In both class of TLRs (lysosomal and plasma membrane TLRs) there are two signaling pathways that are possible right ? Either MyD88 dependent or TRIF dependent. In the TRIF dependent pathway, either TRAF 6 or TRAF 3 is activated. Is whichever one that is activated dependent on the specific ligand that activated the receptor in the first place?
Thank you for your comment! Well the regulation of signaling is still not very well understood. When LPS from bacteria is detected by TLR, the endocytosis pathway delivers Toll-like Receptor 4 (TLR4) to endosomes. I hope the answer was helpful.
Thank you Lokender, for a wonderful video. But maybe it is more appropriate to use the term 'Eukaryote cell' instead of human or animal cell. Just a suggestion :) well done.
A really great explanation helps me a lot better to understand the MAPk and their crosstalks with JAK/STAT and mTOR. Thank you so much. Should one be scared if one reads KRAS overexpressed and upregulated for more than 7 days 200 genes after transfection thinking about that TLR can also myd88 independent act in cancer progression? If one thinks that LNP will activate more than one TLR and also SCAVENGER, NOTCH, NOD and MDA5? (Asking for a friend) What a weird show.... We even start to understand the interactions/ crosstalks amongst the PRR and the intereactions with lncRNA for example via NOTCH.
As for your question, the overexpression and upregulation of KRAS for an extended period and the potential involvement of TLR, especially myd88-independent activation in cancer progression, can indeed be concerning. Additionally, the activation of multiple TLRs, as well as other factors like SCAVENGER, NOTCH, NOD, and MDA5 by LNP, could have complex implications. It's important to carefully consider these factors and their potential impact. I hope it was helpful, let me know if you have any further questions?
@@BasicScienceSeries It was. If you find the time: Knabl L, Lee HK, Wieser M, et al. BNT162b2 vaccination enhances interferon-JAK-STAT-regulated antiviral programs in COVID-19 patients infected with the SARS-CoV-2 Beta variant. Commun Med (Lond). 2022;2(1):17. doi:10.1038/s43856-022-00083-x (They've hidden a lot in the supplementaries.)
Hello Sir, I have studied that dimerization of TLR4 isn't possible it's only possible in the case of TLR1, TLR2 and TLR6. SO, HOW DIMERIZATION OF TLR4 IS POSSIBLE?
Amazing video , TLR s are really amazing ,they can detect pathogens and activate signalling ,my question is that are they conserved through evolution but the mystery is that human beings are more evolved than mouse but yet mouse has 3 extra TLRs then humans How this is possible ?????
*Toll-like receptor signaling! Subscribe to the channel for more videos!*
awesome, thanks. Simplified a confusing explanation from Kuby's immunology!
Glad it helped!
We need more such videos sir. Nicely explained!
Thank you for your valuable feedback, much appreciated, I will try my best to provide more.
What a beautiful explanation 👏🏻👏🏻
Glad you think so!
Your videos are very precise .....👍👍👍👍
Thank you very much Akshay, I thank you for appreciating my effort. It means alot. Thank you!!!!
In both class of TLRs (lysosomal and plasma membrane TLRs) there are two signaling pathways that are possible right ? Either MyD88 dependent or TRIF dependent. In the TRIF dependent pathway, either TRAF 6 or TRAF 3 is activated. Is whichever one that is activated dependent on the specific ligand that activated the receptor in the first place?
Very nice video!
Thank you!
My question - what mediator changes the pathway of nfkb to interferon pathway or vice versa? And when are TLR4 endocyosed?
Thank you for your comment! Well the regulation of signaling is still not very well understood. When LPS from bacteria is detected by TLR, the endocytosis pathway delivers Toll-like Receptor 4 (TLR4) to endosomes. I hope the answer was helpful.
Very good thx for the information
Thanks for the comment 🙏🏼
You are brilliant! Thank you so much!
Thank you so much for your valuable comment 🙏 I am glad you liked the video!
Thank you Lokender, for a wonderful video. But maybe it is more appropriate to use the term 'Eukaryote cell' instead of human or animal cell. Just a suggestion :) well done.
Thank you Tamzid for watching the video and posting your valuable comment! Much appreciated. Thank you for your feedback. 🙏
A really great explanation helps me a lot better to understand the MAPk and their crosstalks with JAK/STAT and mTOR. Thank you so much.
Should one be scared if one reads KRAS overexpressed and upregulated for more than 7 days 200 genes after transfection thinking about that TLR can also myd88 independent act in cancer progression? If one thinks that LNP will activate more than one TLR and also SCAVENGER, NOTCH, NOD and MDA5? (Asking for a friend)
What a weird show.... We even start to understand the interactions/ crosstalks amongst the PRR and the intereactions with lncRNA for example via NOTCH.
As for your question, the overexpression and upregulation of KRAS for an extended period and the potential involvement of TLR, especially myd88-independent activation in cancer progression, can indeed be concerning. Additionally, the activation of multiple TLRs, as well as other factors like SCAVENGER, NOTCH, NOD, and MDA5 by LNP, could have complex implications. It's important to carefully consider these factors and their potential impact. I hope it was helpful, let me know if you have any further questions?
@@BasicScienceSeries
It was. If you find the time:
Knabl L, Lee HK, Wieser M, et al. BNT162b2 vaccination enhances interferon-JAK-STAT-regulated antiviral programs in COVID-19 patients infected with the SARS-CoV-2 Beta variant. Commun Med (Lond). 2022;2(1):17. doi:10.1038/s43856-022-00083-x (They've hidden a lot in the supplementaries.)
May I ask another learning question?: N, H, and KRAS... are they in direct correlation/ Crosstalks?
well explanation
Thank you for your comment 🙏🏼 can you suggest any topic for the future videos?
Hello Sir,
I have studied that dimerization of TLR4 isn't possible it's only possible in the case of TLR1, TLR2 and TLR6.
SO, HOW DIMERIZATION OF TLR4 IS POSSIBLE?
In presence of LPS of bacteria
Very helpful, thanks!
Thanks for your valuable feedback 🙏
Thank you so much!!!
Amazing video , TLR s are really amazing ,they can detect pathogens and activate signalling ,my question is that are they conserved through evolution but the mystery is that human beings are more evolved than mouse but yet mouse has 3 extra TLRs then humans
How this is possible ?????
Great question! This is quiet interesting actually that we have less TLRs than mouse. Thats the beauty of nature.. many things need more research