David A. Wassarman

Localizing transcription factors on chromatin by immunofluorescence.

The SIN3/RPD3 deacetylase complex is essential for G(2) phase cell cycle progression and regulation of SMRTER corepressor levels.

The SIN3 deacetylase complex represses genes encoding mitochondrial proteins: implications for the regulation of energy metabolism.

TAF1 activates transcription by phosphorylation of serine 33 in histone H2B.

DNA binding properties of TAF1 isoforms with two AT-hooks.

ATM and ATR pathways signal alternative splicing of Drosophila TAF1 pre-mRNA in response to DNA damage.

Nucleolar colocalization of TAF1 and testis-specific TAFs during Drosophila spermatogenesis.

Mutations in String/CDC25 inhibit cell cycle re-entry and neurodegeneration in a Drosophila model of Ataxia telangiectasia.

Cyclic Disulfides as Functional Mimics of the Histone Deacetylase Inhibitor FK-228.

A DNA damage signal activates and derepresses exon inclusion in Drosophila TAF1 alternative splicing.

Control of alternative splicing by signal-dependent degradation of splicing-regulatory proteins.

Promoting developmental transcription.

Ubiquilin modifies TDP-43 toxicity in a Drosophila model of amyotrophic lateral sclerosis (ALS).

The effect of ATM knockdown on ionizing radiation-induced neuronal cell cycle reentry in Drosophila.

ATM kinase inhibition in glial cells activates the innate immune response and causes neurodegeneration in Drosophila.

Drosophila innate immune response pathways moonlight in neurodegeneration.

The Drosophila Translational Control Element (TCE) is required for high-level transcription of many genes that are specifically expressed in testes.

The innate immune response transcription factor relish is necessary for neurodegeneration in a Drosophila model of ataxia-telangiectasia.

A Drosophila model of closed head traumatic brain injury.

Death following traumatic brain injury in Drosophila is associated with intestinal barrier dysfunction.

The gut reaction to traumatic brain injury.

Age and Diet Affect Genetically Separable Secondary Injuries that Cause Acute Mortality Following Traumatic Brain Injury in Drosophila.

A pharmacological screen for compounds that rescue the developmental lethality of a Drosophila ATM mutant.

Genetic variability affects absolute and relative potencies and kinetics of the anesthetics isoflurane and sevoflurane in Drosophila melanogaster.

Anesthetics Influence Mortality in a Drosophila Model of Blunt Trauma With Traumatic Brain Injury.

Ageing and genetic background influence anaesthetic effects in a D. melanogaster model of blunt trauma with brain injury.

Loss of the Antimicrobial Peptide Metchnikowin Protects Against Traumatic Brain Injury Outcomes in .

Mitochondrial Complex I Mutations Predispose Drosophila to Isoflurane Neurotoxicity.

Interactions among Genetic Background, Anesthetic Agent, and Oxygen Concentration Shape Blunt Traumatic Brain Injury Outcomes in .

Survival Following Traumatic Brain Injury in Is Increased by Heterozygosity for a Mutation of the NF-κB Innate Immune Response Transcription Factor Relish.

Effects of blunt force injuries in third-instar larvae persist through metamorphosis and reduce adult lifespan.

Ketogenic diet reduces early mortality following traumatic brain injury in Drosophila via the PPARγ ortholog Eip75B.

Beta-blockers reduce intestinal permeability and early mortality following traumatic brain injury in .

Anesthetic Preconditioning of Traumatic Brain Injury Is Ineffective in a Drosophila Model of Obesity.

Lissencephaly-1 mutations enhance traumatic brain injury outcomes in Drosophila.

Mutations in Complex I of the Mitochondrial Electron-Transport Chain Sensitize the Fruit Fly () to Ether and Non-Ether Volatile Anesthetics.