2005
DOI: 10.1182/blood-2004-02-0703
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BMP4 and Madh5 regulate the erythroid response to acute anemia

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Cited by 177 publications
(299 citation statements)
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References 41 publications
(35 reference statements)
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“…It is, however, interesting to note that the BMP pathway has been previously linked to stress erythropoiesis, as will be discussed below. 44,45 The mechanism by which TIF1g cooperates with Smads continues to be a controversial issue. Developmental studies from a variety of species have suggested that TIF1g, also known as Ectodermin, acts as a ubiquitin ligase for Smad4, thus functioning as a direct inhibitor of Smad4 downstream of TGF-b and BMP signaling.…”
Section: Tgf-b Signaling Diversified: a Role For Transcriptional Intementioning
confidence: 99%
“…It is, however, interesting to note that the BMP pathway has been previously linked to stress erythropoiesis, as will be discussed below. 44,45 The mechanism by which TIF1g cooperates with Smads continues to be a controversial issue. Developmental studies from a variety of species have suggested that TIF1g, also known as Ectodermin, acts as a ubiquitin ligase for Smad4, thus functioning as a direct inhibitor of Smad4 downstream of TGF-b and BMP signaling.…”
Section: Tgf-b Signaling Diversified: a Role For Transcriptional Intementioning
confidence: 99%
“…The absence of BMPRIA caused increased numbers of HSC-supporting osteoblastic cells lining the bone surface, which in turn led to an increase in the numbers of HSCs in these mice . A role for BMP signaling in stress erythropoiesis in the spleen has recently been described (Lenox et al, 2005) Interfering with the entire Smad pathway Since Smad7 has been shown to block all Smad signaling pathways, enforced expression of Smad7 can be used to greatly reduce or eliminate Smad signaling in HSC. Recently, overexpression of Smad7 in human CD34 þ hematopoietic cells was found to augment myeloid differentiation at the expense of lymphoid commitment (Chadwick et al, 2005).…”
Section: The Bmps In Adult Hematopoiesismentioning
confidence: 99%
“…However, a subsequent study demonstrated that it was the mutation of Madh5 that affected the ability of f/f mice to respond to acute anemia and the attribution of Sfxn1 mutation to the f/f phenotypes was in doubt (Lenox et al, 2005). Unlike other MCs, SFXN lacks the canonical internal tripartite structure (Azzi et al, 1993;Fleming et al, 2001).…”
Section: Introductionmentioning
confidence: 99%