Difference between revisions of "CHAER1"

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==Annotated Information==
 
==Annotated Information==
 
===Name===
 
===Name===
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''CHAER1'': Cardiac hypertrophy associated epigenetic regulator 1 (HGNC nomenclature), Chaer <ref name="ref1" />.
+
Approved symbol：CHAER1
 +
 
 +
Approved name：cardiac hypertrophy associated epigenetic regulator 1
 +
 
 +
HGNC ID：HGNC:53620
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 +
Alias symbols：Chaer
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RefSeq ID：XR_001741701
  
 
===Characteristics===
 
===Characteristics===

Revision as of 01:43, 26 November 2020

CHAER1, is a long non-coding RNA and act as a critical regulator of cardiac hypertrophy via direct interaction with PRC2.

Annotated Information

Name

Approved symbol：CHAER1

Approved name：cardiac hypertrophy associated epigenetic regulator 1

HGNC ID：HGNC:53620

Alias symbols：Chaer

RefSeq ID：XR_001741701

Characteristics

CHAER1 is 1596 bp long non-coding RNA, located on human chromosome 4q12. CHAER1 transcript contains a bi-tetra-loop motif within the 5′ end that is both sufficient and necessary for PRC2 binding [1].

Function

CHAER1 regulates cardiac hypertrophy. (a) RNA reads of mouse CHAER1 and genomic structure. Three reading frames are shown with stop codon labeled by black lines and the longest open reading frames labeled in red. (b) Northern blot analysis for CHAER1 in adult mouse tissues. Gapdh, Glyceraldehyde 3-phosphate dehydrogenase; SKM, skeletal muscle. (c) In vitro translation assay for Chaer, HOX transcript antisense RNA (Hotair) and GFP. (d) Schematic of Chaer knockout in mouse genome using CRISPR-cas9 system showing two guide RNA sequences used. (e) Wild-type (WT) and CHAER1 knockout (KO) alleles detected by genomic DNA PCR. (f) Effect of Chaer KO on heart weight and myofilament cross-section areas 4 weeks after trans-aortic constriction (TAC) surgery, Data were mean ± s.e.m. Sample numbers were labeled on bars. ***P < 0.001 versus WT; ###P < 0.001 versus sham (Students' t test). (g) Atrial natriuretic factor (Anf; left) and β-myosin heavy chain (Myh7; right) expression. Data were mean ± s.e.m. n = 3. *P < 0.05, ***P < 0.001 versus WT; ##P < 0.01, ###P < 0.001 versus sham (Students' t test). (h) Hematoxylin and Eosin (H&E) staining and Picro Sirius Red (PSR) staining. (i,j) Left ventricular (LV) collagen volume (i) and fractional shortening (j). Data were mean ± s.e.m. Sample numbers were labeled on bars. *P < 0.05, **P < 0.01, ***P < 0.001 versus WT; ##P < 0.01, ###P < 0.001 versus sham (Students' t test).[1]

CHAER1 contributes to the timing and specificity of cardiac epigenetic reprogramming during hypertrophy by coordinating temporal and spatial specific histone methylation and de-methylation [1].

CHAER1 directly interacts with Polycomb Repressor Complex 2 (PRC2) catalytic subunit through a 66-mer motif, interferes with its targeting to genomic locus, and subsequently inhibits histone H3 lysine 27 methylation at hypertrophic genes. This interaction is transiently induced upon hormone or stress stimulation in an mTORC1 dependent manner, and is prerequisite for epigenetic reprogramming and induction of hypertrophic genes. Inhibition of CHAER1 in intact heart before, but not after, the onset of pressure overload significantly attenuates cardiac hypertrophy and dysfunction [1].

Expression

Increase of CHAER1 expression is observed in dilated cardiomyopathy hearts compared with normal controls [1].

Regulation

Please input information here.

Diseases

  • Cardiac hypertrophy [1]

Labs working on this lncRNA

  • Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.[1]
  • Animal Experiment Center–Animal Biosafety Level 3 Laboratory, Wuhan University, Wuhan, China.[1]
  • Medical Research Institute, School of Medicine, Wuhan University, Wuhan, China.[1]
  • Division of Molecular Medicine, Department of Anesthesiology, David Geffen School of Medicine, University of California at Los Angeles (UCLA), Los Angeles, California, USA.[1]
  • Department of Cardiology, Tianjin Institute of Cardiology, Second Hospital of Tianjin Medical University, Tianjin, China.[1]
  • Gladstone Institute of Cardiovascular Diseases, San Francisco, California, USA.[1]
  • University of California San Francisco, School of Medicine, San Francisco, California, USA.[1]
  • Department of Medicine, Cardiology Division, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA.[1]
  • Cardiovascular Research Laboratories, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA.[1]
  • Department of Integrative Biology and Physiology, College of Life Sciences, Molecular Biology Institute, David Geffen School of Medicine, University of California at Los Angeles, Los Angeles, California, USA.[1]
  • Bioinformatics Interdepartmental Program, University of California at Los Angeles, Los Angeles, California, USA.[1]
  • Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.[1]
  • Laboratory of Molecular Cardiology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China.[1]
  • Shanghai Jiao Tong University School of Medicine, Shanghai, China.[1]

References

  1. ↑ 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 1.17 1.18 1.19 Wang Z, Zhang X-J, Ji Y-X, Zhang P, Deng K-Q, Gong J et al. The long noncoding RNA Chaer defines an epigenetic checkpoint in cardiac hypertrophy[J]. Nature medicine. 2016, 22(10):1131-1139.

Sequence

>gi|105377667|ref|XR_001741701.1| Homo sapiens , Cardiac hypertrophy associated epigenetic regulator 1 (CHAER1), long non-coding RNA

000001 TGTTGTTATT GTTGTTTAAA TCTTCCTGGA AGGCAGAAAG AAAGAGATAA AAAGGAAAAA ACAGCATTTG TCACTTATAG 000080
000081 TGCTCTGGTT AGCACAGTAG CTGGGCCCCT GAACCCTCTA CAGGCCTCCC AAGCTGGCAC TGAATAAAAT GTGAGAAATG 000160
000161 AAAGGAACTT TTCCGTGAGT CTGGCAGCGC CGACAGACAC TGAGGTGGCA GAGCTGTCTG GTCCCAGTCC ACATGCAGAG 000240
000241 GCCTGCAGCT CCTCCTTCCA GCCCGCACCC ACCAGAGCTT CTCAGACGGG CCGTGTCCTG AGAAGGTTGT TGCCAATGTA 000320
000321 GATGTTTGAG AGGCTCACTG ATGAACAAAT CAACAGAGCA GATTTAATCT GAAGAGATCC AAATATTGTG CTTCTTTGGA 000400
000401 CTCATAGAAA TGGCGAAAGA TTTAACATCA GGAAGTACTT AAGTCAGCTA ATTTCTAGAG CCTTCTTCCT CCCTGTCACT 000480
000481 TGATTCTAGA TAGGATCACC AGTTAGACAT CAGAACCAGA TCTTTTTATC CAGAGAAGTA CCAGTTTGTT GTTTTTCCTT 000560
000561 CCGAAGCCAA GTCCTCGAGT TTCAGGAAAG CAAAAAGCCC CGAAGAGCCT GGCTTGGAAT AAAAACATGC ACCATACAAG 000640
000641 ATTTTTATGA AGATTAAATA ACTTGGGCTA AAATATTCTG GAAGCTGCCA AGGGCTCTAC AGATGAGCTA TACAGAGGCA 000720
000721 TTTGCTGAAA ACTGGCCTGG ATTGACAAGC GCAATGCAAA CGTGGCTGCG GCAGTTCCAG GCATCACATG GTAACAAGAT 000800
000801 CACATCCAGT GAAGAAGGAA TTCTCATAAG ACAGTCAGCA GATTTTGCAG GTTTTCAACT GATTGGATGA GGTTCACCTA 000880
000881 CATTATGGAG GACAGTCTGC TTTACTCAAA GTCCATCAAT GTAAATTCCT GCAAGGTGGA TATCACTCTC ACCTTCAGCG 000960
000961 CACAAAGAAA GGAGGTATAC AGAAGACACA GAACTCACCA AAGTCACAGG AACTAGGTGA GGATGAACCA GGCTGCATCC 001040
001041 AAGCAGCCCA GCTTCAGGGT CTGTATTCTT TGCCACTACC CAGAACTTTT ACCAATAAGC AAAGCTATTG TTTGCAATAA 001120
001121 CAGGAAGCAA AAATAGCAAA AAGTTCCCTT TAAGGGGGAG TGTTATAATA TACTTAACAA TCAGAATGGC TGAAGCACTG 001200
001201 ATCTGTGAGA GTGGCTACTG GTCATAGCCT GGAGCTGGTC TTTTAGGTCC TCTTTGGTTA CTGGATCCTG GGAGGATGGA 001280
001281 TGAGGAAGTG GTCTCAGGCA AGGGGTGGAG TTAAGTGGCT GTGGAAGGTA CTTTGGAGGC TCAGGCAGCA GCTTTTTTTC 001360
001361 CCCTTAAACT TTTGTTTTAA GTTCTAGGGT ACACGTGCAG GATGTGCAGT TTACATAGGT AAACGTGTGC CGTGGTGGTT 001440
001441 TGCTGTACAG AACAAACCAT CACTCAGGTA TTATTAAGCC CAGCACCCAT TAGCTATTCT TTCTGATGCT TTCCCTCTCC 001520
001521 CAACTTCCAC CCGACAGGCC CCAGTGTGTG TTGTTCCCCT CCCTCTGTTC TCATTGTTCA GCTCCCACTT ATAAGT
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