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Items: 1 to 20 of 98

2.

The dimerization mechanism of LIS1 and its implication for proteins containing the LisH motif.

Mateja A, Cierpicki T, Paduch M, Derewenda ZS, Otlewski J.

J Mol Biol. 2006 Mar 24;357(2):621-31.

PMID:
16445939
3.

The structure of the N-terminal domain of the product of the lissencephaly gene Lis1 and its functional implications.

Kim MH, Cooper DR, Oleksy A, Devedjiev Y, Derewenda U, Reiner O, Otlewski J, Derewenda ZS.

Structure. 2004 Jun;12(6):987-98.

4.

Novel functional features of the Lis-H domain: role in protein dimerization, half-life and cellular localization.

Gerlitz G, Darhin E, Giorgio G, Franco B, Reiner O.

Cell Cycle. 2005 Nov;4(11):1632-40.

PMID:
16258276
5.

Characterization of the nucleolar gene product, treacle, in Treacher Collins syndrome.

Isaac C, Marsh KL, Paznekas WA, Dixon J, Dixon MJ, Jabs EW, Meier UT.

Mol Biol Cell. 2000 Sep;11(9):3061-71.

6.

The lissencephaly protein Lis1 is present in motile mammalian cilia and requires outer arm dynein for targeting to Chlamydomonas flagella.

Pedersen LB, Rompolas P, Christensen ST, Rosenbaum JL, King SM.

J Cell Sci. 2007 Mar 1;120(Pt 5):858-67.

7.

The LisH motif of muskelin is crucial for oligomerization and governs intracellular localization.

Delto CF, Heisler FF, Kuper J, Sander B, Kneussel M, Schindelin H.

Structure. 2015 Feb 3;23(2):364-73. doi: 10.1016/j.str.2014.11.016.

8.

Gross deletions in TCOF1 are a cause of Treacher-Collins-Franceschetti syndrome.

Bowman M, Oldridge M, Archer C, O'Rourke A, McParland J, Brekelmans R, Seller A, Lester T.

Eur J Hum Genet. 2012 Jul;20(7):769-77. doi: 10.1038/ejhg.2012.2.

9.

[Molecular mechanism of lissencephaly--how LIS1 and NDEL1 regulate cytoplasmic dynein?].

Hirotsune S.

Brain Nerve. 2008 Apr;60(4):375-81. Review. Japanese.

PMID:
18421979
11.
12.
13.

Lis1 acts as a "clutch" between the ATPase and microtubule-binding domains of the dynein motor.

Huang J, Roberts AJ, Leschziner AE, Reck-Peterson SL.

Cell. 2012 Aug 31;150(5):975-86. doi: 10.1016/j.cell.2012.07.022.

14.

The role of cytoplasmic dynein in the human brain developmental disease lissencephaly.

Vallee RB, Faulkner NE, Tai CY.

Biochim Biophys Acta. 2000 Mar 17;1496(1):89-98. Review.

15.

Point mutations and an intragenic deletion in LIS1, the lissencephaly causative gene in isolated lissencephaly sequence and Miller-Dieker syndrome.

Lo Nigro C, Chong CS, Smith AC, Dobyns WB, Carrozzo R, Ledbetter DH.

Hum Mol Genet. 1997 Feb;6(2):157-64.

16.
17.

The structure of the coiled-coil domain of Ndel1 and the basis of its interaction with Lis1, the causal protein of Miller-Dieker lissencephaly.

Derewenda U, Tarricone C, Choi WC, Cooper DR, Lukasik S, Perrina F, Tripathy A, Kim MH, Cafiso DS, Musacchio A, Derewenda ZS.

Structure. 2007 Nov;15(11):1467-81.

18.

The location and type of mutation predict malformation severity in isolated lissencephaly caused by abnormalities within the LIS1 gene.

Cardoso C, Leventer RJ, Matsumoto N, Kuc JA, Ramocki MB, Mewborn SK, Dudlicek LL, May LF, Mills PL, Das S, Pilz DT, Dobyns WB, Ledbetter DH.

Hum Mol Genet. 2000 Dec 12;9(20):3019-28.

19.

LIS1 controls mitosis and mitotic spindle organization via the LIS1-NDEL1-dynein complex.

Moon HM, Youn YH, Pemble H, Yingling J, Wittmann T, Wynshaw-Boris A.

Hum Mol Genet. 2014 Jan 15;23(2):449-66. doi: 10.1093/hmg/ddt436.

20.

Abnormal cortical development; towards elucidation of the LIS1 gene product function (review).

Reiner O, Sapir T.

Int J Mol Med. 1998 May;1(5):849-53. Review.

PMID:
9852306
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