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  1. Data from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  2. Data from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  3. Supplementary Figure S1 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  4. Supplementary Figure S1 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  5. Supplementary Figure S2 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  6. Supplementary Figure S2 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  7. Supplementary Figure S3 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  8. Supplementary Figure S3 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  9. Supplementary Figure S4 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  10. Supplementary Figure S4 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  11. Supplementary Figure S5 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  12. Supplementary Figure S5 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  13. Supplementary Table S1 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  14. Supplementary Table S1 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  15. Supplementary Table S2 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  16. Supplementary Table S2 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  17. Supplementary Table S3 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  18. Supplementary Table S3 from Targeting NANOG and FAK via Cx26-derived Cell-penetrating Peptides in Triple-negative Breast Cancer
  19. Data from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  20. Data from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  21. Supplementary Figure 1 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  22. Supplementary Figure 1 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  23. Supplementary Figure 2 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  24. Supplementary Figure 2 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  25. Supplementary Figure 3 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  26. Supplementary Figure 3 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  27. Supplementary Figure 4 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  28. Supplementary Figure 4 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  29. Supplementary Figure 5 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  30. Supplementary Figure 5 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  31. Supplementary Figure 6 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  32. Supplementary Figure 6 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  33. Supplementary Figure 7 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  34. Supplementary Figure 7 from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  35. Supplementary Information from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  36. Supplementary Information from Prostate Cancer Progression Relies on the Mitotic Kinase Citron Kinase
  37. Prostate cancer progression relies on the mitotic kinase citron kinase
  38. Targeting NANOG and FAK via Cx26-derived cell-penetrating peptides in triple-negative breast cancer
  39. Diversity in Androgen Receptor Action Among Treatment-naïve Prostate Cancers Is Reflected in Treatment Response Predictions and Molecular Subtypes
  40. Abstract 390: Prostate cancer progression depends on the activity of the mitotic kinase citron kinase
  41. Abstract 390: Prostate cancer progression depends on the activity of the mitotic kinase citron kinase
  42. Protein Kinase N1 control of androgen-responsive serum response factor action provides rationale for novel prostate cancer treatment strategy
  43. Abstract 3745: Inhibition of Protein Kinase N1 prevents control of AR over SRF action in advanced prostate cancer
  44. Abstract LB-211: The cardiac transcription factor Nkx2-5 contributes to SRF-dependent AR action in prostate cancer
  45. A B3GALT6 variant in patient originally described as Al‐Gazali syndrome and implicating the endoplasmic reticulum quality control in the mechanism of some β3GalT6‐pathy mutations
  46. Compound heterozygous variants in the multiple PDZ domain protein (MPDZ) cause a case of mild non-progressive communicating hydrocephalus
  47. Defect in phosphoinositide signalling through a homozygous variant inPLCB3causes a new form of spondylometaphyseal dysplasia with corneal dystrophy
  48. A comprehensive analysis of coregulator recruitment, androgen receptor function and gene expression in prostate cancer
  49. A homozygous splicing mutation in ELAC2 suggests phenotypic variability including intellectual disability with minimal cardiac involvement
  50. Cover Image, Volume 170A, Number 8, August 2016
  51. A recessive syndrome of intellectual disability, moderate overgrowth, and renal dysplasia predisposing to Wilms tumor is caused by a mutation inFIBPgene
  52. Gonadal mosaicism in ARID1B gene causes intellectual disability and dysmorphic features in three siblings
  53. A Novel Single-Nucleotide Deletion (c.1020delA) in NSUN2 Causes Intellectual Disability in an Emirati Child
  54. A novel splice site deletion in the OFD1 gene is responsible for oral–facial–digital syndrome type1 in an Emirati child
  55. New Arab family with cerebral dysgenesis, neuropathy, ichthyosis and keratoderma syndrome suggests a possible founder effect for the c.223delG mutation
  56. A Novel Whole Exon Deletion in WWOX Gene Causes Early Epilepsy, Intellectual Disability and Optic Atrophy
  57. Transaldolase deficiency caused by the homozygous p.R192C mutation of the TALDO1 gene in four Emirati patients with considerable phenotypic variability
  58. Mutation spectrum of Joubert syndrome and related disorders among Arabs
  59. Asparagine synthetase deficiency detected by whole exome sequencing causes congenital microcephaly, epileptic encephalopathy and psychomotor delay
  60. Identification of the Cellular Mechanisms That Modulate Trafficking of Frizzled Family Receptor 4 (FZD4) Missense Mutants Associated With Familial Exudative Vitreoretinopathy
  61. METTL23, a transcriptional partner of GABPA, is essential for human cognition
  62. The mutational spectrum of the NF1 gene in neurofibromatosis type I patients from UAE
  63. Analysis of two Arab families reveals additional support for a DFNB2 nonsyndromic phenotype of MYO7A
  64. Determination of the CCR5∆32 frequency in Emiratis and Tunisians and the screening of the CCR5 gene for novel alleles in Emiratis
  65. Posterior microphthalmia and nanophthalmia in Tunisia caused by a founder c.1059_1066insC mutation of the PRSS56 gene
  66. Novel mutations in ADAMTSL2 gene underlying geleophysic dysplasia in families from United Arab Emirates
  67. Mutations in DDHD2, Encoding an Intracellular Phospholipase A1, Cause a Recessive Form of Complex Hereditary Spastic Paraplegia
  68. Clinical and molecular analysis of isovaleric acidemia patients in the United Arab Emirates reveals remarkable phenotypes and four novel mutations in the IVD gene
  69. A Novel Aberrant Splice Site Mutation in RAB23 Leads to an Eight Nucleotide Deletion in the mRNA and Is Responsible for Carpenter Syndrome in a Consanguineous Emirati Family
  70. Alteration of the serine protease PRSS56 causes angle-closure glaucoma in mice and posterior microphthalmia in humans and mice
  71. A genome-wide linkage scan in Tunisian families identifies a novel locus for non-syndromic posterior microphthalmia to chromosome 2q37.1