Tgfß2 -/- Tgfß3 -/- double knockout mice display severe midline fusion defects and early embryonic lethality

Dünker, Nicole; Krieglstein, Kerstin

doi:10.1007/s00429-002-0273-6

Cited by 107 publications

(112 citation statements)

References 42 publications

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“…Several mutant mice with body wall abnormalities have been extensively analyzed (Qu et al, 1997;Manley et al, 2001;Dunker and Krieglstein, 2002;Williams, 2004a, 2004b). However, the molecular mechanism of mammalian body wall formation and pathogenesis of body wall abnormalities are still poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Ventral abdominal wall dysmorphogenesis of Msx1/Msx2 double‐mutant mice

Ogi¹,

Suzuki²,

Ogino³

et al. 2005

Anat. Rec.

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Msx1 and Msx2 genes encode the homeodomain transcription factors. Several gene knockout mice and expression studies suggest that they possess functionally redundant roles in embryogenesis. In this study, we revealed that Msx1 and Msx2 were expressed during ventral body wall formation in an overlapping manner. Msx1/Msx2 double-mutant mice displayed embryonic abdominal wall defects with disorganized muscle layers and connective tissues. These findings indicate that Msx1 and Msx2 play roles in concert during embryonic ventral abdominal wall formation.

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Section: Discussionmentioning

confidence: 99%

Ventral abdominal wall dysmorphogenesis of Msx1/Msx2 double‐mutant mice

Ogi¹,

Suzuki²,

Ogino³

et al. 2005

Anat. Rec.

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“…Omphk1 might function in each of these sites complementarily with other serine-threonine kinases. Tgf␤2/Tgf␤3 and Hoxb2/Hoxb4 functions are complementary, respectively, in the formation of primary body wall (Manley et al, 2001;Dunker and Krieglstein, 2002). Omphk2 is not expressed in either primary or secondary ventral body walls (Fig.…”

Section: Omphk1 Mutant Phenotypementioning

confidence: 97%

“…AP-2␣ (Brewer and Williams, 2004a), Hoxb2/b4 double (Manley et al, 2001), Tgf␤2/␤3 double (Dunker and Krieglstein, 2002), and Mab21l2 (Yamada et al, 2004) mutants have defects in the primary body wall formation. The AP-2␣ mutant also lacks sternal and abdominal bands (Brewer and Williams, 2004a), and several mutants are known that have defects in the migration of the bands and/or in the subsequent clo-sure of the ventral body wall (Suzuki et al, 1996;Eggenschwiler et al, 1997;Zhang et al, 1997;Kitamura et al, 1999;Carter et al, 2000;Rauch et al, 2000;Doyonnas et al, 2001;Ogi et al, 2005;Thumkeo et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

A new serine/threonine protein kinase,Omphk1, essential to ventral body wall formation

Hirano¹,

Kanazawa

Furushima

et al. 2006

Developmental Dynamics

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Here, we report a new serine/threonine protein kinase of the SNF1 subfamily Omphk1. Two Omphk homologues exist in each vertebrate species, and one homologue exists in Drosophila and Caenorhabditis elegans; the kinase domain is highly conserved among these homologues, and several domains are conserved among vertebrate Omphk. Omphk1 expression dynamically changes in the developing central nervous system, is found ubiquitously in epidermis, and is present uniquely in several other tissues. Its expression is also found in each tissue associated with the ventral body wall closure: the primary body wall composed of primitive ectoderm and each component of the secondary body wall. Concomitantly, its null mutant exhibits omphalocele with a failure in closure of the secondary body wall. There are no apparent gross morphological defects in brain, however, despite the unique Omphk1 expression in this tissue.

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“…The entire appendicular and most of the axial skeleton have an endochondral origin, forming through a cartilage template that is subsequently replaced by osteoblasts and bone (Soltanoff et al 2009). TGF-b and BMP signaling are crucial for the development of both bone types ) and for regulating chondrogenesis and osteogenesis (Kulkarni et al 1993;Mishina et al 1995;Winnier et al 1995;Zhang and Bradley 1996;Sanford et al 1997;Sirard et al 1998;Gu et al 1999;Beppu et al 2000;Dunker and Krieglstein 2002;Wang et al 2014;Salazar et al 2016;Wu et al 2016).…”

Section: Roles Of Tgf-b and Bmp Signaling In Bone Formation Skeletalmentioning

confidence: 99%

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

MacFarlane

Haupt

Dietz

et al. 2017

Cold Spring Harb Perspect Biol

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The transforming growth factor b (TGF-b) family of signaling molecules, which includes TGF-bs, activins, inhibins, and numerous bone morphogenetic proteins (BMPs) and growth and differentiation factors (GDFs), has important functions in all cells and tissues, including soft connective tissues and the skeleton. Specific TGF-b family members play different roles in these tissues, and their activities are often balanced with those of other TGF-b family members and by interactions with other signaling pathways. Perturbations in TGF-b family pathways are associated with numerous human diseases with prominent involvement of the skeletal and cardiovascular systems. This review focuses on the role of this family of signaling molecules in the pathologies of connective tissues that manifest in rare genetic syndromes (e.g., syndromic presentations of thoracic aortic aneurysm), as well as in more common disorders (e.g., osteoarthritis and osteoporosis). Many of these diseases are caused by or result in pathological alterations of the complex relationship between the TGF-b family of signaling mediators and the extracellular matrix in connective tissues.T he transforming growth factor b (TGF-b) family of cytokines comprises the three TGF-b proteins (TGF-b1, TGF-b2, and TGFb3) and related growth and differentiation factors such as activins, inhibins, bone morphogenic proteins (BMPs), and growth and differentiation factors (GDFs). These molecules play critical roles both in normal development and in several pathological conditions, including inflammation, fibrosis, and cancer (reviewed in Li and Flavell 2006;Gordon and Blobe 2008;Ikushima and Miyazono 2010). This review focuses on the role of these proteins in development and homeostasis of the skeleton and other connective tissues (summarized in Fig. 1) and on the diseases that ensue when these pathways are altered. Aberrant signaling in these pathways has been associated with common connective 6 These authors contributed equally to this work.

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Tgfß2 -/- Tgfß3 -/- double knockout mice display severe midline fusion defects and early embryonic lethality

Cited by 107 publications

References 42 publications

Ventral abdominal wall dysmorphogenesis of Msx1/Msx2 double‐mutant mice

Ventral abdominal wall dysmorphogenesis of Msx1/Msx2 double‐mutant mice

A new serine/threonine protein kinase,Omphk1, essential to ventral body wall formation

TGF-β Family Signaling in Connective Tissue and Skeletal Diseases

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