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23 results on '"Mohadeseh Mehrabian"'

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1. Bridging the gap between in vitro and in vivo models: a way forward to clinical translation of mitochondrial transplantation in acute disease states

2. Cardiac glycoside-mediated turnover of Na, K-ATPases as a rational approach to reducing cell surface levels of the cellular prion protein.

3. The cellular prion protein interacts with and promotes the activity of Na,K-ATPases.

4. The human brain somatostatin interactome: SST binds selectively to P-type family ATPases.

5. NCAM1 Polysialylation

6. Prion Protein Deficiency Causes Diverse Proteome Shifts in Cell Models That Escape Detection in Brain Tissue.

7. The Prion Protein Controls Polysialylation of Neural Cell Adhesion Molecule 1 during Cellular Morphogenesis.

8. CRISPR-Cas9-based knockout of the prion protein and its effect on the proteome.

9. The ZIP5 ectodomain co-localizes with PrP and may acquire a PrP-like fold that assembles into a dimer.

10. SPG11 Presenting with Tremor

11. The <scp>IDIP</scp> framework for assessing protein function and its application to the prion protein

12. The aminoglycoside G418 hinders de novo prion infection in cultured cells

13. The prion protein is embedded in a molecular environment that modulates transforming growth factor β and integrin signaling

14. The human brain somatostatin interactome: SST binds selectively to P-type family ATPases

15. The Human Tau Interactome: Binding to the Ribonucleoproteome, and Impaired Binding of the Proline-to-Leucine Mutant at Position 301 (P301L) to Chaperones and the Proteasome

16. The frequency of spinocerebellar ataxia type 23 in a UK population

17. Quantitative Structure-Activity Relationships and Docking Studies of Calcitonin Gene-Related Peptide Antagonists

18. Prion Protein Deficiency Causes Diverse Proteome Shifts in Cell Models That Escape Detection in Brain Tissue

19. An emerging role of the cellular prion protein as a modulator of a morphogenetic program underlying epithelial-to-mesenchymal transition

20. CRISPR-Cas9-based knockout of the prion protein and its effect on the proteome

21. The ZIP5 ectodomain co-localizes with PrP and may acquire a PrP-like fold that assembles into a dimer

22. LIV-1 ZIP ectodomain shedding in prion-infected mice resembles cellular response to transition metal starvation

23. Quantitative structure-activity relationships and docking studies of calcitonin gene-related peptide antagonists

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