Prader–Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review
Abstract
:1. Introduction
2. Genetics of Prader–Willi Syndrome
3. Clinical Description of Prader–Willi Syndrome and 15q11.2 BP1-BP2 Deletion
4. Description, Evaluation and Gene Expression of Chromosome 15q11.2 BP1-BP2
4.1. Chromosome 15q11.2 BP1-BP2 Region Description
4.2. Chromosome 15q11.2 BP1-BP2 Genes, Functions and Pathway Analysis
4.3. Clinical Evaluation and Findings in 15q11.2 BP1-BP2 Deletion
5. Conclusions
Funding
Acknowledgments
Conflicts of Interest
References
- Butler, M.G. Single Gene and Syndromic Causes of Obesity: Illustrative Examples. Prog. Mol. Biol. Transl. Sci. 2016, 140, 1–45. [Google Scholar] [CrossRef]
- Butler, M.G.; Hartin, S.N.; Hossain, W.A.; Manzardo, A.M.; Kimonis, V.; Dykens, E.; Gold, J.A.; Kim, S.J.; Weisensel, N.; Tamura, R.; et al. Molecular genetic classification in Prader-Willi syndrome: A multisite cohort study. J. Med. Genet. 2019, 56, 149–153. [Google Scholar] [CrossRef]
- Strom, S.P.; Hossain, W.A.; Grigorian, M.; Li, M.; Fierro, J.; Scaringe, W.; Yen, H.Y.; Teguh, M.; Liu, J.; Gao, H.; et al. A Streamlined Approach to Prader-Willi and Angelman Syndrome Molecular Diagnostics. Front Genet. 2021, 12, 608889. [Google Scholar] [CrossRef]
- Duis, J.; Butler, M.G. Syndromic and Nonsyndromic Obesity: Underlying Genetic Causes in Humans. Adv. Biol. 2022, 6, e2101154. [Google Scholar] [CrossRef]
- Butler, M.G.; Duis, J. Chromosome 15 Imprinting Disorders: Genetic Laboratory Methodology and Approaches. Front Pediatr. 2020, 8, 154. [Google Scholar] [CrossRef]
- Cassidy, S.B.; Schwartz, S.; Miller, J.L.; Driscoll, D.J. Prader-Willi syndrome. Genet. Med. 2012, 14, 10–26. [Google Scholar] [CrossRef] [Green Version]
- Butler, M.G.; Lee, P.; Whitman, B. Management of Prader-Willi Syndrome, 4th ed.; Springer Publishers: New York, NY, USA, 2022. [Google Scholar]
- Butler, M.G. Imprinting disorders in humans: A review. Curr. Opin. Pediatr. 2020, 32, 719–729. [Google Scholar] [CrossRef]
- Butler, M.G.; Miller, B.S.; Romano, A.; Ross, J.; Abuzzahab, M.J.; Backeljauw, P.; Bamba, V.; Bhangoo, A.; Mauras, N.; Geffner, M. Genetic conditions of short stature: A review of three classic examples. Front Endocrinol. 2022, 13, 1011960. [Google Scholar] [CrossRef]
- Alves, C.; Franco, R.R. Prader-Willi syndrome: Endocrine manifestations and management. Arch. Endocrinol. Metab. 2020, 64, 223–234. [Google Scholar] [CrossRef]
- Butler, M.G. Prader-Willi syndrome: Current understanding of cause and diagnosis. Am. J. Med. Genet. 1990, 35, 319–332. [Google Scholar] [CrossRef] [Green Version]
- Angulo, M.A.; Butler, M.G.; Hossain, W.A.; Castro-Magana, M.; Corletto, J. Central adrenal insufficiency screening with morning plasma cortisol and ACTH levels in Prader-Willi syndrome. J. Pediatr. Endocrinol. Metab. 2022, 35, 733–740. [Google Scholar] [CrossRef]
- Mahmoud, R.; Kimonis, V.; Butler, M.G. Genetics of Obesity in Humans: A Clinical Review. Int. J. Mol. Sci. 2022, 23, 11005. [Google Scholar] [CrossRef]
- Butler, M.G.; Miller, J.L.; Forster, J.L. Prader-Willi Syndrome—Clinical Genetics, Diagnosis and Treatment Approaches: An Update. Curr. Pediatr. Rev. 2019, 15, 207–244. [Google Scholar] [CrossRef] [PubMed]
- Butler, M.G.; Kimonis, V.; Dykens, E.; Gold, J.A.; Miller, J.; Tamura, R.; Driscoll, D.J. Prader-Willi syndrome and early-onset morbid obesity NIH rare disease consortium: A review of natural history study. Am. J. Med. Genet A 2018, 176, 368–375. [Google Scholar] [CrossRef] [PubMed]
- Driscoll, D.J.; Miller, J.L.; Schwartz, S.; Cassidy, S.B. Prader-Willi Syndrome. In GeneReviews®; Adam, M.P., Everman, D.B., Mirzaa, G.M., Pagon, R.A., Wallace, S.E., Bean, L.J.H., Gripp, K.W., Amemiya, A., Eds.; University of Washington: Seattle, WA, USA, 1998; pp. 1993–2022. [Google Scholar]
- Napolitano, L.; Barone, B.; Morra, S.; Celentano, G.; La Rocca, R.; Capece, M.; Morgera, V.; Turco, C.; Caputo, V.F.; Spena, G.; et al. Hypogonadism in Patients with Prader Willi Syndrome: A Narrative Review. Int. J. Mol. Sci. 2021, 22, 1993. [Google Scholar] [CrossRef]
- Miller, J.L.; Lynn, C.H.; Driscoll, D.C.; Goldstone, A.P.; Gold, J.A.; Kimonis, V.; Dykens, E.; Butler, M.G.; Shuster, J.J.; Driscoll, D.J. Nutritional phases in Prader-Willi syndrome. Am. J. Med. Genet A. 2011, 155A, 1040–1049. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Butler, M.G.; Manzardo, A.M.; Heinemann, J.; Loker, C.; Loker, J. Causes of death in Prader-Willi syndrome: Prader-Willi Syndrome Association (USA) 40-year mortality survey. Genet. Med. 2017, 19, 635–642. [Google Scholar] [CrossRef] [Green Version]
- Manzardo, A.M.; Loker, J.; Heinemann, J.; Loker, C.; Butler, M.G. Survival trends from the Prader-Willi Syndrome Association (USA) 40-year mortality survey. Genet. Med. 2018, 20, 24–30. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Whittington, J.E.; Holland, A.J.; Webb, T.; Butler, J.; Clarke, D.; Boer, H. Population prevalence and estimated birth incidence and mortality rate for people with Prader-Willi syndrome in one UK Health Region. J. Med. Genet. 2001, 38, 792–798. [Google Scholar] [CrossRef] [Green Version]
- Butler, M.G.; Matthews, N.A.; Patel, N.; Surampalli, A.; Gold, J.A.; Khare, M.; Thompson, T.; Cassidy, S.B.; Kimonis, V.E. Impact of genetic subtypes of Prader-Willi syndrome with growth hormone therapy on intelligence and body mass index. Am. J. Med. Genet. A 2019, 179, 1826–1835. [Google Scholar] [CrossRef]
- Huisman, S.; Mulder, P.; Kuijk, J.; Kerstholt, M.; van Eeghen, A.; Leenders, A.; van Balkom, I.; Oliver, C.; Piening, S.; Hennekam, R. Self-injurious behavior. Neurosci. Biobehav. Rev. 2018, 84, 483–491. [Google Scholar] [CrossRef]
- Kimonis, V.E.; Tamura, R.; Gold, J.A.; Patel, N.; Surampalli, A.; Manazir, J.; Miller, J.L.; Roof, E.; Dykens, E.; Butler, M.G.; et al. Early Diagnosis in Prader-Willi Syndrome Reduces Obesity and Associated Co-Morbidities. Genes 2019, 10, 898. [Google Scholar] [CrossRef] [Green Version]
- Nicholls, R.D.; Knepper, J.L. Genome organization, function, and imprinting in Prader-Willi and Angelman syndromes. Annu. Rev. Genomics. Hum. Genet. 2001, 2, 153–175. [Google Scholar] [CrossRef]
- Bittel, D.C.; Butler, M.G. Prader-Willi syndrome: Clinical genetics, cytogenetics and molecular biology. Expert Rev. Mol. Med. 2005, 7, 1–20. [Google Scholar] [CrossRef] [PubMed]
- Butler, M.G. Clinical and genetic aspects of the 15q11.2 BP1-BP2 microdeletion disorder. J. Intellect. Disabil. Res. 2017, 61, 568–579. [Google Scholar] [CrossRef] [PubMed]
- Rafi, S.K.; Butler, M.G. The 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome: In Silico Analyses of the Four Coding Genes Reveal Functional Associations with Neurodevelopmental Phenotypes. Int. J. Mol. Sci. 2020, 21, 3296. [Google Scholar] [CrossRef]
- Kalsner, L.; Chamberlain, S.J. Prader-Willi, Angelman, and 15q11-q13 Duplication Syndromes. Pediatr. Clin. North. Am. 2015, 62, 587–606. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Burnett, L.C.; LeDuc, C.A.; Sulsona, C.R.; Paull, D.; Rausch, R.; Eddiry, S.; Carli, J.F.; Morabito, M.V.; Skowronski, A.A.; Hubner, G.; et al. Deficiency in prohormone convertase PC1 impairs prohormone processing in Prader-Willi syndrome. J. Clin. Investig. 2017, 127, 293–305. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Butler, M.G.; Bittel, D.C.; Kibiryeva, N.; Talebizadeh, Z.; Thompson, T. Behavioral differences among subjects with Prader-Willi syndrome and type I or type II deletion and maternal disomy. Pediatrics 2004, 113, 565–573. [Google Scholar] [CrossRef]
- Roof, E.; Stone, W.; MacLean, W.; Feurer, I.D.; Thompson, T.; Butler, M.G. Intellectual characteristics of Prader-Willi syndrome: Comparison of genetic subtypes. J. Intellect. Disabil. Res. 2000, 44, 25–30. [Google Scholar] [CrossRef] [PubMed]
- Hartley, S.L.; Maclean, W.E., Jr.; Butler, M.G.; Zarcone, J.; Thompson, T. Maladaptive behaviors and risk factors among the genetic subtypes of Prader-Willi syndrome. Am. J. Med. Genet A 2005, 136, 140–145. [Google Scholar] [CrossRef] [Green Version]
- Zarcone, J.; Napolitano, D.; Peterson, C.; Breidbord, J.; Ferraioli, S.; Caruso-Anderson, M.; Holsen, L.; Butler, M.G.; Thompson, T. The relationship between compulsive behaviour and academic achievement across the three genetic subtypes of Prader-Willi syndrome. J. Intellect. Disabil. Res. 2007, 51, 478–487. [Google Scholar] [CrossRef]
- Holsen, L.M.; Zarcone, J.R.; Chambers, R.; Butler, M.G.; Bittel, D.C.; Brooks, W.M.; Thompson, T.I.; Savage, C.R. Genetic subtype differences in neural circuitry of food motivation in Prader-Willi syndrome. Int. J. Obes. 2009, 33, 273–283. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Fox, R.; Sinatra, R.B.; Mooney, M.A.; Feurer, I.D.; Butler, M.G. Visual capacity and Prader-Willi syndrome. J. Pediatr. Ophthalmol. Strabismus. 1999, 36, 331–336. [Google Scholar] [CrossRef]
- Fox, R.; Yang, G.S.; Feurer, I.D.; Butler, M.G.; Thompson, T. Kinetic form discrimination in Prader-Willi syndrome. J. Intellect. Disabil. Res. 2001, 45, 317–325. [Google Scholar] [CrossRef]
- Cox, D.M.; Butler, M.G. The 15q11.2 BP1-BP2 microdeletion syndrome: A review. Int. J. Mol. Sci. 2015, 16, 4068–4082. [Google Scholar] [CrossRef] [Green Version]
- Burnside, R.D.; Pasion, R.; Mikhail, F.M.; Carroll, A.J.; Robin, N.H.; Youngs, E.L.; Gadi, I.K.; Keitges, E.; Jaswaney, V.L.; Papenhausen, P.R.; et al. Microdeletion/microduplication of proximal 15q11.2 between BP1 and BP2: A susceptibility region for neurological dysfunction including developmental and language delay. Hum. Genet. 2011, 130, 517–528. [Google Scholar] [CrossRef]
- Chai, J.H.; Locke, D.P.; Greally, J.M.; Knoll, J.H.; Ohta, T.; Dunai, J.; Yavor, A.; Eichler, E.E.; Nicholls, R.D. Identification of four highly conserved genes between breakpoint hotspots BP1 and BP2 of the Prader-Willi/Angelman syndromes deletion region that have undergone evolutionary transposition mediated by flanking duplicons. Am. J. Hum. Genet. 2003, 73, 898–925. [Google Scholar] [CrossRef] [Green Version]
- Dagli, A.; Buiting, K.; Williams, C.A. Molecular and Clinical Aspects of Angelman Syndrome. Mol. Syndromol. 2012, 2, 100–112. [Google Scholar] [CrossRef] [Green Version]
- Bonello, D.; Camilleri, F.; Calleja-Agius, J. Angelman Syndrome: Identification and Management. Neonatal. Netw. 2017, 36, 142–151. [Google Scholar] [CrossRef]
- Bittel, D.C.; Kibiryeva, N.; Butler, M.G. Expression of 4 genes between chromosome 15 breakpoints 1 and 2 and behavioral outcomes in Prader-Willi syndrome. Pediatrics 2006, 118, e1276–e1283. [Google Scholar] [CrossRef] [Green Version]
- Chen, C.P.; Lin, S.P.; Lee, C.L.; Chern, S.R.; Wu, P.S.; Chen, Y.N.; Chen, S.W.; Wang, W. Familial transmission of recurrent 15q11.2 (BP1-BP2) microdeletion encompassing NIPA1, NIPA2, CYFIP1, and TUBGCP5 associated with phenotypic variability in developmental, speech, and motor delay. Taiwan J. Obstet. Gynecol. 2017, 56, 93–97. [Google Scholar] [CrossRef]
- Clifton, N.E.; Thomas, K.L.; Wilkinson, L.S.; Hall, J.; Trent, S. FMRP and CYFIP1 at the Synapse and Their Role in Psychiatric Vulnerability. Complex Psychiatry 2020, 6, 5–19. [Google Scholar] [CrossRef] [Green Version]
- Salcedo-Arellano, M.J.; Dufour, B.; McLennan, Y.; Martinez-Cerdeno, V.; Hagerman, R. Fragile X syndrome and associated disorders: Clinical aspects and pathology. Neurobiol. Dis. 2020, 136, 104740. [Google Scholar] [CrossRef]
- Butler, M.G. Magnesium Supplement and the 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome: A Potential Treatment? Int. J. Mol. Sci. 2019, 20, 2914. [Google Scholar] [CrossRef] [Green Version]
- Butler, M.G.; Cowen, N.; Bhatnagar, A. Prader-Willi syndrome, deletion subtypes, and magnesium: Potential impact on clinical findings. Am. J. Med. Genet A 2022, 188, 3278–3286. [Google Scholar] [CrossRef] [PubMed]
- Davis, K.W.; Serrano, M.; Loddo, S.; Robinson, C.; Alesi, V.; Dallapiccola, B.; Novelli, A.; Butler, M.G. Parent-of-Origin Effects in 15q11.2 BP1-BP2 Microdeletion (Burnside-Butler) Syndrome. Int. J. Mol. Sci. 2019, 20, 1459. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Ho, K.S.; Wassman, E.R.; Baxter, A.L.; Hensel, C.H.; Martin, M.M.; Prasad, A.; Twede, H.; Vanzo, R.J.; Butler, M.G. Chromosomal Microarray Analysis of Consecutive Individuals with Autism Spectrum Disorders Using an Ultra-High Resolution Chromosomal Microarray Optimized for Neurodevelopmental Disorders. Int. J. Mol. Sci. 2016, 17, 2070. [Google Scholar] [CrossRef] [Green Version]
- Baldwin, I.; Shafer, R.L.; Hossain, W.A.; Gunewardena, S.; Veatch, O.J.; Mosconi, M.W.; Butler, M.G. Genomic, Clinical, and Behavioral Characterization of 15q11.2 BP1-BP2 Deletion (Burnside-Butler) Syndrome in Five Families. Int. J. Mol. Sci. 2021, 22, 1660. [Google Scholar] [CrossRef] [PubMed]
- Vanlerberghe, C.; Petit, F.; Malan, V.; Vincent-Delorme, C.; Bouquillon, S.; Boute, O.; Holder-Espinasse, M.; Delobel, B.; Duban, B.; Vallee, L.; et al. 15q11.2 microdeletion (BP1-BP2) and developmental delay, behaviour issues, epilepsy and congenital heart disease: A series of 52 patients. Eur. J. Med. Genet. 2015, 58, 140–147. [Google Scholar] [CrossRef] [PubMed]
- Farrell, M.; Lichtenstein, M.; Harner, M.K.; Crowley, J.J.; Filmyer, D.M.; Lázaro-Muñoz, G.; Dietterich, T.E.; Bruno, L.M.; Shaughnessy, R.A.; Biondi, T.F.; et al. Treatment-resistant psychotic symptoms and the 15q11.2 BP1-BP2 (Burnside-Butler) deletion syndrome: Case report and review of the literature. Transl. Psychiatry. 2020, 10, 42. [Google Scholar] [CrossRef] [Green Version]
- Jiang, Y.; Zhang, Y.; Zhang, P.; Sang, T.; Zhang, F.; Ji, T.; Huang, Q.; Xie, H.; Du, R.; Cai, B.; et al. NIPA2 located in 15q11.2 is mutated in patients with childhood absence epilepsy. Hum. Genet. 2012, 131, 1217–1224. [Google Scholar] [CrossRef]
- Picinelli, C.; Lintas, C.; Piras, I.S.; Gabriele, S.; Sacco, R.; Brogna, C.; Persico, A.M. Recurrent 15q11.2 BP1-BP2 microdeletions and microduplications in the etiology of neurodevelopmental disorders. Am. J. Med. Genet. B Neuropsychiatr. Genet. 2016, 171, 1088–1098. [Google Scholar] [CrossRef]
- Xie, H.; Zhang, Y.; Zhang, P.; Wang, J.; Wu, Y.; Wu, X.; Netoff, T.; Jiang, Y. Functional study of NIPA2 mutations identified from the patients with childhood absence epilepsy. PLoS ONE 2014, 9, e109749. [Google Scholar] [CrossRef]
- Stefanski, A.; Calle-López, Y.; Leu, C.; Pérez-Palma, E.; Pestana-Knight, E.; Lal, D. Clinical sequencing yield in epilepsy, autism spectrum disorder, and intellectual disability: A systematic review and meta-analysis. Epilepsia 2021, 62, 143–151. [Google Scholar] [CrossRef]
- Genovese, A.; Butler, M.G. Clinical Assessment, Genetics, and Treatment Approaches in Autism Spectrum Disorder (ASD). Int. J. Mol. Sci. 2020, 21, 4726. [Google Scholar] [CrossRef]
- Lord, C.; Brugha, T.S.; Charman, T.; Cusack, J.; Dumas, G.; Frazier, T.; Jones, E.J.H.; Jones, R.M.; Pickles, A.; State, M.W.; et al. Autism spectrum disorder. Nat. Rev. Dis. Primers 2020, 6, 5. [Google Scholar] [CrossRef]
- Rainier, S.; Chai, J.H.; Tokarz, D.; Nicholls, R.D.; Fink, J.K. NIPA1 gene mutations cause autosomal dominant hereditary spastic paraplegia (SPG6). Am. J. Hum. Genet. 2003, 73, 967–971. [Google Scholar] [CrossRef] [Green Version]
- Spagnoli, C.; Schiavoni, S.; Rizzi, S.; Salerno, G.G.; Frattini, D.; Koskenvuo, J.; Fusco, C. SPG6 (NIPA1 variant): A report of a case with early-onset complex hereditary spastic paraplegia and brief literature review. J. Clin. Neurosci. 2021, 94, 281–285. [Google Scholar] [CrossRef]
- Hagerman, R.J.; Berry-Kravis, E.; Hazlett, H.C.; Bailey, D.B., Jr.; Moine, H.; Kooy, R.F.; Tassone, F.; Gantois, I.; Sonenberg, N.; Mandel, J.L.; et al. Fragile X syndrome. Nat. Rev. Dis. Primers 2017, 3, 17065. [Google Scholar] [CrossRef]
- van der Meer, D.; Sønderby, I.E.; Kaufmann, T.; Walters, G.B.; Abdellaoui, A.; Ames, D.; Amunts, K.; Andersson, M.; Armstrong, N.J.; Bernard, M.; et al. Association of Copy Number Variation of the 15q11.2 BP1-BP2 Region With Cortical and Subcortical Morphology and Cognition. JAMA Psychiatry 2020, 77, 420–430. [Google Scholar] [PubMed] [Green Version]
- Chu, F.C.; Shaw, S.W.; Lee, C.H.; Lo, L.M.; Hsu, J.J.; Hung, T.H. Adverse Perinatal and Early Life Outcomes following 15q11.2 CNV Diagnosis. Genes 2021, 12, 1480. [Google Scholar] [CrossRef] [PubMed]
- Huang, X.; Chen, J.; Hu, W.; Li, L.; He, H.; Guo, H.; Liao, Q.; Ye, M.; Tang, D.; Dai, Y. A report on seven fetal cases associated with 15q11-q13 microdeletion and microduplication. Mol.Genet. Genomic. Med. 2021, 9, e160. [Google Scholar] [CrossRef] [PubMed]
- Williams, S.G.; Nakev, A.; Guo, H.; Frain, S.; Tenin, G.; Liakhovitskaia, A.; Saha, P.; Priest, J.R.; Hentges, K.E.; Keavney, B.D. Association of congenital cardiovascular malformation and neuropsychiatric phenotypes with 15q11.2 (BP1-BP2) deletion in the UK Biobank. Eur. J. Hum. Genet. 2020, 28, 1265–1273. [Google Scholar] [CrossRef] [PubMed]
- Usrey, K.M.; Williams, C.A.; Dasouki, M.; Fairbrother, L.C.; Butler, M.G. Congenital Arthrogryposis: An Extension of the 15q11.2 BP1-BP2 Microdeletion Syndrome? Case Rep. Genet. 2014, 2014, 127258. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Wong, D.; Johnson, S.M.; Young, D.; Iwamoto, L.; Sood, S.; Slavin, T.P. Expanding the BP1-BP2 15q11.2 Microdeletion Phenotype: Tracheoesophageal Fistula and Congenital Cataracts. Case Rep. Genet. 2013, 2013, 801094. [Google Scholar] [CrossRef] [PubMed]
- Silva, A.I.; Ulfarsson, M.O.; Stefansson, H.; Gustafsson, O.; Walters, G.B.; Linden, D.E.J.; Wilkinson, L.S.; Drakesmith, M.; Owen, M.J.; Hall, J.; et al. Reciprocal White Matter Changes Associated With Copy Number Variation at 15q11.2 BP1-BP2: A Diffusion Tensor Imaging Study. Biol. Psychiatry 2019, 85, 563–572. [Google Scholar] [CrossRef] [PubMed] [Green Version]
- Silva, A.I.; Haddon, J.E.; Ahmed Syed, Y.; Trent, S.; Lin, T.E.; Patel, Y.; Carter, J.; Haan, N.; Honey, R.C.; Humby, T.; et al. Cyfip1 haploinsufficient rats show white matter changes, myelin thinning, abnormal oligodendrocytes and behavioural inflexibility. Nat. Commun. 2019, 10, 3455. [Google Scholar] [CrossRef] [Green Version]
- Haan, N.; Westacott, L.J.; Carter, J.; Owen, M.J.; Gray, W.P.; Hall, J.; Wilkinson, L.S. Haploinsufficiency of the schizophrenia and autism risk gene Cyfip1 causes abnormal postnatal hippocampal neurogenesis through microglial and Arp2/3 mediated actin dependent mechanisms. Transl. Psychiatry 2021, 11, 313. [Google Scholar] [CrossRef]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. |
© 2023 by the author. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
Share and Cite
Butler, M.G. Prader–Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review. Int. J. Mol. Sci. 2023, 24, 4271. https://doi.org/10.3390/ijms24054271
Butler MG. Prader–Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review. International Journal of Molecular Sciences. 2023; 24(5):4271. https://doi.org/10.3390/ijms24054271
Chicago/Turabian StyleButler, Merlin G. 2023. "Prader–Willi Syndrome and Chromosome 15q11.2 BP1-BP2 Region: A Review" International Journal of Molecular Sciences 24, no. 5: 4271. https://doi.org/10.3390/ijms24054271