Menin molecular interactions: Insights into normal functions and tumorigenesis

S. K. Agarwal, P. A. Kennedy, P. C. Scacheri, E. A. Novotny, A. B. Hickman, A. Cerrato, T. S. Rice, J. B. Moore, S. Rao, Y. Ji, C. Mateo, S. K. Libutti, B. Oliver, S. C. Chandrasekharappa, A. L. Burns, F. S. Collins, Allen M. Spiegel, S. J. Marx

Research output: Contribution to journalArticle

98 Citations (Scopus)

Abstract

Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease predisposed by heterozygous germline mutations in the MEN1 tumor suppressor gene. Biallelic loss of MEN1 resulting from small mutation and/or loss of heterozygosity occurs in a large tissue spectrum of MEN1 tumors or non-hereditary tumors. Mouse models of MEN1 underexpression or overexpression have also supported the tumor-suppressor effect of the MEN1 gene. Menin, the 610-amino-acid protein encoded by MEN1, is expressed ubiquitously and found predominantly in the nucleus. Sequence analyses do not reveal motifs of known function other than two nuclear localization sequences. Menin has been found to partner in vitro with a variety of proteins that comprise transcription factors, DNA processing factors, DNA repair proteins, and cytoskeletal proteins. The diverse functions of menin interactors suggest roles for menin in multiple biological pathways. Inactivation of menin switches its JunD partner from a downstream action of growth suppression to growth promotion. This is a plausible mechanism for menin tumorigenesis.

Original languageEnglish (US)
Pages (from-to)369-374
Number of pages6
JournalHormone and Metabolic Research
Volume37
Issue number6
DOIs
StatePublished - Jun 2005
Externally publishedYes

Fingerprint

Multiple Endocrine Neoplasia Type 1
Molecular interactions
Tumors
Carcinogenesis
Genes
Cytoskeletal Proteins
DNA
Proteins
Repair
Transcription Factors
Switches
Neoplasms
Tissue
Germ-Line Mutation
Loss of Heterozygosity
Amino Acids
Growth
Tumor Suppressor Genes
DNA Repair
Processing

Keywords

  • Hox genes
  • Jund
  • Men1
  • MLL
  • Multiple endocrine neoplasia
  • Oncogene
  • Partners
  • Transcription
  • Tumor suppressor

ASJC Scopus subject areas

  • Biochemistry
  • Endocrinology

Cite this

Agarwal, S. K., Kennedy, P. A., Scacheri, P. C., Novotny, E. A., Hickman, A. B., Cerrato, A., ... Marx, S. J. (2005). Menin molecular interactions: Insights into normal functions and tumorigenesis. Hormone and Metabolic Research, 37(6), 369-374. https://doi.org/10.1055/s-2005-870139

Menin molecular interactions : Insights into normal functions and tumorigenesis. / Agarwal, S. K.; Kennedy, P. A.; Scacheri, P. C.; Novotny, E. A.; Hickman, A. B.; Cerrato, A.; Rice, T. S.; Moore, J. B.; Rao, S.; Ji, Y.; Mateo, C.; Libutti, S. K.; Oliver, B.; Chandrasekharappa, S. C.; Burns, A. L.; Collins, F. S.; Spiegel, Allen M.; Marx, S. J.

In: Hormone and Metabolic Research, Vol. 37, No. 6, 06.2005, p. 369-374.

Research output: Contribution to journalArticle

Agarwal, SK, Kennedy, PA, Scacheri, PC, Novotny, EA, Hickman, AB, Cerrato, A, Rice, TS, Moore, JB, Rao, S, Ji, Y, Mateo, C, Libutti, SK, Oliver, B, Chandrasekharappa, SC, Burns, AL, Collins, FS, Spiegel, AM & Marx, SJ 2005, 'Menin molecular interactions: Insights into normal functions and tumorigenesis', Hormone and Metabolic Research, vol. 37, no. 6, pp. 369-374. https://doi.org/10.1055/s-2005-870139
Agarwal SK, Kennedy PA, Scacheri PC, Novotny EA, Hickman AB, Cerrato A et al. Menin molecular interactions: Insights into normal functions and tumorigenesis. Hormone and Metabolic Research. 2005 Jun;37(6):369-374. https://doi.org/10.1055/s-2005-870139
Agarwal, S. K. ; Kennedy, P. A. ; Scacheri, P. C. ; Novotny, E. A. ; Hickman, A. B. ; Cerrato, A. ; Rice, T. S. ; Moore, J. B. ; Rao, S. ; Ji, Y. ; Mateo, C. ; Libutti, S. K. ; Oliver, B. ; Chandrasekharappa, S. C. ; Burns, A. L. ; Collins, F. S. ; Spiegel, Allen M. ; Marx, S. J. / Menin molecular interactions : Insights into normal functions and tumorigenesis. In: Hormone and Metabolic Research. 2005 ; Vol. 37, No. 6. pp. 369-374.
@article{a87ec3995d50415d86b04070a3d043a8,
title = "Menin molecular interactions: Insights into normal functions and tumorigenesis",
abstract = "Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease predisposed by heterozygous germline mutations in the MEN1 tumor suppressor gene. Biallelic loss of MEN1 resulting from small mutation and/or loss of heterozygosity occurs in a large tissue spectrum of MEN1 tumors or non-hereditary tumors. Mouse models of MEN1 underexpression or overexpression have also supported the tumor-suppressor effect of the MEN1 gene. Menin, the 610-amino-acid protein encoded by MEN1, is expressed ubiquitously and found predominantly in the nucleus. Sequence analyses do not reveal motifs of known function other than two nuclear localization sequences. Menin has been found to partner in vitro with a variety of proteins that comprise transcription factors, DNA processing factors, DNA repair proteins, and cytoskeletal proteins. The diverse functions of menin interactors suggest roles for menin in multiple biological pathways. Inactivation of menin switches its JunD partner from a downstream action of growth suppression to growth promotion. This is a plausible mechanism for menin tumorigenesis.",
keywords = "Hox genes, Jund, Men1, MLL, Multiple endocrine neoplasia, Oncogene, Partners, Transcription, Tumor suppressor",
author = "Agarwal, {S. K.} and Kennedy, {P. A.} and Scacheri, {P. C.} and Novotny, {E. A.} and Hickman, {A. B.} and A. Cerrato and Rice, {T. S.} and Moore, {J. B.} and S. Rao and Y. Ji and C. Mateo and Libutti, {S. K.} and B. Oliver and Chandrasekharappa, {S. C.} and Burns, {A. L.} and Collins, {F. S.} and Spiegel, {Allen M.} and Marx, {S. J.}",
year = "2005",
month = "6",
doi = "10.1055/s-2005-870139",
language = "English (US)",
volume = "37",
pages = "369--374",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "Georg Thieme Verlag",
number = "6",

}

TY - JOUR

T1 - Menin molecular interactions

T2 - Insights into normal functions and tumorigenesis

AU - Agarwal, S. K.

AU - Kennedy, P. A.

AU - Scacheri, P. C.

AU - Novotny, E. A.

AU - Hickman, A. B.

AU - Cerrato, A.

AU - Rice, T. S.

AU - Moore, J. B.

AU - Rao, S.

AU - Ji, Y.

AU - Mateo, C.

AU - Libutti, S. K.

AU - Oliver, B.

AU - Chandrasekharappa, S. C.

AU - Burns, A. L.

AU - Collins, F. S.

AU - Spiegel, Allen M.

AU - Marx, S. J.

PY - 2005/6

Y1 - 2005/6

N2 - Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease predisposed by heterozygous germline mutations in the MEN1 tumor suppressor gene. Biallelic loss of MEN1 resulting from small mutation and/or loss of heterozygosity occurs in a large tissue spectrum of MEN1 tumors or non-hereditary tumors. Mouse models of MEN1 underexpression or overexpression have also supported the tumor-suppressor effect of the MEN1 gene. Menin, the 610-amino-acid protein encoded by MEN1, is expressed ubiquitously and found predominantly in the nucleus. Sequence analyses do not reveal motifs of known function other than two nuclear localization sequences. Menin has been found to partner in vitro with a variety of proteins that comprise transcription factors, DNA processing factors, DNA repair proteins, and cytoskeletal proteins. The diverse functions of menin interactors suggest roles for menin in multiple biological pathways. Inactivation of menin switches its JunD partner from a downstream action of growth suppression to growth promotion. This is a plausible mechanism for menin tumorigenesis.

AB - Multiple endocrine neoplasia type 1 (MEN1) is an autosomal dominant disease predisposed by heterozygous germline mutations in the MEN1 tumor suppressor gene. Biallelic loss of MEN1 resulting from small mutation and/or loss of heterozygosity occurs in a large tissue spectrum of MEN1 tumors or non-hereditary tumors. Mouse models of MEN1 underexpression or overexpression have also supported the tumor-suppressor effect of the MEN1 gene. Menin, the 610-amino-acid protein encoded by MEN1, is expressed ubiquitously and found predominantly in the nucleus. Sequence analyses do not reveal motifs of known function other than two nuclear localization sequences. Menin has been found to partner in vitro with a variety of proteins that comprise transcription factors, DNA processing factors, DNA repair proteins, and cytoskeletal proteins. The diverse functions of menin interactors suggest roles for menin in multiple biological pathways. Inactivation of menin switches its JunD partner from a downstream action of growth suppression to growth promotion. This is a plausible mechanism for menin tumorigenesis.

KW - Hox genes

KW - Jund

KW - Men1

KW - MLL

KW - Multiple endocrine neoplasia

KW - Oncogene

KW - Partners

KW - Transcription

KW - Tumor suppressor

UR - http://www.scopus.com/inward/record.url?scp=22444445436&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=22444445436&partnerID=8YFLogxK

U2 - 10.1055/s-2005-870139

DO - 10.1055/s-2005-870139

M3 - Article

C2 - 16001329

AN - SCOPUS:22444445436

VL - 37

SP - 369

EP - 374

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 6

ER -