Sudden Infant Death Syndrome (SIDS) Susceptibility Pathways (Homo sapiens)

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71606474113125353178480927541, 80, 94673318114584925, 10643, 6311215501043878698512344119851233812378386259631235910, 91, 118278100785093212147488648212123, 86485242, 12123, 86117488648794821864848484852101SIDS Susceptibility PathwaysIncreased brainstem hypoplasia with SIDSTRrCardiac myocytep+Cell MembraneIncreased long-QT with SIDSPutative TRPutative TRsPutative TRK+G2989TBradycardiaPutative TRsSarcoplasmic ReticulumTRrSleepGs signalingThermoregulation2OtherPutative TRsHeartDecreased relative SIDS expressionPutative TRsCaSerotoninTransporterMiscelaneous SIDS Associated2+Focal AdhesionsPutative TRscircadian4R/4RPutative TRHOSIDS associated polymorphismsPutative TRNucleusBrainBrainstem neurondepressionPutative TRrs2856966Increased relative SIDS expressionSerotonin SignalingNucleusSPhPutative TRSPhAssociated with Energy Metabolism and SIDSK+C825TNHGq signalingG5477ASoma MembraneSerotonin Synthesis and MetabolismPutative TRsAssociated with Infection and SIDSrs6295 (-1019) BrownAdiposeNa+Putative TRsSPhHNPutative TRRapidly-activating K+ CurrentTR: Transcriptional RegulationSph: SIDS Phenotype Animal ModelNerve TerminalIVS-191_190insAStabilizationSPhGi signalingG-proteinVagal ToneInfant (<1 year in age) Slowly-Activating K+ Current11611865110118392961959512277LMX1BVIPR2CC2D1AEP300POU3F2NFKB1ESR2ADCYAP1ARSP1GATA3ASCL1THRB5-HIAASP1MIR13ACREB1PPARGC1APHOX2ASP1CHRNB4AVPL-TryptophanDEAF1CREBBP5-HTNEUROD1TPH2IL6CHRNA4MAOAC4APLP1EN1GATA2YBX1FluoxetinePKNOX1TPH1MEF2CFOXM1Glial Cell DifferentiationHTR1AIL6RTNF5-HTVIPR1NKX3-1IL8POU3F2ADCYAP1R1ALDOACREB1RESTRETHSPD1KCNH2ACADMECE1CTCFRUNX3DDCRESTTCF3RESTADCYAP1DDCCREB1RESTHES1PPARGC1BHADHATP73FEVRESTIL10HTR1AHIF1ATACR1TPH2NFKB1HES5TPH1NGF5-HTRYR2CDCA7LSSTR1JUNEGR1SSTR2RYR2CAV3HTR2AMAOAMIR16-1SLC6A4SP1NR3C1KCNQ1NicotineNR3C1HES1TLX3KCNQ1BHLHE40GNB3SP3C4BPHOX2BFEV5-HTPKCNH2 SP1DLX2HIF1ASCN5ACAV3PBX1NKX2-2MAZMIR210RORANFYA997080193110812390671411543105427842045738851895611, 6292102688112481876310376Putative TRsCTNNB1SOX2NANOGPOU5F176MAPK pathway86BDNFNTRK2Gi signalingGABA107GABRA155CHRM2GJA113SNTA1Na+H+28K+KCNJ8GJA1PKC inhibitor 14-3-3Protein Kinase APRKAR2BYWHAEYWHAZPRKAR1BPRKAR2AYWHAQYWHAGPRKAR1AYWHAHYWHABPRKACBPRKACAActivationGAP Junction120SLC9A3CASP3FMO3G6PC32GCK40GPD1L16GRIN1HADHB34HTR3ASCN3BSCN4BSSTNa+Cardiac VagalExcitationChronicHypoxia965-HTGlutamateCa2+72H20H20AQP4ApoptosisCPT1AIL1A22IL1B75IL1RN7557IL1336TSPYL1VEGFA66SCN5A9882DopaminePhenylalanineCHATL-DOPAPAHAcetylcholineCholineTHTyrosineDDCNOS1AP111Gq signalingMAP2TAC153MicrotubleStabilizationSLC1A3SLC25A4GlutamateSNAP25Synaptic Vesicle ReleaseGlutamateSST53TAC153HTR3A64TH60CHAT4779SLC9A3BDNF86NTRK2AQP472125GRIN1SP18NFKB2JUNHDAC997MYB24CEBPB113SNTA113GPD1LSP1JUNNR3C1REST9JUN26CREB1POU2F2CREM83RESTNFKB1CHRNB2CHRNA7Serotinergic NeuronsHDAC1MBD1MECP2NFKB1CREBBPTRrTRrGABRA1107CREB130VAMP2Extracellular SpacePutative TRsPutative TRsPutative TRsPutative TRsPutative TRsPutative TRsPutative TRsPutative TRsPutative TRsTPPPATP1A3GAPDHHSP90B1TFSPTBN1YWHAGHIF1APutative TRs


Description

In this model, we provide an integrated view of Sudden Infant Death Syndrome (SIDS) at the level of implicated tissues, signaling networks and genetics. The purpose of this model is to serve as an overview of research in this field and recommend new candidates for more focused or genome wide analyses. SIDS is the sudden and unexpected death of an infant (less than 1 year of age), almost always during deep sleep, where no cause of death can be found by autopsy. Factors that mediate SIDS are likely to be both biological and behavioral, such as sleeping position, environment and stress during a critical phase of infant development (http://www.nichd.nih.gov/health/topics/Sudden_Infant_Death_Syndrome.cfm). While no clear diagnostic markers currently exist, several polymorphisms have been identified which are significantly over-represented in distinct SIDS ethnic population. The large majority of these polymorphisms exist in genes associated with neuronal signaling, cardiac contraction and inflammatory response. These and other lines of evidence suggest that SIDS has a strong autonomic nervous system component (PMID:12350301, PMID: 20124538). One of the neuronal nuclei most strongly implicated in SIDS has been the raphe nucleus of the brain stem. In this nuclei there are ultrastructural, cellular and molecular changes associated with SIDS relative to controls (PMID:19342987, PMID: 20124538). This region of the brain is responsible for the large majority of neuronal serotonin produced and is functionally important in the regulation of normal cardiopulmonary activity, sleep and thermoregulation (see associated references).

Genes associated with serotonin synthesis and receptivity have some of the strongest genetic association with SIDS. Principle among these genes the serotonin biosynthetic enzyme TPH2, the serotonin transporter SLC6A4 and the serotonin receptor HTR1A. SLC6A4 exhibits decreased expression in the raphe nucleus of the medulla oblongata and polymorphisms specifically associated with SIDS (PMID:19342987). In 75% of infants with SIDS, there is decreased HTR1A expression relative to controls along with an increase in the number of raphe serotonin neurons (PMID:19342987). Over-expression of the mouse orthologue of the HTR1A gene in the juvenile mouse medulla produces an analogous phenotype to SIDS with death due to bradycardia and hypothermia (PMID:18599790). These genes as well as those involved in serotonin synthesis are predicted to be transcriptionally regulated by a common factor, FEV (human orthologue of PET-1). PET-1 knock-out results in up to a 90% loss of serotonin neurons (PMID:12546819), while polymorphisms in FEV are over-represented in African American infants with SIDS. In addition to FEV, other transcription factors implicated in the regulation of these genes (Putative transcriptional regulators (TRs)) and FEV are also listed (see associated references). In addition to serotonin, vasopressin signaling and its regulation by serotonin appear to be important in a common pathway of cardiopulmonary regulation (PMID:2058745). A protein that associates with vasopressin signaling, named pituitary adenylate cyclase-activating polypeptide (ADCYAP1), results in a SIDS like phenotype, characterized by a high increase in spontaneous neonatal death, exacerbated by hypothermia and hypoxia (PMID:14608012), when disrupted in mice. Protein for this gene is widely distributed throughout the central nervous system (CNS), including autonomic control centers (PMID:12389210). ADCYAP1 and HTR1A are both predicted to be transcriptionally regulated by REST promoter binding. Regulation of G-protein coupled signaling pathways is illustrated for these genes, however, it is not clear whether ADCYAP1 acts directly upon raphe serotonin neurons.

Another potentially important class of receptors in SIDS is nicotine. Receptors for nicotine are expressed in serotonin neurons of the raphe throughout development (PMID:18986852). Application of nicotine or cigarette smoke is sufficient to inhibit electrical activity of raphe serotonin neurons (PMID:17515803) and chronic nicotine infusion in rats decreases expression of SLC6A4 (PMID:18778441). Furthermore, nicotine exposure reduces both HTR1A and HTR2A immunoreactivity in several nuclei of the brainstem (PMID:17451658).

In addition to CNS abnormalities, several studies have identified a critical link between cardiac arrhythmia (long QT syndrome) and SIDS (PMID:18928334). A number of genetic association studies identified functionally modifying mutations in critical cardiac channels in as many as 10% of all SIDS cases (PMID:18928334). These mutations have been predicted to predispose infants for long QT syndrome and sudden death. The highest proportion of SIDS associated mutations (both inherited and sporadic) is found in the sodium channel gene SCN5A. Examination of putative transcriptional regulators for these genes, highlights a diverse set of factors as well as a relatively common one (SP1).

Finally, several miscellaneous mutations have been identified in genes associated with inflammatory response and thermoregulation. Infection is considered a significant risk factor for SIDS (PMID:19114412). For inflammatory associated genes, such as TNF alpha, interleukin 10 and complement component 4, many of these mutations are only significant in the presence of infection and SIDS. In addition to these mutations, cerebrospinal fluid levels of IL6 are increased in SIDS cases as well as IL6R levels in the arcuate nucleus of the brain, another major site of serotonin synthesis (PMID:19396608). Genes such as ILR6 and ADCYAP1 are also associated with autoimmune disorders, thus SIDS may also be associated with autoinflammation of autonomic centers in the brain. Regulation of thermogenesis by brown adipose tissue has been proposed be an important component of SIDS, given that SIDS incidence is highest in the winter time and that animal models of SIDS demonstrate variation in body temperature. Interestingly, activation of raphe HTR1A decreases both shivering and peripheral vasoconstriction in piglets (18094064). Although a putative significant polymorphism was identified in the thermoregulator gene HSP60, this only occurred in one SIDS case. It is important to note that in the large majority of all these studies, sleeping position and smoking were among the most significant risk factors for SIDS.

In loving memory of Milo Salomonis (http://www.milosalomonis.org).

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History

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106830view13:31, 17 September 2019MaintBotHMDB identifier normalization
105829view23:06, 15 August 2019Khanspersmodified description
101924view17:05, 17 November 2018EgonwRemoved whitespace in PubMed identifiers.
96990view11:22, 25 April 2018Fehrhartinteractions to graphical lines
96989view10:00, 25 April 2018Fehrhartinteractions to graphical lines
96988view09:55, 25 April 2018Fehrhartinteractions to graphical lines
96900view14:21, 18 April 2018FehrhartInteractions to graphical lines
96897view14:09, 18 April 2018FehrhartInteractions to graphical lines
96896view14:04, 18 April 2018FehrhartConverted interactions to graphical lines
96895view13:58, 18 April 2018FehrhartConverted interactions to graphical lines
92921view11:36, 17 July 2017EgonwReplaced a CAS of a salt with that of the parent compound.
86078view09:59, 29 June 2016MirellaKalafatiModified title
80056view09:31, 3 May 2015LarsEijssenCorrected spelling error: serotinergic -> serotonergic
78533view10:30, 7 January 2015MaintBotadded missing graphIds
74443view07:26, 20 April 2014EgonwFixed a PubMed ID.
73552view18:27, 30 January 2014EgonwH2O not H20....
70114view19:12, 12 July 2013MaintBotupdated to 2013 schema
68050view12:25, 29 June 2013EgonwFixed a few identifier issues.
68049view12:21, 29 June 2013EgonwFixed char encoding issues in references.
67641view11:43, 26 June 2013DdiglesOntology Term : 'serotonin signaling pathway' added !
59166view18:29, 22 February 2013MaintBotUpdated Ensembl data source
55364view18:39, 13 December 2012NsalomonisPeriodical save, work in progress
55358view18:18, 13 December 2012NsalomonisSpecify description
55355view18:08, 13 December 2012NsalomonisPeriodical save, work in progress
55354view17:58, 13 December 2012NsalomonisPeriodical save, work in progress
55353view17:47, 13 December 2012NsalomonisPeriodical save, work in progress
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52816view00:16, 23 October 2012Nsalomonistest-without-DNA
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External references

DataNodes

View all...
NameTypeDatabase referenceComment
5-HIAAMetaboliteHMDB00763 (HMDB)
5-HTMetaboliteHMDB00259 (HMDB)
5-HTPMetaboliteHMDB00472 (HMDB)
ACADMGeneProduct34 (Entrez Gene)
ADCYAP1GeneProduct116 (Entrez Gene)
ADCYAP1R1GeneProduct117 (Entrez Gene)
ALDOAGeneProductENSG00000149925 (Ensembl Human)
AQP4GeneProductENSG00000171885 (Ensembl Human)
ARGeneProduct367 (Entrez Gene)
ASCL1GeneProduct429 (Entrez Gene)
ATP1A3GeneProductENSG00000105409 (Ensembl Human)
AVPGeneProduct551 (Entrez Gene)
AcetylcholineMetabolite51-84-3 (CAS)
BDNFGeneProductENSG00000176697 (Ensembl Human)
BHLHE40GeneProductENSG00000134107 (Ensembl Human)
C4AGeneProduct720 (Entrez Gene)
C4BGeneProduct721 (Entrez Gene)
CASP3GeneProductENSG00000164305 (Ensembl Human)
CAV3GeneProduct859 (Entrez Gene)
CC2D1AGeneProduct54862 (Entrez Gene)
CDCA7LGeneProduct55536 (Entrez Gene)
CEBPBGeneProductENSG00000172216 (Ensembl Human)
CHATGeneProductENSG00000070748 (Ensembl Human)
CHRM2GeneProduct1129 (Entrez Gene)
CHRNA4GeneProduct1137 (Entrez Gene)
CHRNA7GeneProductENSG00000175344 (Ensembl Human)
CHRNB2GeneProduct1141 (Entrez Gene)
CHRNB4GeneProduct1143 (Entrez Gene)
CPT1AGeneProductENSG00000110090 (Ensembl Human)
CREB1GeneProduct1385 (Entrez Gene)
CREB1GeneProductENSG00000118260 (Ensembl Human)
CREBBPGeneProductENSG00000005339 (Ensembl Human)
CREMGeneProductENSG00000095794 (Ensembl Human)
CTCFGeneProduct10664 (Entrez Gene)
CTNNB1GeneProductENSG00000168036 (Ensembl Human)
CholineMetabolite62-49-7 (CAS)
DDCGeneProduct1644 (Entrez Gene)
DEAF1GeneProduct10522 (Entrez Gene)
DLX2GeneProductENSG00000115844 (Ensembl Human)
DopamineMetabolite62-31-7 (CAS)
ECE1GeneProduct1889 (Entrez Gene)
EGR1GeneProductENSG00000120738 (Ensembl Human)
EN1GeneProduct2019 (Entrez Gene)
EP300GeneProduct2033 (Entrez Gene)
ESR2GeneProduct2100 (Entrez Gene)
FEVGeneProduct54738 (Entrez Gene)
FMO3GeneProductENSG00000007933 (Ensembl Human)
FOXM1GeneProduct2305 (Entrez Gene)
FluoxetineMetabolite59333-67-4 (CAS)
G6PCGeneProductENSG00000131482 (Ensembl Human)
GABAMetaboliteHMDB00112 (HMDB)
GABRA1GeneProduct2554 (Entrez Gene)
GAPDHGeneProductENSG00000111640 (Ensembl Human)
GATA2GeneProduct2624 (Entrez Gene)
GATA3GeneProduct2625 (Entrez Gene)
GCKGeneProductENSG00000106633 (Ensembl Human)
GJA1GeneProductENSG00000152661 (Ensembl Human)
GNB3GeneProduct2784 (Entrez Gene)
GPD1LGeneProductENSG00000152642 (Ensembl Human)
GRIN1GeneProductENSG00000176884 (Ensembl Human)
Glial Cell DifferentiationPathwayWP2276
GlutamateMetabolite
GlutamateMetaboliteHMDB04135 (HMDB)
HADHAGeneProduct3030 (Entrez Gene)
HADHBGeneProductENSG00000138029 (Ensembl Human)
HDAC1GeneProductENSG00000116478 (Ensembl Human)
HDAC9GeneProductENSG00000048052 (Ensembl Human)
HES1GeneProduct3280 (Entrez Gene)
HES1GeneProductENSG00000114315 (Ensembl Human)
HES5GeneProduct388585 (Entrez Gene)
HIF1AGeneProductENSG00000100644 (Ensembl Human)
HSP90B1GeneProductENSG00000166598 (Ensembl Human)
HSPD1GeneProduct3329 (Entrez Gene)
HTR1AGeneProduct3350 (Entrez Gene)
HTR2AGeneProduct3356 (Entrez Gene)
HTR3AGeneProductENSG00000166736 (Ensembl Human)
IL10GeneProduct3586 (Entrez Gene)
IL13GeneProductENSG00000169194 (Ensembl Human)
IL1AGeneProductENSG00000115008 (Ensembl Human)
IL1BGeneProductENSG00000125538 (Ensembl Human)
IL1RNGeneProductENSG00000136689 (Ensembl Human)
IL6GeneProduct3569 (Entrez Gene)
IL6RGeneProduct3570 (Entrez Gene)
IL8GeneProduct3576 (Entrez Gene)
JUNGeneProductENSG00000177606 (Ensembl Human)
KCNH2 GeneProduct3757 (Entrez Gene)
KCNH2GeneProduct3757 (Entrez Gene)
KCNJ8GeneProduct3764 (Entrez Gene)
KCNQ1GeneProduct3784 (Entrez Gene)
L-DOPAMetabolite59-92-7 (CAS)
L-TryptophanMetaboliteHMDB00929 (HMDB)
LMX1BGeneProduct4010 (Entrez Gene)
MAOAGeneProduct4128 (Entrez Gene)
MAP2GeneProductENSG00000078018 (Ensembl Human)
MAZGeneProductENSG00000103495 (Ensembl Human)
MBD1GeneProductENSG00000141644 (Ensembl Human)
MECP2GeneProductENSG00000169057 (Ensembl Human)
MEF2CGeneProductENSG00000081189 (Ensembl Human)
MIR13AGeneProductENSG00000208009
MIR16-1GeneProduct406950 (Entrez Gene)
MIR210GeneProductENSG00000199038 (Ens