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==Menin==
==Menin==
* MEN1 [[gene]] encodes a 610 [[amino acid]] (67 Kda) [[nuclear protein]] called Menin.<ref name="pmid10341092">{{cite journal| author=Guru SC, Crabtree JS, Brown KD, Dunn KJ, Manickam P, Prasad NB et al.| title=Isolation, genomic organization, and expression analysis of Men1, the murine homolog of the MEN1 gene. | journal=Mamm Genome | year= 1999 | volume= 10 | issue= 6 | pages= 592-6 | pmid=10341092 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10341092  }} </ref><ref name="pmid10524203">{{cite journal| author=Karges W, Maier S, Wissmann A, Dralle H, Dosch HM, Boehm BO| title=Primary structure, gene expression and chromosomal mapping of rodent homologs of the MEN1 tumor suppressor gene. | journal=Biochim Biophys Acta | year= 1999 | volume= 1446 | issue= 3 | pages= 286-94 | pmid=10524203 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10524203  }} </ref><ref name="pmid10529376">{{cite journal| author=Khodaei S, O'Brien KP, Dumanski J, Wong FK, Weber G| title=Characterization of the MEN1 ortholog in zebrafish. | journal=Biochem Biophys Res Commun | year= 1999 | volume= 264 | issue= 2 | pages= 404-8 | pmid=10529376 | doi=10.1006/bbrc.1999.1529 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10529376  }} </ref><ref name="pmid10818209">{{cite journal| author=Manickam P, Vogel AM, Agarwal SK, Oda T, Spiegel AM, Marx SJ et al.| title=Isolation, characterization, expression and functional analysis of the zebrafish ortholog of MEN1. | journal=Mamm Genome | year= 2000 | volume= 11 | issue= 6 | pages= 448-54 | pmid=10818209 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10818209  }} </ref><ref name="pmid11064160">{{cite journal| author=Maruyama K, Tsukada T, Honda M, Nara-Ashizawa N, Noguchi K, Cheng J et al.| title=Complementary DNA structure and genomic organization of Drosophila menin. | journal=Mol Cell Endocrinol | year= 2000 | volume= 168 | issue= 1-2 | pages= 135-40 | pmid=11064160 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11064160  }} </ref>
* MEN1 [[gene]] encodes a 610 [[amino acid]] (67 Kda) [[nuclear protein]] called menin.<ref name="pmid10341092">{{cite journal| author=Guru SC, Crabtree JS, Brown KD, Dunn KJ, Manickam P, Prasad NB et al.| title=Isolation, genomic organization, and expression analysis of Men1, the murine homolog of the MEN1 gene. | journal=Mamm Genome | year= 1999 | volume= 10 | issue= 6 | pages= 592-6 | pmid=10341092 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10341092  }} </ref><ref name="pmid10524203">{{cite journal| author=Karges W, Maier S, Wissmann A, Dralle H, Dosch HM, Boehm BO| title=Primary structure, gene expression and chromosomal mapping of rodent homologs of the MEN1 tumor suppressor gene. | journal=Biochim Biophys Acta | year= 1999 | volume= 1446 | issue= 3 | pages= 286-94 | pmid=10524203 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10524203  }} </ref><ref name="pmid10529376">{{cite journal| author=Khodaei S, O'Brien KP, Dumanski J, Wong FK, Weber G| title=Characterization of the MEN1 ortholog in zebrafish. | journal=Biochem Biophys Res Commun | year= 1999 | volume= 264 | issue= 2 | pages= 404-8 | pmid=10529376 | doi=10.1006/bbrc.1999.1529 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10529376  }} </ref><ref name="pmid10818209">{{cite journal| author=Manickam P, Vogel AM, Agarwal SK, Oda T, Spiegel AM, Marx SJ et al.| title=Isolation, characterization, expression and functional analysis of the zebrafish ortholog of MEN1. | journal=Mamm Genome | year= 2000 | volume= 11 | issue= 6 | pages= 448-54 | pmid=10818209 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10818209  }} </ref><ref name="pmid11064160">{{cite journal| author=Maruyama K, Tsukada T, Honda M, Nara-Ashizawa N, Noguchi K, Cheng J et al.| title=Complementary DNA structure and genomic organization of Drosophila menin. | journal=Mol Cell Endocrinol | year= 2000 | volume= 168 | issue= 1-2 | pages= 135-40 | pmid=11064160 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11064160  }} </ref>
* The first identified partner of menin was JunD, a transcriptional factor belonging to the AP1 transcription complex family. Menin interacts with the N-terminus of JunD through its N-terminus and central domains (which are critical for this interaction). Wild type menin represses JunD-activated transcription maybe via a histone deacetylase-dependent mechanism.<ref name="pmid9989505">{{cite journal| author=Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY et al.| title=Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription. | journal=Cell | year= 1999 | volume= 96 | issue= 1 | pages= 143-52 | pmid=9989505 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9989505  }} </ref><ref name="pmid10500243">{{cite journal| author=Gobl AE, Berg M, Lopez-Egido JR, Oberg K, Skogseid B, Westin G| title=Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism. | journal=Biochim Biophys Acta | year= 1999 | volume= 1447 | issue= 1 | pages= 51-6 | pmid=10500243 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10500243  }} </ref>.
* The first identified partner of menin was JunD, a [[transcriptional factor]] belonging to the AP1 [[transcription]] complex family. Menin interacts with the N-terminus of [[JunD]] through its N-terminus and central domains. Wild type menin represses [[JunD]]-activated [[transcription]] maybe via a [[histone]] deacetylase-dependent mechanism.<ref name="pmid9989505">{{cite journal| author=Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY et al.| title=Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription. | journal=Cell | year= 1999 | volume= 96 | issue= 1 | pages= 143-52 | pmid=9989505 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9989505  }} </ref><ref name="pmid10500243">{{cite journal| author=Gobl AE, Berg M, Lopez-Egido JR, Oberg K, Skogseid B, Westin G| title=Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism. | journal=Biochim Biophys Acta | year= 1999 | volume= 1447 | issue= 1 | pages= 51-6 | pmid=10500243 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10500243  }} </ref>.
* Menin interacts, directly, with three members of the nuclear factor NF-kB family of transcription regulators: NF-kB1 (p50), NF-kB2 (p52) and RelA (p65)<ref name="pmid11526476">{{cite journal| author=Heppner C, Bilimoria KY, Agarwal SK, Kester M, Whitty LJ, Guru SC et al.| title=The tumor suppressor protein menin interacts with NF-kappaB proteins and inhibits NF-kappaB-mediated transactivation. | journal=Oncogene | year= 2001 | volume= 20 | issue= 36 | pages= 4917-25 | pmid=11526476 | doi=10.1038/sj.onc.1204529 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11526476  }} </ref>.. These proteins modulate the expression of various genes and are involved in the oncogenesis of numerous organs. Menin interacts with NF-kB by its central domain and represses NF-kB-mediated transcription.
* Menin interacts, directly, with three members of the [[nuclear factor]] [[NF-kB]] family of [[transcription]] regulators: [[NF-kB1]] (p50), NF-kB2 (p52) and RelA (p65)<ref name="pmid11526476">{{cite journal| author=Heppner C, Bilimoria KY, Agarwal SK, Kester M, Whitty LJ, Guru SC et al.| title=The tumor suppressor protein menin interacts with NF-kappaB proteins and inhibits NF-kappaB-mediated transactivation. | journal=Oncogene | year= 2001 | volume= 20 | issue= 36 | pages= 4917-25 | pmid=11526476 | doi=10.1038/sj.onc.1204529 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11526476  }} </ref>. These [[protein]]s modulate the expression of various [[gene]]s and are involved in the [[oncogenesis]] of numerous [[organ]]s. Menin interacts with [[NF-kB]] by its central domain and represses [[NF-kB]]-mediated [[transcription]].
* Moreover, menin interferes with the Transforming Growth Factor beta (TGFβ) signalling pathway at the level of Smad3. Alteration of the TGFβ signalling pathways is important in pancreatic carcinogenesis.
* Moreover, menin interferes with the transforming growth factor beta ([[TGFβ]]) signalling pathway at the level of [[Smad3]]. Alteration of the [[TGFβ]] signalling pathways is important in pancreatic [[carcinogenesis]].
* Although menin has been identified primarily as a nuclear protein, recent studies have reported its interaction with the glial fibrillary acid protein (GFAP) and with vimentin (components of intermediate filaments (IFs)), suggesting a putative role in glial cell oncogenesis.
* Although menin has been identified primarily as a nuclear [[protein]], recent studies have reported its interaction with the [[glial fibrillary acid protein]] (GFAP) and with [[vimentin]] (components of intermediate filaments (IFs)), suggesting a putative role in [[glial cell oncogenesis]].
* Finally, menin interacts with the metastasis suppressor Nm23H1<ref name="pmid12145286">{{cite journal| author=Yaguchi H, Ohkura N, Tsukada T, Yamaguchi K| title=Menin, the multiple endocrine neoplasia type 1 gene product, exhibits GTP-hydrolyzing activity in the presence of the tumor metastasis suppressor nm23. | journal=J Biol Chem | year= 2002 | volume= 277 | issue= 41 | pages= 38197-204 | pmid=12145286 | doi=10.1074/jbc.M204132200 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12145286  }} </ref>. This interaction enables menin to act as an atypical GTPase and to hydrolyze GTP. The binding of menin to Nm23H1 may be relevant also to the control of genomic stability, as Nm23H1 is associated to the centrosome that is involved in the maintenance of chromosome integrity.<ref name="pmid1672620">{{cite journal| author=Scappaticci S, Maraschio P, del Ciotto N, Fossati GS, Zonta A, Fraccaro M| title=Chromosome abnormalities in lymphocytes and fibroblasts of subjects with multiple endocrine neoplasia type 1. | journal=Cancer Genet Cytogenet | year= 1991 | volume= 52 | issue= 1 | pages= 85-92 | pmid=1672620 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1672620  }} </ref><ref name="pmid1358429">{{cite journal| author=Scappaticci S, Brandi ML, Capra E, Cortinovis M, Maraschio P, Fraccaro M| title=Cytogenetics of multiple endocrine neoplasia syndrome. II. Chromosome abnormalities in an insulinoma and a glucagonoma from two subjects with MEN1. | journal=Cancer Genet Cytogenet | year= 1992 | volume= 63 | issue= 1 | pages= 17-21 | pmid=1358429 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1358429  }} </ref><ref name="pmid7889502">{{cite journal| author=Tomassetti P, Cometa G, Del Vecchio E, Baserga M, Faccioli P, Bosoni D et al.| title=Chromosomal instability in multiple endocrine neoplasia type 1. Cytogenetic evaluation with DEB test. | journal=Cancer Genet Cytogenet | year= 1995 | volume= 79 | issue= 2 | pages= 123-6 | pmid=7889502 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7889502  }} </ref><ref name="pmid10087948">{{cite journal| author=Sakurai A, Katai M, Itakura Y, Ikeo Y, Hashizume K| title=Premature centromere division in patients with multiple endocrine neoplasia type 1. | journal=Cancer Genet Cytogenet | year= 1999 | volume= 109 | issue= 2 | pages= 138-40 | pmid=10087948 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10087948  }} </ref>
* Finally, menin interacts with the [[metastasis]] suppressor [[Nm23H1]]<ref name="pmid12145286">{{cite journal| author=Yaguchi H, Ohkura N, Tsukada T, Yamaguchi K| title=Menin, the multiple endocrine neoplasia type 1 gene product, exhibits GTP-hydrolyzing activity in the presence of the tumor metastasis suppressor nm23. | journal=J Biol Chem | year= 2002 | volume= 277 | issue= 41 | pages= 38197-204 | pmid=12145286 | doi=10.1074/jbc.M204132200 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12145286  }} </ref>. This interaction enables menin to act as an atypical GTPase and to hydrolyze GTP. The binding of menin to Nm23H1 may be relevant also to the control of genomic stability, as Nm23H1 is associated to the [[centrosome]] that is involved in the maintenance of chromosome integrity.<ref name="pmid1672620">{{cite journal| author=Scappaticci S, Maraschio P, del Ciotto N, Fossati GS, Zonta A, Fraccaro M| title=Chromosome abnormalities in lymphocytes and fibroblasts of subjects with multiple endocrine neoplasia type 1. | journal=Cancer Genet Cytogenet | year= 1991 | volume= 52 | issue= 1 | pages= 85-92 | pmid=1672620 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1672620  }} </ref><ref name="pmid1358429">{{cite journal| author=Scappaticci S, Brandi ML, Capra E, Cortinovis M, Maraschio P, Fraccaro M| title=Cytogenetics of multiple endocrine neoplasia syndrome. II. Chromosome abnormalities in an insulinoma and a glucagonoma from two subjects with MEN1. | journal=Cancer Genet Cytogenet | year= 1992 | volume= 63 | issue= 1 | pages= 17-21 | pmid=1358429 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1358429  }} </ref><ref name="pmid7889502">{{cite journal| author=Tomassetti P, Cometa G, Del Vecchio E, Baserga M, Faccioli P, Bosoni D et al.| title=Chromosomal instability in multiple endocrine neoplasia type 1. Cytogenetic evaluation with DEB test. | journal=Cancer Genet Cytogenet | year= 1995 | volume= 79 | issue= 2 | pages= 123-6 | pmid=7889502 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=7889502  }} </ref><ref name="pmid10087948">{{cite journal| author=Sakurai A, Katai M, Itakura Y, Ikeo Y, Hashizume K| title=Premature centromere division in patients with multiple endocrine neoplasia type 1. | journal=Cancer Genet Cytogenet | year= 1999 | volume= 109 | issue= 2 | pages= 138-40 | pmid=10087948 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=10087948  }} </ref>

Latest revision as of 18:34, 4 September 2015

  • The gene locus causing MEN1 has been localised to chromosome 11q13 by studies of loss of heterozigosity (LOH) on MEN1-associated tumors and by linkage analysis in MEN1 families[1][2][3][4]
  • MEN1, spans about 10 Kb and consists of ten exons encoding a 610 amino acid nuclear protein, named menin.
  • MEN1 gene is a putative tumor suppressor gene and causes type 1 multiple endocrine neoplasia by Knudson's "two hits" model for tumor development.[5]
  • Knudson's "two hits" model for tumor development suggest that there is a germline mutation present in all cells at birth and the second mutation is a somatic mutation that occurs in the predisposed endocrine cell and leads to loss of the remaining wild type allele. This "two hits" model gives cells the survival advantage needed for tumor development.
  • Mutations are distributed over the entire coding region without showing any significant hot spot region[6][7][8][9][10][11]
  • Approximately 20% of mutations are nonsense mutations, about 50% are frameshift insertions and deletions, 20% are missense mutations and about 7% are splice site defects.

Menin

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  2. Thakker RV, Bouloux P, Wooding C, Chotai K, Broad PM, Spurr NK; et al. (1989). "Association of parathyroid tumors in multiple endocrine neoplasia type 1 with loss of alleles on chromosome 11". N Engl J Med. 321 (4): 218–24. doi:10.1056/NEJM198907273210403. PMID 2568587.
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  4. Byström C, Larsson C, Blomberg C, Sandelin K, Falkmer U, Skogseid B; et al. (1990). "Localization of the MEN1 gene to a small region within chromosome 11q13 by deletion mapping in tumors". Proc Natl Acad Sci U S A. 87 (5): 1968–72. PMC 53606. PMID 1968641.
  5. Knudson AG (1993). "Antioncogenes and human cancer". Proc Natl Acad Sci U S A. 90 (23): 10914–21. PMC 47892. PMID 7902574.
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  7. Giraud S, Zhang CX, Serova-Sinilnikova O, Wautot V, Salandre J, Buisson N; et al. (1998). "Germ-line mutation analysis in patients with multiple endocrine neoplasia type 1 and related disorders". Am J Hum Genet. 63 (2): 455–67. doi:10.1086/301953. PMC 1377295. PMID 9683585.
  8. Teh BT, Kytölä S, Farnebo F, Bergman L, Wong FK, Weber G; et al. (1998). "Mutation analysis of the MEN1 gene in multiple endocrine neoplasia type 1, familial acromegaly and familial isolated hyperparathyroidism". J Clin Endocrinol Metab. 83 (8): 2621–6. doi:10.1210/jcem.83.8.5059. PMID 9709921.
  9. Poncin J, Abs R, Velkeniers B, Bonduelle M, Abramowicz M, Legros JJ; et al. (1999). "Mutation analysis of the MEN1 gene in Belgian patients with multiple endocrine neoplasia type 1 and related diseases". Hum Mutat. 13 (1): 54–60. doi:10.1002/(SICI)1098-1004(1999)13:1<54::AID-HUMU6>3.0.CO;2-K. PMID 9888389.
  10. Hai N, Aoki N, Matsuda A, Mori T, Kosugi S (1999). "Germline MEN1 mutations in sixteen Japanese families with multiple endocrine neoplasia type 1 (MEN1)". Eur J Endocrinol. 141 (5): 475–80. PMID 10576763.
  11. Morelli A, Falchetti A, Martineti V, Becherini L, Mark M, Friedman E; et al. (2000). "MEN1 gene mutation analysis in Italian patients with multiple endocrine neoplasia type 1". Eur J Endocrinol. 142 (2): 131–7. PMID 10664520.
  12. Guru SC, Crabtree JS, Brown KD, Dunn KJ, Manickam P, Prasad NB; et al. (1999). "Isolation, genomic organization, and expression analysis of Men1, the murine homolog of the MEN1 gene". Mamm Genome. 10 (6): 592–6. PMID 10341092.
  13. Karges W, Maier S, Wissmann A, Dralle H, Dosch HM, Boehm BO (1999). "Primary structure, gene expression and chromosomal mapping of rodent homologs of the MEN1 tumor suppressor gene". Biochim Biophys Acta. 1446 (3): 286–94. PMID 10524203.
  14. Khodaei S, O'Brien KP, Dumanski J, Wong FK, Weber G (1999). "Characterization of the MEN1 ortholog in zebrafish". Biochem Biophys Res Commun. 264 (2): 404–8. doi:10.1006/bbrc.1999.1529. PMID 10529376.
  15. Manickam P, Vogel AM, Agarwal SK, Oda T, Spiegel AM, Marx SJ; et al. (2000). "Isolation, characterization, expression and functional analysis of the zebrafish ortholog of MEN1". Mamm Genome. 11 (6): 448–54. PMID 10818209.
  16. Maruyama K, Tsukada T, Honda M, Nara-Ashizawa N, Noguchi K, Cheng J; et al. (2000). "Complementary DNA structure and genomic organization of Drosophila menin". Mol Cell Endocrinol. 168 (1–2): 135–40. PMID 11064160.
  17. Agarwal SK, Guru SC, Heppner C, Erdos MR, Collins RM, Park SY; et al. (1999). "Menin interacts with the AP1 transcription factor JunD and represses JunD-activated transcription". Cell. 96 (1): 143–52. PMID 9989505.
  18. Gobl AE, Berg M, Lopez-Egido JR, Oberg K, Skogseid B, Westin G (1999). "Menin represses JunD-activated transcription by a histone deacetylase-dependent mechanism". Biochim Biophys Acta. 1447 (1): 51–6. PMID 10500243.
  19. Heppner C, Bilimoria KY, Agarwal SK, Kester M, Whitty LJ, Guru SC; et al. (2001). "The tumor suppressor protein menin interacts with NF-kappaB proteins and inhibits NF-kappaB-mediated transactivation". Oncogene. 20 (36): 4917–25. doi:10.1038/sj.onc.1204529. PMID 11526476.
  20. Yaguchi H, Ohkura N, Tsukada T, Yamaguchi K (2002). "Menin, the multiple endocrine neoplasia type 1 gene product, exhibits GTP-hydrolyzing activity in the presence of the tumor metastasis suppressor nm23". J Biol Chem. 277 (41): 38197–204. doi:10.1074/jbc.M204132200. PMID 12145286.
  21. Scappaticci S, Maraschio P, del Ciotto N, Fossati GS, Zonta A, Fraccaro M (1991). "Chromosome abnormalities in lymphocytes and fibroblasts of subjects with multiple endocrine neoplasia type 1". Cancer Genet Cytogenet. 52 (1): 85–92. PMID 1672620.
  22. Scappaticci S, Brandi ML, Capra E, Cortinovis M, Maraschio P, Fraccaro M (1992). "Cytogenetics of multiple endocrine neoplasia syndrome. II. Chromosome abnormalities in an insulinoma and a glucagonoma from two subjects with MEN1". Cancer Genet Cytogenet. 63 (1): 17–21. PMID 1358429.
  23. Tomassetti P, Cometa G, Del Vecchio E, Baserga M, Faccioli P, Bosoni D; et al. (1995). "Chromosomal instability in multiple endocrine neoplasia type 1. Cytogenetic evaluation with DEB test". Cancer Genet Cytogenet. 79 (2): 123–6. PMID 7889502.
  24. Sakurai A, Katai M, Itakura Y, Ikeo Y, Hashizume K (1999). "Premature centromere division in patients with multiple endocrine neoplasia type 1". Cancer Genet Cytogenet. 109 (2): 138–40. PMID 10087948.