Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome (Q34063471)

30 July 2017

title

Inhibiting farnesylation reverses the nuclear morphology defect in a HeLa cell model for Hutchinson-Gilford progeria syndrome (English)

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30 July 2017

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Monica P Mallampalli

1

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30 July 2017

Gregory Huyer

2

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30 July 2017

Pravin Bendale

3

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30 July 2017

Michael H Gelb

4

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30 July 2017

Susan Michaelis

5

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30 July 2017

language of work or name

English

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publication date

26 September 2005

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Proceedings of the National Academy of Sciences of the United States of America

30 July 2017

number of pages

6

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based on heuristic

inferred from page(s)

published in

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30 July 2017

volume

102

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30 July 2017

issue

40

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30 July 2017

page(s)

14416-14421

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Nuclear lamins: building blocks of nuclear structure and function

30 July 2017

cites work

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Reversal of the cellular phenotype in the premature aging disease Hutchinson-Gilford progeria syndrome

5 July 2018

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Heterozygosity for Lmna deficiency eliminates the progeria-like phenotypes in Zmpste24-deficient mice

5 July 2018

1 reference

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A-type lamins: guardians of the soma?

5 July 2018

1 reference

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Hutchinson-Gilford progeria syndrome

5 July 2018

1 reference

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Prelamin A endoproteolytic processing in vitro by recombinant Zmpste24

5 July 2018

1 reference

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The nuclear envelope and human disease

5 July 2018

1 reference

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Genome-scale expression profiling of Hutchinson-Gilford progeria syndrome reveals widespread transcriptional misregulation leading to mesodermal/mesenchymal defects and accelerated atherosclerosis

5 July 2018

1 reference

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Accumulation of mutant lamin A causes progressive changes in nuclear architecture in Hutchinson-Gilford progeria syndrome

5 July 2018

1 reference

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Aging and nuclear organization: lamins and progeria

5 July 2018

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Lamin A/C deficiency causes defective nuclear mechanics and mechanotransduction.

5 July 2018

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Farnesyl transferase inhibitors: mechanism of action, translational studies and clinical evaluation

5 July 2018

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Zinc metalloproteinase, ZMPSTE24, is mutated in mandibuloacral dysplasia

5 July 2018

1 reference

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Recurrent de novo point mutations in lamin A cause Hutchinson–Gilford progeria syndrome

5 July 2018

1 reference

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Lamin a truncation in Hutchinson-Gilford progeria.

5 July 2018

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Zmpste24 deficiency in mice causes spontaneous bone fractures, muscle weakness, and a prelamin A processing defect.

5 July 2018

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Life at the edge: the nuclear envelope and human disease

5 July 2018

1 reference

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Mutations in the gene encoding the lamin B receptor produce an altered nuclear morphology in granulocytes (Pelger-Huët anomaly)

5 July 2018

1 reference

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The multispanning membrane protein Ste24p catalyzes CAAX proteolysis and NH2-terminal processing of the yeast a-factor precursor

5 July 2018

1 reference

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Discovery of (R)-7-cyano-2,3,4, 5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3- (phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine (BMS-214662), a farnesyltransferase inhibitor with potent preclinical antitumor activity

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Prenylated prelamin A interacts with Narf, a novel nuclear protein

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Dual roles for Ste24p in yeast a-factor maturation: NH2-terminal proteolysis and COOH-terminal CAAX processing

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

A novel membrane-associated metalloprotease, Ste24p, is required for the first step of NH2-terminal processing of the yeast a-factor precursor

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Protein prenylation: molecular mechanisms and functional consequences

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Primary structure analysis and lamin B and DNA binding of human LBR, an integral protein of the nuclear envelope inner membrane

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

The CaaX motif of lamin A functions in conjunction with the nuclear localization signal to target assembly to the nuclear envelope

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Isoprenylation is required for the processing of the lamin A precursor

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Nucleoplasmic localization of prelamin A: implications for prenylation-dependent lamin A assembly into the nuclear lamina

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Loss of ZMPSTE24 (FACE-1) causes autosomal recessive restrictive dermopathy and accumulation of Lamin A precursors.

5 July 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

Defective prelamin A processing and muscular and adipocyte alterations in Zmpste24 metalloproteinase-deficient mice.

28 October 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

The role of isoprenylation in membrane attachment of nuclear lamins. A single point mutation prevents proteolytic cleavage of the lamin A precursor and confers membrane binding properties

28 October 2018

1 reference

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pmc&linkname=pmc_refs_pubmed&retmode=json&id=1242289

28 October 2018

Identifiers

DOI

10.1073/PNAS.0503712102

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30 July 2017

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30 July 2017

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