Details of Drug Off-Target (DOT)

General Information of Drug Off-Target (DOT) (ID: OT7Z2YRP)

• DOT Name: A-kinase anchor protein 9 (AKAP9)
• Synonyms: AKAP-9; A-kinase anchor protein 350 kDa; AKAP 350; hgAKAP 350; A-kinase anchor protein 450 kDa; AKAP 450; AKAP 120-like protein; Centrosome- and Golgi-localized PKN-associated protein; CG-NAP; Protein hyperion; Protein kinase A-anchoring protein 9; PRKA9; Protein yotiao
• Gene Name: AKAP9
• Related Disease:
  Melanoma
  Thyroid tumor
  Alzheimer disease
  Breast cancer
  Breast carcinoma
  Breast neoplasm
  Brugada syndrome
  Familial long QT syndrome
  Hypertrophic cardiomyopathy
  Neoplasm
  Schizophrenia
  Skin disease
  Thyroid cancer
  Thyroid gland carcinoma
  Thyroid gland papillary carcinoma
  Advanced cancer
  Obsolete male infertility with azoospermia or oligozoospermia due to single gene mutation
  Long QT syndrome
  Colorectal carcinoma
  Long QT syndrome 11
• UniProt ID: AKAP9_HUMAN
• Pfam ID: PF10495
• Sequence:
  MEDEERQKKLEAGKAKLAQFRQRKAQSDGQSPSKKQKKKRKTSSSKHDVSAHHDLNIDQS
  QCNEMYINSSQRVESTVIPESTIMRTLHSGEITSHEQGFSVELESEISTTADDCSSEVNG
  CSFVMRTGKPTNLLREEEFGVDDSYSEQGAQDSPTHLEMMESELAGKQHEIEELNRELEE
  MRVTYGTEGLQQLQEFEAAIKQRDGIITQLTANLQQARREKDETMREFLELTEQSQKLQI
  QFQQLQASETLRNSTHSSTAADLLQAKQQILTHQQQLEEQDHLLEDYQKKKEDFTMQISF
  LQEKIKVYEMEQDKKVENSNKEEIQEKETIIEELNTKIIEEEKKTLELKDKLTTADKLLG
  ELQEQIVQKNQEIKNMKLELTNSKQKERQSSEEIKQLMGTVEELQKRNHKDSQFETDIVQ
  RMEQETQRKLEQLRAELDEMYGQQIVQMKQELIRQHMAQMEEMKTRHKGEMENALRSYSN
  ITVNEDQIKLMNVAINELNIKLQDTNSQKEKLKEELGLILEEKCALQRQLEDLVEELSFS
  REQIQRARQTIAEQESKLNEAHKSLSTVEDLKAEIVSASESRKELELKHEAEVTNYKIKL
  EMLEKEKNAVLDRMAESQEAELERLRTQLLFSHEEELSKLKEDLEIEHRINIEKLKDNLG
  IHYKQQIDGLQNEMSQKIETMQFEKDNLITKQNQLILEISKLKDLQQSLVNSKSEEMTLQ
  INELQKEIEILRQEEKEKGTLEQEVQELQLKTELLEKQMKEKENDLQEKFAQLEAENSIL
  KDEKKTLEDMLKIHTPVSQEERLIFLDSIKSKSKDSVWEKEIEILIEENEDLKQQCIQLN
  EEIEKQRNTFSFAEKNFEVNYQELQEEYACLLKVKDDLEDSKNKQELEYKSKLKALNEEL
  HLQRINPTTVKMKSSVFDEDKTFVAETLEMGEVVEKDTTELMEKLEVTKREKLELSQRLS
  DLSEQLKQKHGEISFLNEEVKSLKQEKEQVSLRCRELEIIINHNRAENVQSCDTQVSSLL
  DGVVTMTSRGAEGSVSKVNKSFGEESKIMVEDKVSFENMTVGEESKQEQLILDHLPSVTK
  ESSLRATQPSENDKLQKELNVLKSEQNDLRLQMEAQRICLSLVYSTHVDQVREYMENEKD
  KALCSLKEELIFAQEEKIKELQKIHQLELQTMKTQETGDEGKPLHLLIGKLQKAVSEECS
  YFLQTLCSVLGEYYTPALKCEVNAEDKENSGDYISENEDPELQDYRYEVQDFQENMHTLL
  NKVTEEYNKLLVLQTRLSKIWGQQTDGMKLEFGEENLPKEETEFLSIHSQMTNLEDIDVN
  HKSKLSSLQDLEKTKLEEQVQELESLISSLQQQLKETEQNYEAEIHCLQKRLQAVSESTV
  PPSLPVDSVVITESDAQRTMYPGSCVKKNIDGTIEFSGEFGVKEETNIVKLLEKQYQEQL
  EEEVAKVIVSMSIAFAQQTELSRISGGKENTASSKQAHAVCQQEQHYFNEMKLSQDQIGF
  QTFETVDVKFKEEFKPLSKELGEHGKEILLSNSDPHDIPESKDCVLTISEEMFSKDKTFI
  VRQSIHDEISVSSMDASRQLMLNEEQLEDMRQELVRQYQEHQQATELLRQAHMRQMERQR
  EDQEQLQEEIKRLNRQLAQRSSIDNENLVSERERVLLEELEALKQLSLAGREKLCCELRN
  SSTQTQNGNENQGEVEEQTFKEKELDRKPEDVPPEILSNERYALQKANNRLLKILLEVVK
  TTAAVEETIGRHVLGILDRSSKSQSSASLIWRSEAEASVKSCVHEEHTRVTDESIPSYSG
  SDMPRNDINMWSKVTEEGTELSQRLVRSGFAGTEIDPENEELMLNISSRLQAAVEKLLEA
  ISETSSQLEHAKVTQTELMRESFRQKQEATESLKCQEELRERLHEESRAREQLAVELSKA
  EGVIDGYADEKTLFERQIQEKTDIIDRLEQELLCASNRLQELEAEQQQIQEERELLSRQK
  EAMKAEAGPVEQQLLQETEKLMKEKLEVQCQAEKVRDDLQKQVKALEIDVEEQVSRFIEL
  EQEKNTELMDLRQQNQALEKQLEKMRKFLDEQAIDREHERDVFQQEIQKLEQQLKVVPRF
  QPISEHQTREVEQLANHLKEKTDKCSELLLSKEQLQRDIQERNEEIEKLEFRVRELEQAL
  LVSADTFQKVEDRKHFGAVEAKPELSLEVQLQAERDAIDRKEKEITNLEEQLEQFREELE
  NKNEEVQQLHMQLEIQKKESTTRLQELEQENKLFKDDMEKLGLAIKESDAMSTQDQHVLF
  GKFAQIIQEKEVEIDQLNEQVTKLQQQLKITTDNKVIEEKNELIRDLETQIECLMSDQEC
  VKRNREEEIEQLNEVIEKLQQELANIGQKTSMNAHSLSEEADSLKHQLDVVIAEKLALEQ
  QVETANEEMTFMKNVLKETNFKMNQLTQELFSLKRERESVEKIQSIPENSVNVAIDHLSK
  DKPELEVVLTEDALKSLENQTYFKSFEENGKGSIINLETRLLQLESTVSAKDLELTQCYK
  QIKDMQEQGQFETEMLQKKIVNLQKIVEEKVAAALVSQIQLEAVQEYAKFCQDNQTISSE
  PERTNIQNLNQLREDELGSDISALTLRISELESQVVEMHTSLILEKEQVEIAEKNVLEKE
  KKLLELQKLLEGNEKKQREKEKKRSPQDVEVLKTTTELFHSNEESGFFNELEALRAESVA
  TKAELASYKEKAEKLQEELLVKETNMTSLQKDLSQVRDHLAEAKEKLSILEKEDETEVQE
  SKKACMFEPLPIKLSKSIASQTDGTLKISSSNQTPQILVKNAGIQINLQSECSSEEVTEI
  ISQFTEKIEKMQELHAAEILDMESRHISETETLKREHYVAVQLLKEECGTLKAVIQCLRS
  KEGSSIPELAHSDAYQTREICSSDSGSDWGQGIYLTHSQGFDIASEGRGEESESATDSFP
  KKIKGLLRAVHNEGMQVLSLTESPYSDGEDHSIQQVSEPWLEERKAYINTISSLKDLITK
  MQLQREAEVYDSSQSHESFSDWRGELLLALQQVFLEERSVLLAAFRTELTALGTTDAVGL
  LNCLEQRIQEQGVEYQAAMECLQKADRRSLLSEIQALHAQMNGRKITLKREQESEKPSQE
  LLEYNIQQKQSQMLEMQVELSSMKDRATELQEQLSSEKMVVAELKSELAQTKLELETTLK
  AQHKHLKELEAFRLEVKDKTDEVHLLNDTLASEQKKSRELQWALEKEKAKLGRSEERDKE
  ELEDLKFSLESQKQRNLQLNLLLEQQKQLLNESQQKIESQRMLYDAQLSEEQGRNLELQV
  LLESEKVRIREMSSTLDRERELHAQLQSSDGTGQSRPPLPSEDLLKELQKQLEEKHSRIV
  ELLNETEKYKLDSLQTRQQMEKDRQVHRKTLQTEQEANTEGQKKMHELQSKVEDLQRQLE
  EKRQQVYKLDLEGQRLQGIMQEFQKQELEREEKRESRRILYQNLNEPTTWSLTSDRTRNW
  VLQQKIEGETKESNYAKLIEMNGGGTGCNHELEMIRQKLQCVASKLQVLPQKASERLQFE
  TADDEDFIWVQENIDEIILQLQKLTGQQGEEPSLVSPSTSCGSLTERLLRQNAELTGHIS
  QLTEEKNDLRNMVMKLEEQIRWYRQTGAGRDNSSRFSLNGGANIEAIIASEKEVWNREKL
  TLQKSLKRAEAEVYKLKAELRNDSLLQTLSPDSEHVTLKRIYGKYLRAESFRKALIYQKK
  YLLLLLGGFQECEDATLALLARMGGQPAFTDLEVITNRPKGFTRFRSAVRVSIAISRMKF
  LVRRWHRVTGSVSININRDGFGLNQGAEKTDSFYHSSGGLELYGEPRHTTYRSRSDLDYI
  RSPLPFQNRYPGTPADFNPGSLACSQLQNYDPDRALTDYITRLEALQRRLGTIQSGSTTQ
  FHAGMRR
• Function: Scaffolding protein that assembles several protein kinases and phosphatases on the centrosome and Golgi apparatus. Required to maintain the integrity of the Golgi apparatus. Required for microtubule nucleation at the cis-side of the Golgi apparatus. Required for association of the centrosomes with the poles of the bipolar mitotic spindle during metaphase. In complex with PDE4DIP isoform 13/MMG8/SMYLE, recruits CAMSAP2 to the Golgi apparatus and tethers non-centrosomal minus-end microtubules to the Golgi, an important step for polarized cell movement. In complex with PDE4DIP isoform 13/MMG8/SMYLE, EB1/MAPRE1 and CDK5RAP2, contributes to microtubules nucleation and extension also from the centrosome to the cell periphery ; [Isoform 4]: Associated with the N-methyl-D-aspartate receptor and is specifically found in the neuromuscular junction (NMJ) as well as in neuronal synapses, suggesting a role in the organization of postsynaptic specializations.
• Tissue Specificity: Widely expressed . Isoform 4: Highly expressed in skeletal muscle and in pancreas .
• Reactome Pathway:
  Loss of Nlp from mitotic centrosomes (R-HSA-380259)
  Recruitment of mitotic centrosome proteins and complexes (R-HSA-380270)
  Loss of proteins required for interphase microtubule organization from the centrosome (R-HSA-380284)
  Recruitment of NuMA to mitotic centrosomes (R-HSA-380320)
  Phase 3 - rapid repolarisation (R-HSA-5576890)
  Phase 2 - plateau phase (R-HSA-5576893)
  Anchoring of the basal body to the plasma membrane (R-HSA-5620912)
  Signaling by BRAF and RAF1 fusions (R-HSA-6802952)
  AURKA Activation by TPX2 (R-HSA-8854518)
  Regulation of PLK1 Activity at G2/M Transition (R-HSA-2565942)

Molecular Interaction Atlas (MIA) of This DOT

20 Disease(s) Related to This DOT

Disease Name	Disease ID	Evidence Level	Mode of Inheritance	REF
Melanoma	DIS1RRCY	Definitive	Genetic Variation	[1]
Thyroid tumor	DISLVKMD	Definitive	Biomarker	[2]
Alzheimer disease	DISF8S70	Strong	Genetic Variation	[3]
Breast cancer	DIS7DPX1	Strong	Biomarker	[4]
Breast carcinoma	DIS2UE88	Strong	Biomarker	[4]
Breast neoplasm	DISNGJLM	Strong	Genetic Variation	[5]
Brugada syndrome	DISSGN0E	Strong	Biomarker	[6]
Familial long QT syndrome	DISRNNCY	Strong	Biomarker	[7]
Hypertrophic cardiomyopathy	DISQG2AI	Strong	Genetic Variation	[8]
Neoplasm	DISZKGEW	Strong	Biomarker	[9]
Schizophrenia	DISSRV2N	Strong	Genetic Variation	[10]
Skin disease	DISDW8R6	Strong	Biomarker	[11]
Thyroid cancer	DIS3VLDH	Strong	Biomarker	[12]
Thyroid gland carcinoma	DISMNGZ0	Strong	Biomarker	[12]
Thyroid gland papillary carcinoma	DIS48YMM	Strong	Biomarker	[13]
Advanced cancer	DISAT1Z9	moderate	Biomarker	[14]
Obsolete male infertility with azoospermia or oligozoospermia due to single gene mutation	DIS56JR8	Moderate	Autosomal recessive	[15]
Long QT syndrome	DISMKWS3	Disputed	Autosomal dominant	[16]
Colorectal carcinoma	DIS5PYL0	Limited	Altered Expression	[17]
Long QT syndrome 11	DISL0NEK	Limited	Autosomal dominant	[18]

1 Drug(s) Affected the Post-Translational Modifications of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Valproate	DMCFE9I	Approved	Valproate decreases the methylation of A-kinase anchor protein 9 (AKAP9).	[19]

18 Drug(s) Affected the Gene/Protein Processing of This DOT

Drug Name	Drug ID	Highest Status	Interaction	REF
Ciclosporin	DMAZJFX	Approved	Ciclosporin affects the expression of A-kinase anchor protein 9 (AKAP9).	[20]
Tretinoin	DM49DUI	Approved	Tretinoin decreases the expression of A-kinase anchor protein 9 (AKAP9).	[21]
Acetaminophen	DMUIE76	Approved	Acetaminophen decreases the expression of A-kinase anchor protein 9 (AKAP9).	[22]
Cupric Sulfate	DMP0NFQ	Approved	Cupric Sulfate decreases the expression of A-kinase anchor protein 9 (AKAP9).	[23]
Estradiol	DMUNTE3	Approved	Estradiol decreases the expression of A-kinase anchor protein 9 (AKAP9).	[24]
Arsenic	DMTL2Y1	Approved	Arsenic decreases the expression of A-kinase anchor protein 9 (AKAP9).	[11]
Arsenic trioxide	DM61TA4	Approved	Arsenic trioxide increases the expression of A-kinase anchor protein 9 (AKAP9).	[26]
Progesterone	DMUY35B	Approved	Progesterone decreases the expression of A-kinase anchor protein 9 (AKAP9).	[27]
Menadione	DMSJDTY	Approved	Menadione affects the expression of A-kinase anchor protein 9 (AKAP9).	[28]
Demecolcine	DMCZQGK	Approved	Demecolcine increases the expression of A-kinase anchor protein 9 (AKAP9).	[29]
Clorgyline	DMCEUJD	Approved	Clorgyline increases the expression of A-kinase anchor protein 9 (AKAP9).	[30]
Tamibarotene	DM3G74J	Phase 3	Tamibarotene decreases the expression of A-kinase anchor protein 9 (AKAP9).	[21]
Epigallocatechin gallate	DMCGWBJ	Phase 3	Epigallocatechin gallate decreases the expression of A-kinase anchor protein 9 (AKAP9).	[31]
APR-246	DMNFADH	Phase 2	APR-246 decreases the expression of A-kinase anchor protein 9 (AKAP9).	[32]
(+)-JQ1	DM1CZSJ	Phase 1	(+)-JQ1 increases the expression of A-kinase anchor protein 9 (AKAP9).	[33]
PMID28870136-Compound-52	DMFDERP	Patented	PMID28870136-Compound-52 decreases the expression of A-kinase anchor protein 9 (AKAP9).	[31]
Trichostatin A	DM9C8NX	Investigative	Trichostatin A decreases the expression of A-kinase anchor protein 9 (AKAP9).	[34]
Formaldehyde	DM7Q6M0	Investigative	Formaldehyde decreases the expression of A-kinase anchor protein 9 (AKAP9).	[35]

References

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• [2] Mechanisms of chromosomal rearrangements in solid tumors: the model of papillary thyroid carcinoma.Mol Cell Endocrinol. 2010 May 28;321(1):36-43. doi: 10.1016/j.mce.2009.09.013. Epub 2009 Sep 18.
• [3] Tau Phosphorylation is Impacted by Rare AKAP9 Mutations Associated with Alzheimer Disease in African Americans.J Neuroimmune Pharmacol. 2018 Jun;13(2):254-264. doi: 10.1007/s11481-018-9781-x. Epub 2018 Mar 7.
• [4] Role of exchange protein directly activated by cAMP (EPAC1) in breast cancer cell migration and apoptosis.Mol Cell Biochem. 2017 Jun;430(1-2):115-125. doi: 10.1007/s11010-017-2959-3. Epub 2017 Feb 16.
• [5] Association of a common AKAP9 variant with breast cancer risk: a collaborative analysis.J Natl Cancer Inst. 2008 Mar 19;100(6):437-42. doi: 10.1093/jnci/djn037. Epub 2008 Mar 11.
• [6] Brugada syndrome & AKAP9: Reconciling clinical findings with diagnostic uncertainty.J Electrocardiol. 2019 Nov-Dec;57:119-121. doi: 10.1016/j.jelectrocard.2019.09.013. Epub 2019 Sep 7.
• [7] AKAP9 is a genetic modifier of congenital long-QT syndrome type 1.Circ Cardiovasc Genet. 2014 Oct;7(5):599-606. doi: 10.1161/CIRCGENETICS.113.000580. Epub 2014 Aug 2.
• [8] Targeted next-generation sequencing detects novel gene-phenotype associations and expands the mutational spectrum in cardiomyopathies.PLoS One. 2017 Jul 27;12(7):e0181842. doi: 10.1371/journal.pone.0181842. eCollection 2017.
• [9] Cell-free DNA mutations as biomarkers in breast cancer patients receiving tamoxifen.Oncotarget. 2016 Jul 12;7(28):43412-43418. doi: 10.18632/oncotarget.9727.
• [10] Resequencing and association analysis of coding regions at twenty candidate genes suggest a role for rare risk variation at AKAP9 and protective variation at NRXN1 in schizophrenia susceptibility.J Psychiatr Res. 2015 Jul-Aug;66-67:38-44. doi: 10.1016/j.jpsychires.2015.04.013. Epub 2015 Apr 22.
• [11] Gene expression profiles in peripheral lymphocytes by arsenic exposure and skin lesion status in a Bangladeshi population. Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1367-75. doi: 10.1158/1055-9965.EPI-06-0106.
• [12] Oncogenic AKAP9-BRAF fusion is a novel mechanism of MAPK pathway activation in thyroid cancer.J Clin Invest. 2005 Jan;115(1):94-101. doi: 10.1172/JCI23237.
• [13] Cytogenetic and molecular events in adenoma and well-differentiated thyroid follicular-cell neoplasia.Cancer Genet Cytogenet. 2010 Nov;203(1):21-9. doi: 10.1016/j.cancergencyto.2010.08.025.
• [14] A surprising cross-species conservation in the genomic landscape of mouse and human oral cancer identifies a transcriptional signature predicting metastatic disease.Clin Cancer Res. 2014 Jun 1;20(11):2873-84. doi: 10.1158/1078-0432.CCR-14-0205. Epub 2014 Mar 25.
• [15] A genomics approach to male infertility. Genet Med. 2020 Dec;22(12):1967-1975. doi: 10.1038/s41436-020-0916-0. Epub 2020 Jul 28.
• [16] Technical standards for the interpretation and reporting of constitutional copy-number variants: a joint consensus recommendation of the American College of Medical Genetics and Genomics (ACMG) and the Clinical Genome Resource (ClinGen). Genet Med. 2020 Feb;22(2):245-257. doi: 10.1038/s41436-019-0686-8. Epub 2019 Nov 6.
• [17] Long non-coding RNA MALAT1 increases AKAP-9 expression by promoting SRPK1-catalyzed SRSF1 phosphorylation in colorectal cancer cells.Oncotarget. 2016 Mar 8;7(10):11733-43. doi: 10.18632/oncotarget.7367.
• [18] Requirement of a macromolecular signaling complex for beta adrenergic receptor modulation of the KCNQ1-KCNE1 potassium channel. Science. 2002 Jan 18;295(5554):496-9. doi: 10.1126/science.1066843.
• [19] Integrative omics data analyses of repeated dose toxicity of valproic acid in vitro reveal new mechanisms of steatosis induction. Toxicology. 2018 Jan 15;393:160-170.
• [20] Integrating multiple omics to unravel mechanisms of Cyclosporin A induced hepatotoxicity in vitro. Toxicol In Vitro. 2015 Apr;29(3):489-501.
• [21] Differential modulation of PI3-kinase/Akt pathway during all-trans retinoic acid- and Am80-induced HL-60 cell differentiation revealed by DNA microarray analysis. Biochem Pharmacol. 2004 Dec 1;68(11):2177-86.
• [22] Gene expression analysis of precision-cut human liver slices indicates stable expression of ADME-Tox related genes. Toxicol Appl Pharmacol. 2011 May 15;253(1):57-69.
• [23] Physiological and toxicological transcriptome changes in HepG2 cells exposed to copper. Physiol Genomics. 2009 Aug 7;38(3):386-401.
• [24] 17-Estradiol Activates HSF1 via MAPK Signaling in ER-Positive Breast Cancer Cells. Cancers (Basel). 2019 Oct 11;11(10):1533. doi: 10.3390/cancers11101533.
• [25] Gene expression profiles in peripheral lymphocytes by arsenic exposure and skin lesion status in a Bangladeshi population. Cancer Epidemiol Biomarkers Prev. 2006 Jul;15(7):1367-75. doi: 10.1158/1055-9965.EPI-06-0106.
• [26] Essential role of cell cycle regulatory genes p21 and p27 expression in inhibition of breast cancer cells by arsenic trioxide. Med Oncol. 2011 Dec;28(4):1225-54.
• [27] Coordinate up-regulation of TMEM97 and cholesterol biosynthesis genes in normal ovarian surface epithelial cells treated with progesterone: implications for pathogenesis of ovarian cancer. BMC Cancer. 2007 Dec 11;7:223.
• [28] Global gene expression analysis reveals differences in cellular responses to hydroxyl- and superoxide anion radical-induced oxidative stress in caco-2 cells. Toxicol Sci. 2010 Apr;114(2):193-203. doi: 10.1093/toxsci/kfp309. Epub 2009 Dec 31.
• [29] Characterization of formaldehyde's genotoxic mode of action by gene expression analysis in TK6 cells. Arch Toxicol. 2013 Nov;87(11):1999-2012.
• [30] Anti-oncogenic and pro-differentiation effects of clorgyline, a monoamine oxidase A inhibitor, on high grade prostate cancer cells. BMC Med Genomics. 2009 Aug 20;2:55. doi: 10.1186/1755-8794-2-55.
• [31] Comparative proteomics reveals concordant and discordant biochemical effects of caffeine versus epigallocatechin-3-gallate in human endothelial cells. Toxicol Appl Pharmacol. 2019 Sep 1;378:114621. doi: 10.1016/j.taap.2019.114621. Epub 2019 Jun 10.
• [32] Mutant p53 reactivation by PRIMA-1MET induces multiple signaling pathways converging on apoptosis. Oncogene. 2010 Mar 4;29(9):1329-38. doi: 10.1038/onc.2009.425. Epub 2009 Nov 30.
• [33] Inhibition of BRD4 attenuates tumor cell self-renewal and suppresses stem cell signaling in MYC driven medulloblastoma. Oncotarget. 2014 May 15;5(9):2355-71.
• [34] From transient transcriptome responses to disturbed neurodevelopment: role of histone acetylation and methylation as epigenetic switch between reversible and irreversible drug effects. Arch Toxicol. 2014 Jul;88(7):1451-68.
• [35] Gene expression changes in primary human nasal epithelial cells exposed to formaldehyde in vitro. Toxicol Lett. 2010 Oct 5;198(2):289-95.