Thank you, for yet another interesting conversation. Given that the demethylase JMD3 has been shown to have both demethylation-dependent and -independent functions in T-cell activation, differentiation and lineage stability and that JMJD3 works in synergy with the master transcription factor T-bet in forming the SWI/SNF complex, could it be interesting to consider the immunological processes of Alzheimers as an abberrant immune activation resulting in both upregulation of a specific gene signature as well as a downregulation of another?
Yes, it could be very interesting to consider the immunological processes in Alzheimer's disease as a result of aberrant immune activation, with involvement of factors like JMJD3. JMJD3 (a histone demethylase) plays a key role in T-cell activation, differentiation, and lineage stability, often through epigenetic modifications. Its interaction with the master transcription factor T-bet, which is crucial for driving immune responses, particularly in the SWI/SNF complex, suggests a regulatory pathway that controls the expression of specific immune genes. In Alzheimer's disease, there is growing evidence of immune dysregulation, particularly in microglial activation, which parallels some of the processes seen in T-cell activation. The hypothesis of JMJD3-driven aberrant immune activation could provide a mechanistic basis for the upregulation of genes associated with neuroinflammation and immune responses, while concurrently leading to downregulation of protective or regulatory genes. If JMJD3's activity in Alzheimer’s involves both demethylation-dependent and independent functions, this might result in a specific epigenetic signature. Such dysregulation could shift the balance towards chronic inflammation and neurodegeneration, while suppressing pathways that normally protect the brain or resolve inflammation.
It has been shown that another demethylase, namely the H3K27me3/2 demethylase JMJD3 cooperates with Tau to specifically control VGLUT1 and VGLUT2 expression for proper synaptic transmission and normal neuron functions under physiological conditions. JMJD3, in immun cell activation, plays a prominent role as providing chromatin accessability for transcription factors and, thus, for gene expression.
That's a fascinating connection! The demethylase JMJD3 indeed plays critical roles both in neuronal function and immune cell activation, highlighting its versatile regulatory abilities.
Thank you, for yet another interesting conversation.
Given that the demethylase JMD3 has been shown to have both demethylation-dependent and -independent functions in T-cell activation, differentiation and lineage stability and that JMJD3 works in synergy with the master transcription factor T-bet in forming the SWI/SNF complex, could it be interesting to consider the immunological processes of Alzheimers as an abberrant immune activation resulting in both upregulation of a specific gene signature as well as a downregulation of another?
Yes, it could be very interesting to consider the immunological processes in Alzheimer's disease as a result of aberrant immune activation, with involvement of factors like JMJD3. JMJD3 (a histone demethylase) plays a key role in T-cell activation, differentiation, and lineage stability, often through epigenetic modifications. Its interaction with the master transcription factor T-bet, which is crucial for driving immune responses, particularly in the SWI/SNF complex, suggests a regulatory pathway that controls the expression of specific immune genes.
In Alzheimer's disease, there is growing evidence of immune dysregulation, particularly in microglial activation, which parallels some of the processes seen in T-cell activation. The hypothesis of JMJD3-driven aberrant immune activation could provide a mechanistic basis for the upregulation of genes associated with neuroinflammation and immune responses, while concurrently leading to downregulation of protective or regulatory genes.
If JMJD3's activity in Alzheimer’s involves both demethylation-dependent and independent functions, this might result in a specific epigenetic signature. Such dysregulation could shift the balance towards chronic inflammation and neurodegeneration, while suppressing pathways that normally protect the brain or resolve inflammation.
It has been shown that another demethylase, namely the H3K27me3/2 demethylase JMJD3 cooperates with Tau to specifically control VGLUT1 and VGLUT2 expression for proper synaptic transmission and normal neuron functions under physiological conditions. JMJD3, in immun cell activation, plays a prominent role as providing chromatin accessability for transcription factors and, thus, for gene expression.
That's a fascinating connection! The demethylase JMJD3 indeed plays critical roles both in neuronal function and immune cell activation, highlighting its versatile regulatory abilities.
You are left handed?
Yes!!
@@everythingepigenetics So am i they do not making many thing for us left handed people it sucks