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3. Recycling of memory B cells between germinal center and lymph node subcapsular sinus supports affinity maturation to antigenic drift

4. Dissecting the contribution of human chromosome 21 syntenic regions to recognition memory processes in adult and aged mouse models of Down syndrome.

5. Increased dosage of DYRK1A leads to congenital heart defects in a mouse model of Down syndrome

6. Maternal iron deficiency perturbs embryonic cardiovascular development in mice

8. Investigating Brain Alterations in the Dp1Tyb Mouse Model of Down Syndrome

9. Genetic dissection of triplicated chromosome 21 orthologs yields varying skeletal traits in Down syndrome model mice

10. NKG2D triggers cytotoxicity in mouse NK cells lacking DAP12 or Syk family kinases.

15. Craniofacial dysmorphology in Down syndrome is caused by increased dosage of Dyrk1a and at least three other genes.

22. Comprehensive phenotypic analysis of the Dp1Tyb mouse strain reveals a broad range of Down syndrome-related phenotypes

26. Memory-like B cells emerging from germinal centres recycle through the subcapsular sinus

27. Species-specific pace of development is associated with differences in protein stability

28. Maternal iron deficiency perturbs embryonic cardiovascular development

29. Critical role of WNK1 in MYC-dependent early thymocyte development

30. Tumour angiogenesis is reduced in the Tc1 mouse model of Down’s syndrome

31. An Aneuploid Mouse Strain Carrying Human Chromosome 21 with Down Syndrome Phenotypes

36. Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP

40. Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models.

46. Analysis of motor dysfunction in Down Syndrome reveals motor neuron degeneration

48. Fully-automated μMRI morphometric phenotyping of the Tc1 mouse model of Down Syndrome

49. Tc1 mouse model of trisomy-21 dissociates properties of short- and long-term recognition memory

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