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  1. Epigenetic mechanisms linking early-life adversities and mental health
  2. Oxidative stress associated with spatial memory impairment and social olfactory deterioration in female mice reveals premature aging aroused by perinatal protein malnutrition
  3. Early life stress induces visual dysfunction and retinal structural alterations in adult mice
  4. Impaired social cognition caused by perinatal protein malnutrition evokes neurodevelopmental disorder symptoms and is intergenerationally transmitted
  5. Limited contextual memory and transcriptional dysregulation in the medial prefrontal cortex of mice exposed to early protein malnutrition are intergenerationally transmitted
  6. Perinatal protein malnutrition results in genome-wide disruptions of 5-hydroxymethylcytosine at regions that can be restored to control levels by an enriched environment
  7. Perinatal protein malnutrition induces the emergence of enduring effects and age-related impairment behaviors, increasing the death risk in a mouse model
  8. Nutritional stress timing differentially programs cognitive abilities in young adult male mice
  9. Effects of cocaine base paste on anxiety-like behavior and immediate-early gene expression in nucleus accumbens and medial prefrontal cortex of female mice
  10. Exposure to enriched environment rescues anxiety-like behavior and miRNA deregulated expression induced by perinatal malnutrition while altering oligodendrocyte morphology
  11. Multimodal neurocognitive markers of interoceptive tuning in smoked cocaine
  12. Intergenerational transmission of maternal care deficiency and offspring development delay induced by perinatal protein malnutrition
  13. Altered miRNA biogenesis in early life malnutrition
  14. Oxidative stress-induced CREB upregulation promotes DNA damage repair prior to neuronal cell death protection
  15. Depressive-like behavior in perinatal malnutrition
  16. E2F transcription factor and maintenance of genomic stability
  17. Nuclear translocation of p19INK4d in response to oxidative DNA damage promotes chromatin relaxation
  18. CDK5-mediated phosphorylation of p19INK4d avoids DNA damage-induced neurodegeneration in mouse hippocampus and prevents loss of cognitive functions
  19. p19INK4d is involved in the cellular senescence mechanism contributing to heterochromatin formation
  20. Early protein malnutrition negatively impacts physical growth and neurological reflexes and evokes anxiety and depressive-like behaviors
  21. Chromatin Relaxation-Mediated Induction of p19INK4d Increases the Ability of Cells to Repair Damaged DNA
  22. Inhibitor of growth 1 (ING1) acts at early steps of multiple DNA repair pathways
  23. CDK2 and PKA Mediated-Sequential Phosphorylation Is Critical for p19INK4d Function in the DNA Damage Response
  24. E2F1 induces p19INK4d, a protein involved in the DNA damage response, following UV irradiation
  25. E2F1-Mediated Upregulation of p19INK4d Determines Its Periodic Expression during Cell Cycle and Regulates Cellular Proliferation
  26. Transcriptional upregulation of p19INK4d upon diverse genotoxic stress is critical for optimal DNA damage response
  27. E2F1 transcription is induced by genotoxic stress through ATM/ATR activation
  28. Cell cycle inhibitor, p19INK4d, promotes cell survival and decreases chromosomal aberrations after genotoxic insult due to enhanced DNA repair
  29. INK4 proteins, a family of mammalian CDK inhibitors with novel biological functions
  30. Cell growth-dependent subcellular localization of p8
  31. Repression of 5-aminolevulinate synthase gene by the potent tumor promoter, TPA, involves multiple signal transduction pathways
  32. Induction of p19INK4d in response to ultraviolet light improves DNA repair and confers resistance to apoptosis in neuroblastoma cells
  33. Hepatic Nuclear Factor 3 and Nuclear Factor 1 Regulate 5-Aminolevulinate Synthase Gene Expression and Are Involved in Insulin Repression
  34. Inhibitory Effect of AP-1 Complex on 5-Aminolevulinate Synthase Gene Expression through Sequestration of cAMP-response Element Protein (CRE)-binding Protein (CBP) Coactivator
  35. Cloning and expression of the human p8, a nuclear protein with mitogenic activity
  36. Phosphatidylinositol 3-Kinase and Ras/Mitogen-Activated Protein Kinase Signaling Pathways Are Required for the Regulation of 5-Aminolevulinate Synthase Gene Expression by Insulin
  37. Transforming growth factor β-1 enhances Smad transcriptional activity through activation of p8 gene expression
  38. 5-Aminolaevulinate synthase gene promoter contains two cAMP-response element (CRE)-like sites that confer positive and negative responsiveness to CRE-binding protein (CREB)
  39. Human p8 Is a HMG-I/Y-like Protein with DNA Binding Activity Enhanced by Phosphorylation
  40. Transcriptional Regulation of 5-Aminolevulinate Synthase by Phenobarbital and cAMP-Dependent Protein Kinase
  41. Structural and functional characterization of the mouse p8 gene: promotion of transcription by the CAAT-enhancer binding protein α (C/EBPα) and C/EBPβ trans-acting factors involves a C/EBP cis-acting element and other regions of the promoter
  42. Insulin Inhibits δ-Aminolevulinate Synthase Gene Expression in Rat Hepatocytes and Human Hepatoma Cells
  43. Evidence That Protein Kinase C Is Involved in δ-Aminolevulinate Synthase Expression in Rat Hepatocytes
  44. cAMP regulation of phenobarbital-mediated induction of δ-aminolevulinate synthase mRNA in hepatocytes from normal and experimental diabetic rats
  45. Regulation of phenobarbital-induced ferrochelatase mRNA activity by dibutyryl cAMP and glucose in normal and diabetic rat hepatocytes
  46. Studies on induction of δ-aminolevulinic acid synthase, ferrochelatase, cytochrome P-450 and cyclic AMP by phenformin
  47. Studies on regulatory mechanisms of heme biosynthesis in hepatocytes from normal and experimental-diabetic rats. Role of insulin
  48. Studies on regulatory mechanisms of heme biosynthesis in hepatocytes from normal and experimental-diabetic rats. Role of cAMP
  49. Purification and characterization of ferro- and cobalto-chelatases
  50. Studies on regulatory mechanisms of heme biosynthesis in hepatocytes from experimental-diabetic rats
  51. Effect of glucose on induction of δ-aminolevulinic acid synthase, ferrochelatase and cytochrome P-450 hemoproteins in isolated rat hepatocytes by phenobarbital and lead
  52. Effect of glucose on the induction of δ-aminolevulinic acid synthase and ferrochelatase in isolated rat hepatocytes by allylisopropylacetamide