Skip to search form
Skip to main content
Skip to account menu
Semantic Scholar
Semantic Scholar's Logo
Search 218,291,051 papers from all fields of science
Search
Sign In
Create Free Account
ELOVL4 gene
Known as:
ELOVL4
, CT118
, ELOVL fatty acid elongase 4
Expand
National Institutes of Health
Create Alert
Alert
Related topics
Related topics
1 relation
ELOVL2 gene
Papers overview
Semantic Scholar uses AI to extract papers important to this topic.
2017
2017
Elongation of very Long-Chain (>C24) Fatty Acids in Clarias gariepinus: Cloning, Functional Characterization and Tissue Expression of elovl4 Elongases
A. Oboh
,
J. Navarro
,
D. Tocher
,
Ó. Monroig
Lipids
2017
Corpus ID: 4016273
Elongation of very long-chain fatty acid 4 (Elovl4) proteins participate in the biosynthesis of very long-chain (>C24) saturated…
Expand
Highly Cited
2015
Highly Cited
2015
A Novel Mutation in ELOVL4 Leading to Spinocerebellar Ataxia (SCA) With the Hot Cross Bun Sign but Lacking Erythrokeratodermia: A Broadened Spectrum of SCA34.
K. Ozaki
,
H. Doi
,
+20 authors
K. Ishikawa
JAMA Neurology
2015
Corpus ID: 6416150
IMPORTANCE Although mutations in 26 causative genes have been identified in the spinocerebellar ataxias (SCAs), the causative…
Expand
Highly Cited
2013
Highly Cited
2013
Role of ELOVL4 and very long-chain polyunsaturated fatty acids in mouse models of Stargardt type 3 retinal degeneration
P. Barabas
,
Aihua Liu
,
+6 authors
D. Križaj
Proceedings of the National Academy of Sciences…
2013
Corpus ID: 32386845
Stargardt type 3 (STGD3) disease is a juvenile macular dystrophy caused by mutations in the ELOVL4 (Elongation of very long chain…
Expand
2013
2013
Deciphering mutant ELOVL4 activity in autosomal-dominant Stargardt macular dystrophy
Sreemathi Logan
,
M. Agbaga
,
+4 authors
R. Anderson
Proceedings of the National Academy of Sciences…
2013
Corpus ID: 22690116
Autosomal-dominant Stargardt-like macular dystrophy [Stargardt3 (STGD3)] results from single allelic mutations in the elongation…
Expand
2007
2007
Elovl4 haploinsufficiency does not induce early onset retinal degeneration in mice
Wenmei Li
,
Yali Chen
,
+9 authors
Kang Zhang
Vision Research
2007
Corpus ID: 17373375
Highly Cited
2005
Highly Cited
2005
Lipofuscin accumulation, abnormal electrophysiology, and photoreceptor degeneration in mutant ELOVL4 transgenic mice: a model for macular degeneration.
Goutam Karan
,
C. Lillo
,
+9 authors
Kang Zhang
Proceedings of the National Academy of Sciences…
2005
Corpus ID: 14190182
Macular degeneration is a heterogeneous group of disorders characterized by photoreceptor degeneration and atrophy of the retinal…
Expand
Highly Cited
2004
Highly Cited
2004
Characterization of mouse orthologue of ELOVL4: genomic organization and spatial and temporal expression.
M. A. Mandal
,
R. Ambasudhan
,
P. Wong
,
P. Gage
,
P. Sieving
,
R. Ayyagari
Genomics
2004
Corpus ID: 26624089
2004
2004
Expression of wild type and mutant ELOVL4 in cell culture: subcellular localization and cell viability.
Goutam Karan
,
Zhenglin Yang
,
Kang Zhang
Molecular Vision
2004
Corpus ID: 20626667
PURPOSE ELOVL4 is a member of the fatty acid elongase (ELO) family of genes. Mutations of this gene are responsible for autosomal…
Expand
2003
2003
Elovl4 mRNA distribution in the developing mouse retina and phylogenetic conservation of Elovl4 genes.
Xian-mei Zhang
,
Zhenglin Yang
,
+4 authors
Kang Zhang
Molecular Vision
2003
Corpus ID: 45421032
PURPOSE Stargardt-like macular dystrophy (STGD3) is an autosomal dominant form of early onset macular degeneration. The disease…
Expand
2002
2002
Molecular cloning of ELOVL4 gene from cynomolgus monkey (Macaca fascicularis).
S. Umeda
,
R. Ayyagari
,
+8 authors
T. Iwata
Experimental animals
2002
Corpus ID: 11152924
ELOVL4, elongation factor of very long chain fatty acids-4, is known to be responsible for autosomal dominant macular…
Expand
By clicking accept or continuing to use the site, you agree to the terms outlined in our
Privacy Policy
(opens in a new tab)
,
Terms of Service
(opens in a new tab)
, and
Dataset License
(opens in a new tab)
ACCEPT & CONTINUE