Menin suppresses osteoblast differentiation by antagonizing the AP-1 factor, JunD (Q24316533)

negative regulation of osteoblast differentiation

1 reference

Jun D proto-oncogene

1 reference

Multiple endocrine neoplasia 1

1 reference

author name string

Junko Naito

1

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Hiroshi Kaji

2

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Hideaki Sowa

3

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Geoffrey N Hendy

4

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Toshitsugu Sugimoto

5

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Kazuo Chihara

Journal of Biological Chemistry

6

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language of work or name

English

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publication date

11 February 2005

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published in

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volume

280

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issue

6

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page(s)

4785-91

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cites work

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Menin, the product of the MEN1 gene, is a nuclear protein

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Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription

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Inactivation of menin, a Smad3-interacting protein, blocks transforming growth factor type beta signaling

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Menin associates with a trithorax family histone methyltransferase complex and with the hoxc8 locus

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Leukemia proto-oncoprotein MLL forms a SET1-like histone methyltransferase complex with menin to regulate Hox gene expression

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A mouse model of multiple endocrine neoplasia, type 1, develops multiple endocrine tumors

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Inactivation of menin, the product of the multiple endocrine neoplasia type 1 gene, inhibits the commitment of multipotential mesenchymal stem cells into the osteoblast lineage

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Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism

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Parathyroid Hormone-Smad3 Axis Exerts Anti-apoptotic Action and Augments Anabolic Action of Transforming Growth Factor β in Osteoblasts

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JunD protects against chronic kidney disease by regulating paracrine mitogens.

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MAP and src kinases control the induction of AP-1 members in response to changes in mechanical environment in osteoblastic cells.

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Menin inactivation leads to loss of transforming growth factor beta inhibition of parathyroid cell proliferation and parathyroid hormone secretion.

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The multiple endocrine neoplasia type 1 gene product, menin, inhibits the human prolactin promoter activity

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Activin inhibits pituitary prolactin expression and cell growth through Smads, Pit-1 and menin

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Transcription factor JunD, deprived of menin, switches from growth suppressor to growth promoter

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Smads bind directly to the Jun family of AP-1 transcription factors

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The comparative role of activator protein 1 and Smad factors in the regulation of Timp-1 and MMP-1 gene expression by transforming growth factor-beta 1

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Transforming growth factor-beta1 induces interleukin-6 expression via activating protein-1 consisting of JunD homodimers in primary human lung fibroblasts.

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Three activator protein-1-binding sites bound by the Fra-2.JunD complex cooperate for the regulation of murine laminin alpha3A (lama3A) promoter activity by transforming growth factor-beta

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Transforming growth factor-beta stimulates interleukin-11 transcription via complex activating protein-1-dependent pathways

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Increased bone formation and osteosclerosis in mice overexpressing the transcription factor Fra-1

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Bone and haematopoietic defects in mice lacking c-fos

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Functions of AP1 (Fos/Jun) in bone development

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inferred from DOI database lookup

7 January 2021

based on heuristic

Decreased AP-1 activity and interleukin-11 expression by bone marrow stromal cells may be associated with impaired bone formation in aged mice

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