(Q28272957)

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

review article

1 reference

title

Prelamin A farnesylation and progeroid syndromes (English)

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

1

1 reference

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21 December 2019

4

Loren G Fong

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

2

Margarita Meta

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

author name string

Shao H Yang

series ordinal

3

1 reference

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21 December 2019

language of work or name

English

0 references

publication date

7 November 2006

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

Journal of Biological Chemistry

21 December 2019

published in

1 reference

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21 December 2019

volume

281

1 reference

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21 December 2019

issue

52

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

page(s)

39741-39745

1 reference

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

Nuclear lamins: laminopathies and their role in premature ageing.

21 December 2019

cites work

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Loss of A-type lamin expression compromises nuclear envelope integrity leading to muscular dystrophy

21 January 2018

1 reference

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Homozygous defects in LMNA, encoding lamin A/C nuclear-envelope proteins, cause autosomal recessive axonal neuropathy in human (Charcot-Marie-Tooth disorder type 2) and mouse

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Lamins A and C but not lamin B1 regulate nuclear mechanics.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Drosophila syntaxin 16 is a Q-SNARE implicated in Golgi dynamics.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Prelamin A and lamin A appear to be dispensable in the nuclear lamina

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Protein prenylation: molecular mechanisms and functional consequences

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Prelamin A endoproteolytic processing in vitro by recombinant Zmpste24

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Modulation of Ras and a-factor function by carboxyl-terminal proteolysis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

The CaaX proteases, Afc1p and Rce1p, have overlapping but distinct substrate specificities

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

The Arabidopsis AtSTE24 is a CAAX protease with broad substrate specificity

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Disruption of the mouse Rce1 gene results in defective Ras processing and mislocalization of Ras within cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Biochemical studies of Zmpste24-deficient mice

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Prelamin A, Zmpste24, misshapen cell nuclei, and progeria--new evidence suggesting that protein farnesylation could be important for disease pathogenesis

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Posttranslational modification of the Ha-ras oncogene protein: evidence for a third class of protein carboxyl methyltransferases

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Mammalian prenylcysteine carboxyl methyltransferase is in the endoplasmic reticulum

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Maturation of nuclear lamin A involves a specific carboxy-terminal trimming, which removes the polyisoprenylation site from the precursor; implications for the structure of the nuclear lamina

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Isoprenylation is required for the processing of the lamin A precursor

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Edible vaccines: not quite ready for prime time

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Head and/or CaaX domain deletions of lamin proteins disrupt preformed lamin A and C but not lamin B structure in mammalian cells

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Blocking protein farnesyltransferase improves nuclear blebbing in mouse fibroblasts with a targeted Hutchinson-Gilford progeria syndrome mutation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Homozygous and compound heterozygous mutations in ZMPSTE24 cause the laminopathy restrictive dermopathy

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Zinc metalloproteinase, ZMPSTE24, is mutated in mandibuloacral dysplasia

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Compound heterozygous ZMPSTE24 mutations reduce prelamin A processing and result in a severe progeroid phenotype

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

A farnesyltransferase inhibitor improves disease phenotypes in mice with a Hutchinson-Gilford progeria syndrome mutation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Accelerated ageing in mice deficient in Zmpste24 protease is linked to p53 signalling activation.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Blocking protein farnesyltransferase improves nuclear shape in fibroblasts from humans with progeroid syndromes

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Inhibiting farnesylation of progerin prevents the characteristic nuclear blebbing of Hutchinson-Gilford progeria syndrome

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Incomplete processing of mutant lamin A in Hutchinson-Gilford progeria leads to nuclear abnormalities, which are reversed by farnesyltransferase inhibition

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Farnesyltransferase inhibitor tipifarnib is well tolerated, induces stabilization of disease, and inhibits farnesylation and oncogenic/tumor survival pathways in patients with advanced multiple myeloma

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

A protein farnesyltransferase inhibitor ameliorates disease in a mouse model of progeria.

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Antitumor activity of orally bioavailable farnesyltransferase inhibitor, ABT-100, is mediated by antiproliferative, proapoptotic, and antiangiogenic effects in xenograft models

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

The truncated prelamin A in Hutchinson-Gilford progeria syndrome alters segregation of A-type and B-type lamin homopolymers

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Novel lamin A/C gene (LMNA) mutations in atypical progeroid syndromes

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

K- and N-Ras are geranylgeranylated in cells treated with farnesyl protein transferase inhibitors

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Farnesylated lamins, progeroid syndromes and farnesyl transferase inhibitors

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

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

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Genomic instability in laminopathy-based premature aging

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Mutant nuclear lamin A leads to progressive alterations of epigenetic control in premature aging

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

Distinct structural and mechanical properties of the nuclear lamina in Hutchinson-Gilford progeria syndrome

21 January 2018

1 reference

https://api.crossref.org/works/10.1074%2FJBC.R600033200

21 January 2018

Identifiers

DOI

10.1074/JBC.R600033200

2 references

Consolidated OpenCitations Corpus – April 2017

5102476

https://www.ebi.ac.uk/europepmc/webservices/rest/search?query=EXT_ID:17090536%20AND%20SRC:MED&resulttype=core&format=json

21 December 2019

5102476

1 reference

Consolidated OpenCitations Corpus – April 2017

Consolidated OpenCitations Corpus – April 2017

2 references

5102476