On Sunday, April 20th 2025, starting 8:30am GMT, there will be maintenance work that will involve the website being unavailable during parts of the day. We apologize for any inconvenience this may cause and appreciate your understanding.
We noted you are experiencing viewing problems
-
Check with your IT department that JWPlatform, JWPlayer and Amazon AWS & CloudFront are not being blocked by your network. The relevant domains are *.jwplatform.com, *.jwpsrv.com, *.jwpcdn.com, jwpltx.com, jwpsrv.a.ssl.fastly.net, *.amazonaws.com and *.cloudfront.net. The relevant ports are 80 and 443.
-
Check the following talk links to see which ones work correctly:
Auto Mode
HTTP Progressive Download Send us your results from the above test links at access@hstalks.com and we will contact you with further advice on troubleshooting your viewing problems. -
No luck yet? More tips for troubleshooting viewing issues
-
Contact HST Support access@hstalks.com
-
Please review our troubleshooting guide for tips and advice on resolving your viewing problems.
-
For additional help, please don't hesitate to contact HST support access@hstalks.com
We hope you have enjoyed this limited-length demo
This is a limited length demo talk; you may
login or
review methods of
obtaining more access.
Printable Handouts
Navigable Slide Index
- Introduction
- Molecular redundancy
- Redundant molecules replace disrupted genes
- Genomic structure of the CD44 molecule
- CD44 - alternative splicing
- CD44 ligands
- Dr. Lora Eshkar Sebban
- CD44 functions
- The three steps model of Dr. Springer
- Rolling and migration of CD44-positive cells
- The migration process
- Anti-CD44 mAbs reduce pathological activities
- Anti-CD44 mAbs reduce diabetogenic activity
- Anti-CD44 mAbs reduce arthritic activity
- Generation of CIA model experimental protocol
- In-vivo efficacy in CIA model
- The CD44-dependency of CIA
- CIA is a CD44-dependent disease
- Effect of type 2 collagen injection
- CD44 DNA analysis of CD44-deficient mice
- Flow cytometry: CD44-deficient mice spleen cells
- Sensitivity to CIA: CD44-knockout vs. WT mice
- Histopathology of joints from CD44+/+ and -/- mice
- Photo imaging of histochemical staining revealed
- CD44-deficient mice: hyaluronic acid accumulation
- Anti-CD44 mAb inhibits CIA in WT DBA/1 mice
- Support of collagen-induced arthritis in mice
- Inhibition of CIA by hyaluronidase in WT mice
- Inhibition of CIA in WT and CD44-K/O mice
- CD44-deficient spleen cells bind to HA
- HA-binding protein compensates for CD44 in mice
- The HA binding protein that compensates for CD44
- RHAMM: receptor for hyaluronan-mediated motility
- RHAMM reagents
- RHAMM regulation in CD44-deficient mice (1)
- RHAMM regulation in CD44-deficient mice (2)
- Transwell migration assay
- Spleen cells migration from CD44-deficient mice
- Anti-RHAMM inhibits mice spleen cells migration
- Anti-RHAMM mAb and soluble RHAMM inhibit CIA
- CD44 affect the disease activity
- CD44 deletion affect embryonic development
- RHAMM regulation after CD44 genetic deletion
- RHAMM functions
- Interpretation of the redundancy mechanism
- Disease-specific CD44 (1)
- Disease-specific CD44 (2)
- Exploring CD44 isoforms
- Genomic sequence of: V4/V5 junction, CD44vRA
- Single amino acid exchange and proteins function
- Levels of CD44vRA Abs in mice splenocytes
- Binding F8:33 anti-CD44 mAb to synovial cells
- Synovial fluid cells from an RA and OA patient
- F8:33 anti-CD44vRA mAb bindings
- Does anti-CD44vRA Ab promote apoptosis?
- Anti-CD44vRA mAb induces apoptosis in RA (1)
- Anti-CD44vRA mAb induces apoptosis in RA (2)
- Disease-specific CD44
- Conclusions
- Acknowledgements
- Albert Einstein's wisdom...
- References
- References
Topics Covered
- CD44 and RHAMM (receptor for hyaluronan-mediated motility) are cell adhesion and cell homing receptors
- Cell migration
- Generation of different CD44 isoforms
- RHAMM also supports cell motility and is engaged in intracellular signalling
- Collagen-induced arthritis and type 1 diabetes are CD44-dependent pathologies
- Molecular redundancy
- CD44 targeting by anti-CD44 mAb may eradicate not only malignant cells and destructive inflammatory cells but also CD44-expressing normal cells which are committed to physiological functions
Links
Series:
Categories:
Therapeutic Areas:
Talk Citation
Naor, D. (2017, November 28). CD44 genetic deletion enhances and CD44 antibody targeting attenuates autoimmune inflammation [Video file]. In The Biomedical & Life Sciences Collection, Henry Stewart Talks. Retrieved April 15, 2025, from https://doi.org/10.69645/SZIG6778.Export Citation (RIS)
Publication History
Financial Disclosures
- Prof. David Naor has not informed HSTalks of any commercial/financial relationship that it is appropriate to disclose.
CD44 genetic deletion enhances and CD44 antibody targeting attenuates autoimmune inflammation
A selection of talks on Immunology & Inflammation
Hide