2003
DOI: 10.1128/mcb.23.11.3951-3964.2003
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Activin Induces x-Zone Apoptosis That Inhibits Luteinizing Hormone-Dependent Adrenocortical Tumor Formation in Inhibin-Deficient Mice

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Cited by 71 publications
(72 citation statements)
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“…PCSK6 was found to be essential for maintaining a high proliferative state in prostate cancer cell lines (Couture et al 2012). Activin A and TGFb2 were believed to be proapoptosis factors in various tissue and cell types such as murine adrenal X-zone (Beuschlein et al 2003), intestinal mucosa (Dunker et al 2002), trophoblast cells (Yu et al 2012), granulosa cells (Quezada et al 2012), oligodendrocytes (Quezada et al 2012), hepatocytes (Hughes & Evans 2003), and endometrial stromal cells (Moulton 1994). However, follistatin acted as an antagonist to activin and was considered as an anti-apoptosis factor in cells such as hepatocytes (Patella et al 2006) and renal tubular cells (Maeshima et al 2001).…”
Section: Discussionmentioning
confidence: 99%
“…PCSK6 was found to be essential for maintaining a high proliferative state in prostate cancer cell lines (Couture et al 2012). Activin A and TGFb2 were believed to be proapoptosis factors in various tissue and cell types such as murine adrenal X-zone (Beuschlein et al 2003), intestinal mucosa (Dunker et al 2002), trophoblast cells (Yu et al 2012), granulosa cells (Quezada et al 2012), oligodendrocytes (Quezada et al 2012), hepatocytes (Hughes & Evans 2003), and endometrial stromal cells (Moulton 1994). However, follistatin acted as an antagonist to activin and was considered as an anti-apoptosis factor in cells such as hepatocytes (Patella et al 2006) and renal tubular cells (Maeshima et al 2001).…”
Section: Discussionmentioning
confidence: 99%
“…Based on the inh -/-observations it was initially suggested that either the overexpression of gonadotropins or the lack of some gonadal factor might be the cause of tumor formation after gonadectomy (Matzuk et al 1994, Kananen et al 1996, Kananen et al 1997. Later studies have indicated that the development of tumors requires a high level of LH (Kero et al 2000) and a drop in the levels of gonadal activin, which normally inhibits the adrenal tumor growth by apoptosis (Beuschlein et al 2003). Smad 3, the intracellular signal transducer for TGFβ, has shown to be upregulated in inh -/--mice and its expression has also been found in the stem cell compartment indicating that tumors might arise from dys-regulated stem cells.…”
Section: Transgenic (Tg) Murine Models For Adrenocortical Tumorigenesismentioning
confidence: 99%
“…Recent work on inh -/--LH-CTP mice (Risma et al 1995, Beuschlein et al 2003 showed that when inh -/-mice are crossbreed with LH-overexpressing LH-CTP mice, they produce large activinsecreting ovarian tumors (Beuschlein et al 2003). While gonadectomized, they produce large, steroid-producing adrenal tumors putatively arising from the X-zone (Beuschlein et 13 al.…”
Section: Transgenic (Tg) Murine Models For Adrenocortical Tumorigenesismentioning
confidence: 99%
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“…The adrenal is also a site of action for both activin and BMP (Spencer et al 1999, Beuschlein et al 2003, Suzuki et al 2004. We wished to test the hypotheses that the expression of known inhibin binding proteins is the basis for adrenal gland binding of inhibin, and also that inhibin is potentially a paracrine/autocrine antagonist of activin and BMP actions in the adrenal.…”
Section: Introductionmentioning
confidence: 99%