PubMed (OMIM) for id: 331400

Year	Number of Results
1980	1
1990	1
1994	1
1996	6
1997	1
1998	9
1999	1
2000	1
2002	7
2003	1
2004	2
2024	0

1

The prevalence of MADH4 and BMPR1A mutations in juvenile polyposis and absence of BMPR2, BMPR1B, and ACVR1 mutations.

Howe JR, Sayed MG, Ahmed AF, Ringold J, Larsen-Haidle J, Merg A, Mitros FA, Vaccaro CA, Petersen GM, Giardiello FM, Tinley ST, Aaltonen LA, Lynch HT. Howe JR, et al. J Med Genet. 2004 Jul;41(7):484-91. doi: 10.1136/jmg.2004.018598. J Med Genet. 2004. PMID: 15235019 Free PMC article.

2

A combined syndrome of juvenile polyposis and hereditary haemorrhagic telangiectasia associated with mutations in MADH4 (SMAD4).

Gallione CJ, Repetto GM, Legius E, Rustgi AK, Schelley SL, Tejpar S, Mitchell G, Drouin E, Westermann CJ, Marchuk DA. Gallione CJ, et al. Lancet. 2004 Mar 13;363(9412):852-9. doi: 10.1016/S0140-6736(04)15732-2. Lancet. 2004. PMID: 15031030

3

Role of Smad4 (DPC4) inactivation in human cancer.

Miyaki M, Kuroki T. Miyaki M, et al. Biochem Biophys Res Commun. 2003 Jul 11;306(4):799-804. doi: 10.1016/s0006-291x(03)01066-0. Biochem Biophys Res Commun. 2003. PMID: 12821112 Review.

4

Structural mechanism of Smad4 recognition by the nuclear oncoprotein Ski: insights on Ski-mediated repression of TGF-beta signaling.

Wu JW, Krawitz AR, Chai J, Li W, Zhang F, Luo K, Shi Y. Wu JW, et al. Cell. 2002 Nov 1;111(3):357-67. doi: 10.1016/s0092-8674(02)01006-1. Cell. 2002. PMID: 12419246 Free article.

5

Nucleocytoplasmic shuttling of Smads 2, 3, and 4 permits sensing of TGF-beta receptor activity.

Inman GJ, Nicolás FJ, Hill CS. Inman GJ, et al. Mol Cell. 2002 Aug;10(2):283-94. doi: 10.1016/s1097-2765(02)00585-3. Mol Cell. 2002. PMID: 12191474 Free article.

6

E2F4/5 and p107 as Smad cofactors linking the TGFbeta receptor to c-myc repression.

Chen CR, Kang Y, Siegel PM, Massagué J. Chen CR, et al. Cell. 2002 Jul 12;110(1):19-32. doi: 10.1016/s0092-8674(02)00801-2. Cell. 2002. PMID: 12150994 Free article.

7

Juvenile polyposis: massive gastric polyposis is more common in MADH4 mutation carriers than in BMPR1A mutation carriers.

Friedl W, Uhlhaas S, Schulmann K, Stolte M, Loff S, Back W, Mangold E, Stern M, Knaebel HP, Sutter C, Weber RG, Pistorius S, Burger B, Propping P. Friedl W, et al. Hum Genet. 2002 Jul;111(1):108-11. doi: 10.1007/s00439-002-0748-9. Epub 2002 Jun 13. Hum Genet. 2002. PMID: 12136244

8

Novel de novo mutation of MADH4/SMAD4 in a patient with juvenile polyposis.

Burger B, Uhlhaas S, Mangold E, Propping P, Friedl W, Jenne D, Dockter G, Back W. Burger B, et al. Am J Med Genet. 2002 Jul 1;110(3):289-91. doi: 10.1002/ajmg.10411. Am J Med Genet. 2002. PMID: 12116240 No abstract available.

9

Common deletion of SMAD4 in juvenile polyposis is a mutational hotspot.

Howe JR, Shellnut J, Wagner B, Ringold JC, Sayed MG, Ahmed AF, Lynch PM, Amos CI, Sistonen P, Aaltonen LA. Howe JR, et al. Am J Hum Genet. 2002 May;70(5):1357-62. doi: 10.1086/340258. Epub 2002 Mar 27. Am J Hum Genet. 2002. PMID: 11920286 Free PMC article.

10

SMIF, a Smad4-interacting protein that functions as a co-activator in TGFbeta signalling.

Bai RY, Koester C, Ouyang T, Hahn SA, Hammerschmidt M, Peschel C, Duyster J. Bai RY, et al. Nat Cell Biol. 2002 Mar;4(3):181-90. doi: 10.1038/ncb753. Nat Cell Biol. 2002. PMID: 11836524

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