MIAT (gene)

Last updated
MIAT
Identifiers
Aliases MIAT , C22orf35, GOMAFU, LINC00066, NCRNA00066, RNCR2, lncRNA-myocardial infarction associated transcript (non-protein coding), myocardial infarction associated transcript
External IDs OMIM: 611082; GeneCards: MIAT; OMA:MIAT - orthologs
Orthologs
SpeciesHumanMouse
Entrez

440823

n/a

Ensembl

ENSG00000225783

n/a

UniProt

n
a

n/a

RefSeq (mRNA)

n/a

n/a

RefSeq (protein)

n/a

n/a

Location (UCSC) Chr 22: 26.65 – 26.68 Mb n/a
PubMed search [2] n/a
Wikidata
View/Edit Human
Location of MIAT within Chromosome 22 Location of MIAT on Chromosome 22.png
Location of MIAT within Chromosome 22

MIAT (myocardial infarction-associated transcript), also known as RNCR2 (retinal non-coding RNA 2) or Gomafu, is a long non-coding RNA. Single nucleotide polymorphisms (SNPs) in MIAT are associated with a risk of myocardial infarction. [3] It is expressed in neurons, and located in the nucleus. [4] It plays a role in the regulation of retinal cell fate specification. [5] Crea and collaborators have shown that MIAT is highly up-regulated in aggressive prostate cancer samples, [6] raising the possibility that this gene plays a role in cancer progression. [7]

Contents

Structure

The MIAT gene is located on Chromosome 22 and is 30,051 bases in length. [8] MIAT's other name, gomafu, is a word in Japanese that means “spotted pattern”. [9] The reason it is named as so is because Gomafu is distributed in the nucleoplasm in a spotted pattern. [9] Moreover, its orientation is a plus strand. [8]

It is also found that MIAT has five exons and is likely to be a functional RNA, since MIAT hasn’t been shown to encode any translational product. [8] Furthermore, the gene encodes a spliced, long non-coding RNA. [8]

The gene is found not only in humans, but also in mice and rats. [9] Orthologs are present in syntenic positions of frog and chicken. [10] It is also found that all gomafu RNA contain tandem repeats of UACUAAC that binds to SPF1, which is a splicing factor. [9]

MIAT was originally discovered as long intergenic noncoding RNAs quite enriched in specific neurons in mouse retina and later more widely expressed in the nervous system and cultured neurons, where it specifies cell identity. [9] Moreover, the gomafu RNA is also quite insoluble [9] and is enriched in PolyA +. Also, there are putative polyadenylation signals (ATTAAA) found at the 3’ end of this gene. The presence of a PolyA tail and multiple exons and introns fulfills the feature of mRNAs transcribed by RNA polymerase II. The stability of the gene is not significantly different from β-actin mRNA. [9]

Function in Pathology

Myocardial Infarction

Myocardial infarction is more commonly known as a heart attack. It is the irreversible death of the heart muscle due to prolonged obstruction of blood supply to the organ. Case-controlled large scale studies utilizing Single Nucleotide Polymorphisms(SNPs) throughout the genome demonstrated that altered expression at 6 SNPs in the MIAT gene might confer genetic susceptibility to myocardial infarctions. MIAT has been demonstrated to encode a nonfunctional RNA. Although the exact function of MIAT is still unclear, knowledge of some of the genetic factors that contribute to the pathogenesis of myocardial infarction can lend itself to better diagnosis, prevention, and treatment. Despite all that has been discovered about MIAT, a causal link between MIAT and myocardial infarctions has not yet been demonstrated. [8]

Model of the molecular mechanism of Gomafu Model of the molecular mechanism of Gomafu.png
Model of the molecular mechanism of Gomafu

Additionally, one study demonstrated that expression levels of MIAT are shown to change in peripheral blood cells of patients with acute myocardial infarction. In particular, researchers studied the association between levels of lncRNAs and inflammation markers in patients who have suffered a myocardial infarction. MIAT levels were found to be positively associated with lymphocytes and negatively associated with neutrophils and platelets. In another portion of this study, researchers looked at the association between cardiovascular risk factors and levels of lncRNAs. Smoking was a cardiovascular risk factor that was found to be positively associated with MIAT. Several researchers have reported that levels of lncRNAs are regulated in the cardiac tissue following a heart attack, but it is not known for sure whether it is the myocardial infarction that affects the levels of lncRNAs in peripheral blood cells. [6] MIAT has various genotypes of SNPs and it is possible that only one of them relates to heart disease. [11]

Schizophrenia

The long non-coding RNA(lncRNA) MIAT is located in the same chromosomal region which is linked to Schizophrenia (SZ) 22Q12.1. [12]

MIAT is upregulated in the nucleus accumbens of cocaine and heroin users. [13] [14] The nucleus accumbens is a region involved in behavior and addiction, [15] suggesting that dysregulation of MIAT can influence behavior.

It is well accepted that alternative splicing has a role in SZ pathology. [16] MIAT is associated with alternative splicing through its interaction with splicing factor 1(SF1) [10] and with genes DISC1 and ERBB4. [17] MIAT binds directly to the splicing regulator quaking homolog (QKI) and serine/arginine-rich splicing factor 1 (SRSF1). [18] QKI gene expression is decreased in specific brain regions in SZ [19] [20] and it has been proposed to be involved in SZ. [21] [22]

Post -mortem SZ brains have upregulated expression of both DISC1 and ERBB4. [18] Overexpression of MIAT in human-induced pluripotent stem cell (HiPSC)-derived neurons shows a significant decrease in expression of both DISC1 and ERBB4 and their alternative spliced variants. [18] This is opposite to the upregulated expression seen in SZ patient brains. [18] ASO mediated knockdown of MIAT in (HiPSC)-derived neurons increase the expression of both DISC1 and ERBB4 splice variants, but not their unspliced transcripts. [18] This is almost exactly matching the aberrant splicing pattern seen in post-mortem SZ patient’s brains. [18] These results suggests that loss of function mutations or decreased expression of MIAT is involved in driving aberrant cortical splicing patterns observed in SZ post-mortem brains. [18]

Other Pathologies

MIAT up-regulation and down-regulation has been linked to various types of cancer and other pathologies.

In a study of glioblastoma multiforme, increased expression of MIAT was linked to increased survival rates. [23] In addition, the glioma cells were found to how significantly down-regulated MIAT. [23] The role of MIAT in lymphocytic leukemia is very different from that of glioblastoma. In certain aggressive cell lines of chronic lymphocytic leukemias, MIAT is upregulated and depends on the presence of a transcriptional regulator, OCT4. [24] OCT4 serves a positive regulator of MIAT transcription and as of now is the only known regulator. However, analysis of relative concentrations of MIAT and OCT4 have indicated that other regulatory factors are in play. [24]

Beyond its role in cancer, MIAT misexpression has also been linked to neurovascular dysfunction. [25]

Related Research Articles

An intron is any nucleotide sequence within a gene that is not expressed or operative in the final RNA product. The word intron is derived from the term intragenic region, i.e., a region inside a gene. The term intron refers to both the DNA sequence within a gene and the corresponding RNA sequence in RNA transcripts. The non-intron sequences that become joined by this RNA processing to form the mature RNA are called exons.

<span class="mw-page-title-main">Non-coding RNA</span> Class of ribonucleic acid that is not translated into proteins

A non-coding RNA (ncRNA) is a functional RNA molecule that is not translated into a protein. The DNA sequence from which a functional non-coding RNA is transcribed is often called an RNA gene. Abundant and functionally important types of non-coding RNAs include transfer RNAs (tRNAs) and ribosomal RNAs (rRNAs), as well as small RNAs such as microRNAs, siRNAs, piRNAs, snoRNAs, snRNAs, exRNAs, scaRNAs and the long ncRNAs such as Xist and HOTAIR.

<span class="mw-page-title-main">Regulation of gene expression</span> Modifying mechanisms used by cells to increase or decrease the production of specific gene products

Regulation of gene expression, or gene regulation, includes a wide range of mechanisms that are used by cells to increase or decrease the production of specific gene products. Sophisticated programs of gene expression are widely observed in biology, for example to trigger developmental pathways, respond to environmental stimuli, or adapt to new food sources. Virtually any step of gene expression can be modulated, from transcriptional initiation, to RNA processing, and to the post-translational modification of a protein. Often, one gene regulator controls another, and so on, in a gene regulatory network.

<span class="mw-page-title-main">DISC1</span> Protein-coding gene in the species Homo sapiens

Disrupted in schizophrenia 1 is a protein that in humans is encoded by the DISC1 gene. In coordination with a wide array of interacting partners, DISC1 has been shown to participate in the regulation of cell proliferation, differentiation, migration, neuronal axon and dendrite outgrowth, mitochondrial transport, fission and/or fusion, and cell-to-cell adhesion. Several studies have shown that unregulated expression or altered protein structure of DISC1 may predispose individuals to the development of schizophrenia, clinical depression, bipolar disorder, and other psychiatric conditions. The cellular functions that are disrupted by permutations in DISC1, which lead to the development of these disorders, have yet to be clearly defined and are the subject of current ongoing research. Although, recent genetic studies of large schizophrenia cohorts have failed to implicate DISC1 as a risk gene at the gene level, the DISC1 interactome gene set was associated with schizophrenia, showing evidence from genome-wide association studies of the role of DISC1 and interacting partners in schizophrenia susceptibility.

<span class="mw-page-title-main">ERBB4</span> Protein-coding gene in the species Homo sapiens

Receptor tyrosine-protein kinase erbB-4 is an enzyme that in humans is encoded by the ERBB4 gene. Alternatively spliced variants that encode different protein isoforms have been described; however, not all variants have been fully characterized.

<span class="mw-page-title-main">QKI</span> Protein

Quaking homolog, KH domain RNA binding (mouse), also known as QKI, is a protein which in humans is encoded by the QKI gene.

<span class="mw-page-title-main">Long non-coding RNA</span> Non-protein coding transcripts longer than 200 nucleotides

Long non-coding RNAs are a type of RNA, generally defined as transcripts more than 200 nucleotides that are not translated into protein. This arbitrary limit distinguishes long ncRNAs from small non-coding RNAs, such as microRNAs (miRNAs), small interfering RNAs (siRNAs), Piwi-interacting RNAs (piRNAs), small nucleolar RNAs (snoRNAs), and other short RNAs. Given that some lncRNAs have been reported to have the potential to encode small proteins or micro-peptides, the latest definition of lncRNA is a class of RNA molecules of over 200 nucleotides that have no or limited coding capacity. Long intervening/intergenic noncoding RNAs (lincRNAs) are sequences of lncRNA which do not overlap protein-coding genes.

<span class="mw-page-title-main">MEG3</span>

MEG3 is a maternally expressed, imprinted long non-coding RNA gene. At least 12 different isoforms of MEG3 are generated by alternative splicing. Expression of MEG3 is lost in cancer cells. It acts as a growth suppressor in tumour cells, and activates p53. A pituitary transcript variant has been associated with inhibited cell proliferation. Studies in mouse and sheep suggest that an upstream intergenic differentially methylated region (IG-DMR) regulates imprinting of the region. The expression profile in mouse of the co-regulated Meg3 and Dlk1 genes suggests a causative role in the pathologies found in uniparental disomy animals, characterized by defects in skeletal muscle maturation, bone formation, placenta size and organization and prenatal lethality. The sheep homolog is associated with the callipyge mutation which in heterozygous individuals affects a muscle-specific long-range control element located in the DLK1-GTL2 intergenic region and results in the callipyge muscular hypertrophy. The non-Mendelian inheritance pattern, known as polar overdominance, likely results from the combination of the cis-effect on the expression levels of genes in the DLK1-GTL2 imprinted domain, and trans interaction between the products of reciprocally imprinted genes. MEG3 is thought to play a role in the development of Alzheimer's disease by triggering necroptosis.

<span class="mw-page-title-main">Neuregulin 3</span> Protein-coding gene in Homo sapiens

Neuregulin 3, also known as NRG3, is a neural-enriched member of the neuregulin protein family which in humans is encoded by the NRG3 gene. The NRGs are a group of signaling proteins part of the superfamily of epidermal growth factor, EGF like polypeptide growth factor. These groups of proteins possess an 'EGF-like domain' that consists of six cysteine residues and three disulfide bridges predicted by the consensus sequence of the cysteine residues.

<span class="mw-page-title-main">HOTAIR</span> Gene found in humans

HOTAIR is a human gene located between HOXC11 and HOXC12 on chromosome 12. It is the first example of an RNA expressed on one chromosome that has been found to influence the transcription of the HOXD cluster posterior genes located on chromosome 2. The sequence and function of HOTAIR are different in humans and mice. Sequence analysis of HOTAIR revealed that it exists in mammals, has poorly conserved sequences and considerably conserved structures, and has evolved faster than nearby HoxC genes. A subsequent study identified HOTAIR has 32 nucleotides long conserved noncoding element (CNE) that has a paralogous copy in HOXD cluster region, suggesting that the HOTAIR conserved sequences predate whole genome duplication events at the root of vertebrate. While the conserved sequence paralogous with HOXD cluster is 32 nucleotide long, the HOTAIR sequence conserved from human to fish is about 200 nucleotide long and is marked by active enhancer features.

<span class="mw-page-title-main">GAS5</span> Non-coding RNA in the species Homo sapiens

Growth arrest-specific 5 is a non-protein coding RNA that in humans is encoded by the GAS5 gene.

<span class="mw-page-title-main">MALAT1</span>

MALAT 1 also known as NEAT2 is a large, infrequently spliced non-coding RNA, which is highly conserved amongst mammals and highly expressed in the nucleus. It regulates the expression of metastasis-associated genes. It also positively regulates cell motility via the transcriptional and/or post-transcriptional regulation of motility-related genes. MALAT1 may play a role in temperature-dependent sex determination in the Red-eared slider turtle.

<span class="mw-page-title-main">CDKN2BAS</span> Non-coding RNA in the species Homo sapiens

CDKN2B-AS, also known as ANRIL is a long non-coding RNA consisting of 19 exons, spanning 126.3kb in the genome, and its spliced product is a 3834bp RNA. It is located within the p15/CDKN2B-p16/CDKN2A-p14/ARF gene cluster, in the antisense direction. Single nucleotide polymorphisms (SNPs) which alter the expression of CDKN2B-AS are associated with human healthy life expectancy, as well as with multiple diseases, including coronary artery disease, diabetes and many cancers. It binds to chromobox 7 (CBX7) within the polycomb repressive complex 1 and to SUZ12, a component of polycomb repression complex 2 and through these interactions is involved in transcriptional repression.

In molecular biology, disrupted in schizophrenia 2 , also known as DISC2, is a long non-coding RNA molecule. In humans, the DISC2 gene that produces the DISC2 RNA molecule is located on chromosome 1, at the breakpoint associated with the chromosomal translocation found in Schizophrenia. It is antisense to the DISC1 gene and may regulate the expression of DISC1. DISC2 may also contribute to other psychiatric disorders.

<span class="mw-page-title-main">HOXA11-AS1</span> Long non-coding RNA from the antisense strand in the homeobox A (HOXA gene).

HOXA11-AS lncRNA is a long non-coding RNA from the antisense strand in the homeobox A. The HOX gene contains four clusters. The sense strand of the HOXA gene codes for proteins. Alternative names for HOXA11-AS lncRNA are: HOXA-AS5, HOXA11S, HOXA11-AS1, HOXA11AS, or NCRNA00076. This gene is 3,885 nucleotides long and resides at chromosome 7 (7p15.2) and is transcribed from an independent gene promoter. Being a lncRNA, it is longer than 200 nucleotides in length, in contrast to regular non-coding RNAs.

Epigenetics of human development is the study of how epigenetics effects human development.

<span class="mw-page-title-main">Zinc transporter ZIP12</span> Protein found in humans

Solute carrier family 39 member 12 is a protein that in humans is encoded by the SLC39A12 gene.

<span class="mw-page-title-main">BC200 lncRNA</span>

Brain cytoplasmic 200 long-noncoding RNA is a 200 nucleotide RNA transcript found predominantly in the brain with a primary function of regulating translation by inhibiting its initiation. As a long non-coding RNA, it belongs to a family of RNA transcripts that are not translated into protein (ncRNAs). Of these ncRNAs, lncRNAs are transcripts of 200 nucleotides or longer and are almost three times more prevalent than protein-coding genes. Nevertheless, only a few of the almost 60,000 lncRNAs have been characterized, and little is known about their diverse functions. BC200 is one lncRNA that has given insight into their specific role in translation regulation, and implications in various forms of cancer as well as Alzheimer's disease.

Small nucleolar RNA host gene 1 is a non-protein coding RNA that in humans is encoded by the SNHG1 gene.

ncRNA therapy

A majority of the human genome is made up of non-protein coding DNA. It infers that such sequences are not commonly employed to encode for a protein. However, even though these regions do not code for protein, they have other functions and carry necessary regulatory information.They can be classified based on the size of the ncRNA. Small noncoding RNA is usually categorized as being under 200 bp in length, whereas long noncoding RNA is greater than 200bp. In addition, they can be categorized by their function within the cell; Infrastructural and Regulatory ncRNAs. Infrastructural ncRNAs seem to have a housekeeping role in translation and splicing and include species such as rRNA, tRNA, snRNA.Regulatory ncRNAs are involved in the modification of other RNAs.

References

  1. 1 2 3 GRCh38: Ensembl release 89: ENSG00000225783 – Ensembl, May 2017
  2. ↑ "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
  3. ↑ Ishii N, Ozaki K, Sato H, Mizuno H, Saito S, Takahashi A, Miyamoto Y, Ikegawa S, Kamatani N, Hori M, Saito S, Nakamura Y, Tanaka T (2006). "Identification of a novel non-coding RNA, MIAT, that confers risk of myocardial infarction". Journal of Human Genetics. 51 (12): 1087–1099. doi: 10.1007/s10038-006-0070-9 . PMID   17066261.
  4. ↑ Sone M, Hayashi T, Tarui H, Agata K, Takeichi M, Nakagawa S (August 2007). "The mRNA-like noncoding RNA Gomafu constitutes a novel nuclear domain in a subset of neurons". Journal of Cell Science. 120 (Pt 15): 2498–2506. doi:10.1242/jcs.009357. PMID   17623775. S2CID   11790043.
  5. ↑ Rapicavoli NA, Poth EM, Blackshaw S (May 2010). "The long noncoding RNA RNCR2 directs mouse retinal cell specification". BMC Developmental Biology. 10: 49. doi: 10.1186/1471-213X-10-49 . PMC   2876091 . PMID   20459797.
  6. 1 2 Vausort M, Wagner DR, Devaux Y (September 2014). "Long noncoding RNAs in patients with acute myocardial infarction". Circulation Research. 115 (7): 668–677. doi:10.1161/CIRCRESAHA.115.303836. PMID   25035150. S2CID   26576988.
  7. ↑ Crea F, Venalainen E, Ci X, Cheng H, Pikor L, Parolia A, Xue H, Nur Saidy NR, Lin D, Lam W, Collins C, Wang Y (2016). "The role of epigenetics and long noncoding RNA MIAT in neuroendocrine prostate cancer" (PDF). Epigenomics. 8 (5): 721–731. doi:10.2217/epi.16.6. PMID   27096814.
  8. 1 2 3 4 5 Ishii N, Ozaki K, Sato H, Mizuno H, Saito S, Takahashi A, Miyamoto Y, Ikegawa S, Kamatani N, Hori M, Saito S, Nakamura Y, Tanaka T (2006-10-26). "Identification of a novel non-coding RNA, MIAT, that confers risk of myocardial infarction". Journal of Human Genetics. 51 (12): 1087–1099. doi: 10.1007/s10038-006-0070-9 . PMID   17066261.
  9. 1 2 3 4 5 6 7 Sone M, Hayashi T, Tarui H, Agata K, Takeichi M, Nakagawa S (August 2007). "The mRNA-like noncoding RNA Gomafu constitutes a novel nuclear domain in a subset of neurons". Journal of Cell Science. 120 (Pt 15): 2498–2506. doi:10.1242/jcs.009357. PMID   17623775. S2CID   11790043.
  10. 1 2 Tsuiji H, Yoshimoto R, Hasegawa Y, Furuno M, Yoshida M, Nakagawa S (May 2011). "Competition between a noncoding exon and introns: Gomafu contains tandem UACUAAC repeats and associates with splicing factor-1". Genes to Cells. 16 (5): 479–490. doi:10.1111/j.1365-2443.2011.01502.x. PMC   3116199 . PMID   21463453.
  11. ↑ Tsunoda T, Lathrop GM, Sekine A, Yamada R, Takahashi A, Ohnishi Y, Tanaka T, Nakamura Y (August 2004). "Variation of gene-based SNPs and linkage disequilibrium patterns in the human genome". Human Molecular Genetics. 13 (15): 1623–1632. doi: 10.1093/hmg/ddh177 . PMID   15190013.
  12. ↑ Takahashi S, Ohtsuki T, Yu SY, Tanabe EI, Yara K, Kamioka M, Matsushima E, Matsuura M, Ishikawa K, Minowa Y, Noguchi E, Nakayama J, Yamakawa-Kobayashi K, Arinami T, Kojima T (2003). "Significant linkage to chromosome 22q for exploratory eye movement dysfunction in schizophrenia". American Journal of Medical Genetics. 123B (1): 27–32. doi:10.1002/ajmg.b.10046. PMID   14582142. S2CID   20876993.
  13. ↑ Albertson DN, Schmidt CJ, Kapatos G, Bannon MJ (October 2006). "Distinctive profiles of gene expression in the human nucleus accumbens associated with cocaine and heroin abuse". Neuropsychopharmacology. 31 (10): 2304–2312. doi:10.1038/sj.npp.1301089. PMC   2239258 . PMID   16710320.
  14. ↑ Michelhaugh SK, Lipovich L, Blythe J, Jia H, Kapatos G, Bannon MJ (February 2011). "Mining Affymetrix microarray data for long non-coding RNAs: altered expression in the nucleus accumbens of heroin abusers". Journal of Neurochemistry. 116 (3): 459–466. doi:10.1111/j.1471-4159.2010.07126.x. PMC   3061462 . PMID   21128942.
  15. ↑ Di Chiara G, Bassareo V, Fenu S, De Luca MA, Spina L, Cadoni C, Acquas E, Carboni E, Valentini V, Lecca D (2004-01-01). "Dopamine and drug addiction: the nucleus accumbens shell connection". Neuropharmacology. Frontiers in Addiction Research: Celebrating the 30th Anniversary of the National Institute on Drug Abuse. 47 (Suppl 1): 227–241. doi:10.1016/j.neuropharm.2004.06.032. PMID   15464140. S2CID   25983940.
  16. ↑ Morikawa T, Manabe T (December 2010). "Aberrant regulation of alternative pre-mRNA splicing in schizophrenia". Neurochemistry International. 57 (7): 691–704. doi:10.1016/j.neuint.2010.08.012. PMID   20813145. S2CID   7113952.
  17. ↑ Law AJ, Kleinman JE, Weinberger DR, Weickert CS (January 2007). "Disease-associated intronic variants in the ErbB4 gene are related to altered ErbB4 splice-variant expression in the brain in schizophrenia". Human Molecular Genetics. 16 (2): 129–141. doi: 10.1093/hmg/ddl449 . PMID   17164265.
  18. 1 2 3 4 5 6 7 Barry G, Briggs JA, Vanichkina DP, Poth EM, Beveridge NJ, Ratnu VS, Nayler SP, Nones K, Hu J, Bredy TW, Nakagawa S, Rigo F, Taft RJ, Cairns MJ, Blackshaw S, Wolvetang EJ, Mattick JS (April 2014). "The long non-coding RNA Gomafu is acutely regulated in response to neuronal activation and involved in schizophrenia-associated alternative splicing". Molecular Psychiatry. 19 (4): 486–494. doi: 10.1038/mp.2013.45 . PMID   23628989.
  19. ↑ Haroutunian V, Katsel P, Dracheva S, Davis KL (October 2006). "The human homolog of the QKI gene affected in the severe dysmyelination "quaking" mouse phenotype: downregulated in multiple brain regions in schizophrenia". The American Journal of Psychiatry. 163 (10): 1834–1837. doi:10.1176/ajp.2006.163.10.1834. PMID   17012699.
  20. ↑ McCullumsmith RE, Gupta D, Beneyto M, Kreger E, Haroutunian V, Davis KL, Meador-Woodruff JH (February 2007). "Expression of transcripts for myelination-related genes in the anterior cingulate cortex in schizophrenia". Schizophrenia Research. 90 (1–3): 15–27. doi:10.1016/j.schres.2006.11.017. PMC   1880890 . PMID   17223013.
  21. ↑ Aberg K, Saetre P, Jareborg N, Jazin E (May 2006). "Human QKI, a potential regulator of mRNA expression of human oligodendrocyte-related genes involved in schizophrenia". Proceedings of the National Academy of Sciences of the United States of America. 103 (19): 7482–7487. Bibcode:2006PNAS..103.7482A. doi: 10.1073/pnas.0601213103 . PMC   1464365 . PMID   16641098.
  22. ↑ Aberg K, Saetre P, Lindholm E, Ekholm B, Pettersson U, Adolfsson R, Jazin E (January 2006). "Human QKI, a new candidate gene for schizophrenia involved in myelination". American Journal of Medical Genetics. Part B, Neuropsychiatric Genetics. 141B (1): 84–90. doi:10.1002/ajmg.b.30243. PMID   16342280. S2CID   11733591.
  23. 1 2 Zhang XQ, Sun S, Lam KF, Kiang KM, Pu JK, Ho AS, Lui WM, Fung CF, Wong TS, Leung GK (October 2013). "A long non-coding RNA signature in glioblastoma multiforme predicts survival". Neurobiology of Disease. 58: 123–131. doi:10.1016/j.nbd.2013.05.011. PMID   23726844. S2CID   23522086.
  24. 1 2 Sattari A, Siddiqui H, Moshiri F, Ngankeu A, Nakamura T, Kipps TJ, Croce CM (August 2016). "Upregulation of long noncoding RNA MIAT in aggressive form of chronic lymphocytic leukemias". Oncotarget. 7 (34): 54174–54182. doi:10.18632/oncotarget.11099. PMC   5338916 . PMID   27527866.
  25. ↑ Jiang Q, Shan K, Qun-Wang X, Zhou RM, Yang H, Liu C, Li YJ, Yao J, Li XM, Shen Y, Cheng H, Yuan J, Zhang YY, Yan B (July 2016). "Long non-coding RNA-MIAT promotes neurovascular remodeling in the eye and brain". Oncotarget. 7 (31): 49688–49698. doi:10.18632/oncotarget.10434. PMC   5226539 . PMID   27391072.
This page is based on this Wikipedia article
Text is available under the CC BY-SA 4.0 license; additional terms may apply.
Images, videos and audio are available under their respective licenses.