“Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing”. Nature Genetics40 (12): 1413–5. (December 2008). doi:10.1038/ng.259. PMID18978789.
“Understanding alternative splicing: towards a cellular code”. Nature Reviews. Molecular Cell Biology6 (5): 386–98. (May 2005). doi:10.1038/nrm1645. PMID15956978.
“Alternative splicing in cancer: noise, functional, or systematic?”. The International Journal of Biochemistry & Cell Biology39 (7-8): 1432–49. (2007). doi:10.1016/j.biocel.2007.02.016. PMID17416541.
“Complex transcriptional units: diversity in gene expression by alternative RNA processing”. Annual Review of Biochemistry55 (1): 1091–117. (1986). doi:10.1146/annurev.bi.55.070186.005303. PMID3017190.
“Steps in the processing of Ad2 mRNA: poly(A)+ nuclear sequences are conserved and poly(A) addition precedes splicing”. Cell15 (4): 1477–93. (December 1978). doi:10.1016/0092-8674(78)90071-5. PMID729004.
“The role of DNA rearrangement and alternative RNA processing in the expression of immunoglobulin delta genes”. Cell24 (2): 353–65. (May 1981). doi:10.1016/0092-8674(81)90325-1. PMID6786756.
“Drosophila Dscam is an axon guidance receptor exhibiting extraordinary molecular diversity”. Cell101 (6): 671–84. (June 2000). doi:10.1016/S0092-8674(00)80878-8. PMID10892653.
“The Function of DNA Methylation Marks in Social Insects”. Frontiers in Ecology and Evolution4: 57. (2016). doi:10.3389/fevo.2016.00057.
“Physiological and molecular mechanisms of nutrition in honey bees.”. Advances in insect physiology. 49. Academic Press. (January 2015). pp. 25–58. doi:10.1016/bs.aiip.2015.06.002
“Assembly of specific SR protein complexes on distinct regulatory elements of the Drosophila doublesex splicing enhancer”. Genes & Development10 (16): 2089–101. (August 1996). doi:10.1101/gad.10.16.2089. PMID8769651.
“Expression of CD95 (Fas) in sun-exposed human skin and cutaneous carcinomas”. Cancer94 (3): 814–9. (February 2002). doi:10.1002/cncr.10277. PMID11857317.
“Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition”. Molecular Cell19 (4): 475–84. (August 2005). doi:10.1016/j.molcel.2005.06.015. PMID16109372.
“SC35 and heterogeneous nuclear ribonucleoprotein A/B proteins bind to a juxtaposed exonic splicing enhancer/exonic splicing silencer element to regulate HIV-1 tat exon 2 splicing”. The Journal of Biological Chemistry279 (11): 10077–84. (March 2004). doi:10.1074/jbc.M312743200. PMID14703516.
“A second exon splicing silencer within human immunodeficiency virus type 1 tat exon 2 represses splicing of Tat mRNA and binds protein hnRNP H”. The Journal of Biological Chemistry276 (44): 40464–75. (November 2001). doi:10.1074/jbc.M104070200. PMID11526107.
“Analysis of expressed sequence tags indicates 35,000 human genes”. Nature Genetics25 (2): 232–4. (June 2000). doi:10.1038/76115. PMID10835644.
“Estimate of human gene number provided by genome-wide analysis using Tetraodon nigroviridis DNA sequence”. Nature Genetics25 (2): 235–8. (June 2000). doi:10.1038/76118. PMID10835645.
“Insights into the connection between cancer and alternative splicing”. Trends in Genetics24 (1): 7–10. (January 2008). doi:10.1016/j.tig.2007.10.001. PMID18054115.
“Cell motility is controlled by SF2/ASF through alternative splicing of the Ron protooncogene”. Molecular Cell20 (6): 881–90. (December 2005). doi:10.1016/j.molcel.2005.10.026. PMID16364913.
“Identification of alternatively spliced mRNA variants related to cancers by genome-wide ESTs alignment”. Oncogene23 (17): 3013–23. (April 2004). doi:10.1038/sj.onc.1207362. PMID15048092.
“Abnormally spliced beta-globin mRNAs: a single point mutation generates transcripts sensitive and insensitive to nonsense-mediated mRNA decay”. Blood99 (5): 1811–6. (March 2002). doi:10.1182/blood.V99.5.1811. PMID11861299.
“Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. The American Journal of Drug and Alcohol Abuse40 (6): 428–37. (November 2014). doi:10.3109/00952990.2014.933840. PMID25083822. "ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."
“Revealing global regulatory features of mammalian alternative splicing using a quantitative microarray platform”. Molecular Cell16 (6): 929–41. (December 2004). doi:10.1016/j.molcel.2004.12.004. PMID15610736.
“Deep surveying of alternative splicing complexity in the human transcriptome by high-throughput sequencing”. Nature Genetics40 (12): 1413–5. (December 2008). doi:10.1038/ng.259. PMID18978789.
“Understanding alternative splicing: towards a cellular code”. Nature Reviews. Molecular Cell Biology6 (5): 386–98. (May 2005). doi:10.1038/nrm1645. PMID15956978.
“Alternative splicing in cancer: noise, functional, or systematic?”. The International Journal of Biochemistry & Cell Biology39 (7-8): 1432–49. (2007). doi:10.1016/j.biocel.2007.02.016. PMID17416541.
“Complex transcriptional units: diversity in gene expression by alternative RNA processing”. Annual Review of Biochemistry55 (1): 1091–117. (1986). doi:10.1146/annurev.bi.55.070186.005303. PMID3017190.
“Steps in the processing of Ad2 mRNA: poly(A)+ nuclear sequences are conserved and poly(A) addition precedes splicing”. Cell15 (4): 1477–93. (December 1978). doi:10.1016/0092-8674(78)90071-5. PMID729004.
“The role of DNA rearrangement and alternative RNA processing in the expression of immunoglobulin delta genes”. Cell24 (2): 353–65. (May 1981). doi:10.1016/0092-8674(81)90325-1. PMID6786756.
“Drosophila Dscam is an axon guidance receptor exhibiting extraordinary molecular diversity”. Cell101 (6): 671–84. (June 2000). doi:10.1016/S0092-8674(00)80878-8. PMID10892653.
“Assembly of specific SR protein complexes on distinct regulatory elements of the Drosophila doublesex splicing enhancer”. Genes & Development10 (16): 2089–101. (August 1996). doi:10.1101/gad.10.16.2089. PMID8769651.
“Expression of CD95 (Fas) in sun-exposed human skin and cutaneous carcinomas”. Cancer94 (3): 814–9. (February 2002). doi:10.1002/cncr.10277. PMID11857317.
“Regulation of Fas alternative splicing by antagonistic effects of TIA-1 and PTB on exon definition”. Molecular Cell19 (4): 475–84. (August 2005). doi:10.1016/j.molcel.2005.06.015. PMID16109372.
“SC35 and heterogeneous nuclear ribonucleoprotein A/B proteins bind to a juxtaposed exonic splicing enhancer/exonic splicing silencer element to regulate HIV-1 tat exon 2 splicing”. The Journal of Biological Chemistry279 (11): 10077–84. (March 2004). doi:10.1074/jbc.M312743200. PMID14703516.
“A second exon splicing silencer within human immunodeficiency virus type 1 tat exon 2 represses splicing of Tat mRNA and binds protein hnRNP H”. The Journal of Biological Chemistry276 (44): 40464–75. (November 2001). doi:10.1074/jbc.M104070200. PMID11526107.
“Analysis of expressed sequence tags indicates 35,000 human genes”. Nature Genetics25 (2): 232–4. (June 2000). doi:10.1038/76115. PMID10835644.
“Estimate of human gene number provided by genome-wide analysis using Tetraodon nigroviridis DNA sequence”. Nature Genetics25 (2): 235–8. (June 2000). doi:10.1038/76118. PMID10835645.
“Insights into the connection between cancer and alternative splicing”. Trends in Genetics24 (1): 7–10. (January 2008). doi:10.1016/j.tig.2007.10.001. PMID18054115.
“Cell motility is controlled by SF2/ASF through alternative splicing of the Ron protooncogene”. Molecular Cell20 (6): 881–90. (December 2005). doi:10.1016/j.molcel.2005.10.026. PMID16364913.
“Identification of alternatively spliced mRNA variants related to cancers by genome-wide ESTs alignment”. Oncogene23 (17): 3013–23. (April 2004). doi:10.1038/sj.onc.1207362. PMID15048092.
“Abnormally spliced beta-globin mRNAs: a single point mutation generates transcripts sensitive and insensitive to nonsense-mediated mRNA decay”. Blood99 (5): 1811–6. (March 2002). doi:10.1182/blood.V99.5.1811. PMID11861299.
“Cellular basis of memory for addiction”. Dialogues in Clinical Neuroscience15 (4): 431–43. (December 2013). PMC3898681. PMID24459410. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681/. "DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement"
“Molecular neurobiology of addiction: what's all the (Δ)FosB about?”. The American Journal of Drug and Alcohol Abuse40 (6): 428–37. (November 2014). doi:10.3109/00952990.2014.933840. PMID25083822. "ΔFosB is an essential transcription factor implicated in the molecular and behavioral pathways of addiction following repeated drug exposure. The formation of ΔFosB in multiple brain regions, and the molecular pathway leading to the formation of AP-1 complexes is well understood. The establishment of a functional purpose for ΔFosB has allowed further determination as to some of the key aspects of its molecular cascades, involving effectors such as GluR2 (87,88), Cdk5 (93) and NFkB (100). Moreover, many of these molecular changes identified are now directly linked to the structural, physiological and behavioral changes observed following chronic drug exposure (60,95,97,102). New frontiers of research investigating the molecular roles of ΔFosB have been opened by epigenetic studies, and recent advances have illustrated the role of ΔFosB acting on DNA and histones, truly as a ‘‘molecular switch’’ (34). As a consequence of our improved understanding of ΔFosB in addiction, it is possible to evaluate the addictive potential of current medications (119), as well as use it as a biomarker for assessing the efficacy of therapeutic interventions (121,122,124). Some of these proposed interventions have limitations (125) or are in their infancy (75). However, it is hoped that some of these preliminary findings may lead to innovative treatments, which are much needed in addiction."
“Epigenetic regulation in drug addiction”. Annals of Agricultural and Environmental Medicine19 (3): 491–6. (2012). PMID23020045. "For these reasons, ΔFosB is considered a primary and causative transcription factor in creating new neural connections in the reward centre, prefrontal cortex, and other regions of the limbic system. This is reflected in the increased, stable and long-lasting level of sensitivity to cocaine and other drugs, and tendency to relapse even after long periods of abstinence. These newly constructed networks function very efficiently via new pathways as soon as drugs of abuse are further taken"
“Revealing global regulatory features of mammalian alternative splicing using a quantitative microarray platform”. Molecular Cell16 (6): 929–41. (December 2004). doi:10.1016/j.molcel.2004.12.004. PMID15610736.
“Cellular basis of memory for addiction”. Dialogues in Clinical Neuroscience15 (4): 431–43. (December 2013). PMC3898681. PMID24459410. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3898681/. "DESPITE THE IMPORTANCE OF NUMEROUS PSYCHOSOCIAL FACTORS, AT ITS CORE, DRUG ADDICTION INVOLVES A BIOLOGICAL PROCESS: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type NAc neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement"
