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Microbes & Immunity RANTES/CCL5 and ezrin peptide RepG3 for long COVID

presence of proinflammatory cytokines. More research is involved in the regulation of MEK > ERK1/2 and PKC > p38
81
needed to unravel the complex control pathways triggered MAPK signaling. As part of the cell membrane multi-protein
by infection and proinflammatory cytokines that regulate complex, EBP50 and CFTR regulate proinflammatory IL-8
CCL5 gene expression, which are modulated by the expression and anti-inflammatory IL-10 expression. 82
CFTR+EBP50+ICAM+Ezrin+PKC+PI3 K multiprotein Under inflammatory conditions, NF-κB increases EBP50
complex (Figure 7).
expression, which potentiates systemic inflammation by
6.3. CFTR+EBP50+PKC and ezrin regulation of promoting macrophage recruitment and activation. Ezrin-
proinflammatory gene expression binding phosphoprotein 50 increases inflammatory responses
in vascular smooth muscle cells (VSMC), including the
Ezrin-binding phosphoprotein 50 plays a central role in expression of adhesion molecules such as ICAM-1 bound to
the activation of inflammatory cytokine expression. Ezrin- the FERM domain of ezrin, which are critical for the homing
binding phosphoprotein 50 is a submembrane protein with of macrophages to sites of damage. Activated EBP50 also
two tandem PDZ domains and a carboxy-terminal ezrin- increases the secretion of proinflammatory cytokines, which
binding (EB) site. The C-terminus of CFTR binds to PDZ-1 are important factors for further induction of proliferation,
of EPB50 through its C-terminal PDZ-interacting domain migration, and adhesion of macrophages.
(TRL). Ezrin-binding phosphoprotein 50 also contains a
second PDZ-binding domain (PDZ-2), which can engage Ezrin-binding phosphoprotein 50 assembles signal
with other kinases, such as PKC, RhoA, and Ras, and is transduction complexes through its two PDZ domains.

Figure 7. Translational control of transcription factor RFLAT-1/KLF13 in T-cells and delayed RANTES/CCL5 expression. Translational control of
transcription factor RFLAT-1/KLF13 in T-cells, and hence, RANTES/CCL5, can be traced back to cell membrane-associated multi-protein complexes of
ezrin protein. ERK-1/2 activation is caused by the activation of Ras, which binds to the FERM domain of ezrin and signals down the Ras > Raf > MEK >
ERK > RSK pathway and triggers CREB transcription. PI3K is bound to the alpha domain of ezrin and signals down the PI3K > AKT/PKB > FRAP/mTOR
pathway, resulting in de-repression of the translation initiation factor eIF4E.

Volume 1 Issue 1 (2024) 16 doi: 10.36922/mi.2474