, they are overexpressed in various cancers (reviewed in refs.…”

Section: Introductionmentioning

confidence: 99%

HMGA2 Regulates Transcription of the Imp2 Gene via an Intronic Regulatory Element in Cooperation with Nuclear Factor-κB

Cleynen

Brants

Peeters

et al. 2007

Molecular Cancer Research

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IMP2 (insulin-like growth factor-II mRNA binding protein 2) is an oncofetal protein that is aberrantly expressed in several types of cancer. We recently identified the Imp2 gene as a target gene of the architectural transcription factor HMGA2 (high mobility group A2) and its tumor-specific truncated form HMGA2Tr. In this study, we investigated the mechanism via which HMGA2 regulates Imp2 gene expression. We show that HMGA2 and HMGA2Tr directly regulate transcription of the Imp2 gene by binding to an AT-rich regulatory region located in the first intron.In reporter experiments, we show that this AT-rich regulatory region mimics the response of the endogenous Imp2 gene to HMGA2 and HMGA2Tr. Furthermore, we show that a consensus nuclear factor-KB (NF-KB) binding site located immediately adjacent to the AT-rich regulatory region binds NF-KB and that NF-KB and HMGA2 cooperate to regulate Imp2 gene expression. Finally, we provide evidence that there is a strong and statistically significant correlation between HMGA2 and IMP2 gene expression in human liposarcomas.

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Expression of mouse igf2 mRNA‐binding protein 3 and its implications for the developing central nervous system

Cited by 55 publications

References 18 publications

Expression of IGF-II mRNA-binding proteins (IMPs) in gonads and testicular cancer

Expression of IGF-II mRNA-binding proteins (IMPs) in gonads and testicular cancer

LIN28 alters cell fate succession and acts independently of the let-7 microRNA during neurogliogenesis in vitro

HMGA2 Regulates Transcription of the Imp2 Gene via an Intronic Regulatory Element in Cooperation with Nuclear Factor-κB

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