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Posted On: 06/12/2024 7:33:56 PM
Post# of 148863
Re: chazzledazzle #144437
Leronlimab Regulator List (a work in progress)
[+] = upregulation
[-] = downregulation
a-SMA [-],
a1-antitrypsin [+],
ADA2 (CCL5 migration to site of injury) [-],
AKT (via blockade of CCL4)[-], AMPK [+],
arachidonic acid (upregulated by CCL2, CCL3, CCL4, CCL5, CCL7 [-],
CCL8)[-],
ARG1 [-],
ASC proteins (via NLRP3 downreg)[-],
ATP (via CCL5 downreg) [-,]
b-arrestin [-],
BACH2 (via decrease of inflammatory TREG reaponse) [+],
Bcl-2 [-],
BDNF [+],
bradykinin[-],
beta- catenin (via downreg CCL5/CCL2) [-],
bFGF (-),
BTK (via SYK) [-],
caspase-1 (via NLRP3/ASC downreg) [-],
capase-3 [-],
capase 9 [-],
C5a, CA-2+[-],
Calcineurin (via downreg CA-2+[-],
cAMP (via CD38)[-],
CCL2 (MCP-1)[-],
CCL3 (MIP-1a)[-],
CCL4 (MIP-1b)[-],
CCL5 (RANTES)[-],
CCL7 (MCP-3)[-],
CCL8 (MCP-2)[-],
CCL11(Eotaxin-1)(low binding affinity) (high binding of CCR3)[-]
CCL13 (MCP-4)[-],
CCL14 (HCC-1)[-],
CCL16 (HCC-4)[-],
CCL18 [-],
CCL20 (LARC MIP3A)(not a CCR5 ligand) (via NF-kB downreg)[-],
CCR1 (via TNF-a and IL-4) [-],
CD25 (aka p55)(IL-2 receptor) [-],
CD69 [+],
CDK2 (via CCL5 downreg) [-],
CDK4 (via CCL5 downreg) [-],
CDK6 (via CCL5 downreg) [-],
CREB [+],
CTLA-4 (via IFN-a downreg)[-],
CX3CL1 (fractalkine) (NF-kB /TNF-a downregulation)[-],
CXCL1 [-],
CXCL8 [-],
CXCR4 (via downreg IL-17a, cyclin D1 (via CCL5 downreg) [-],
cyclin E (via CCL5 downreg) [-],
cytochrome c (via CCL5 downreg)[-],
DNMT1 (vis downreg of STAT3)[-],
ECM [-],
EGF/EGFR (in cancer via downreg fibroblasts, downreg GRP78) [-],
eIF2a (via PKR downreg) [-],
eIF4E [-],
EN-RAGE [-],
Erk 1 and 2[-],
FAK (via CCL5) [-],
FLNa, FOXP3 (downregulation of PKB/Akt pathway)[+],
GLP-1 [+],
GLUT-1 (via CCL5 downreg) [-],
GM-CSF (CSF2)[-],
GPR75 (increased binding of CCL5 to GPR75 due to CCR5 blockade) [effect is downreg CA2[+],
GRP78 (via M2 to M1 machrophage switch, via PI3K/AKT pathway downreg) [-],
Gsdmd [-] ,
inositol monophosphate (IP-1) IP-1 implicated in bi-polar disorder)), HbA1c (correlated with CCL5), HDL (high density lipoprotein) [+],
HGF, HIF-1a (via STAT3 downreg)[-],
HIF-2a (via NF-kb downreg)[-],
ICAM-1(intercellular adhesion molecule-)[-],
IDO (via IFN-y downreg) [-],
IFN-a (via downreg GM-CSF) [-],
IFNy (BACH2 upregulation)[-],
IL-1b (via caspase-1 downreg)[-],
IL-1Ra [+],
IL-2 [-],
IL-4 (-),
IL-5, IL-6 (via CCL5) [-],
IL-8 [-],
IL-10 [?],
IL-13 [-],
IL-16 [-],
IL-17a (via upregulation of CD69 and subsequent downregulation of TH17 cells)[-],
IL-18 (via caspase-1 downreg)[-],
IL-33, IL-36 (via TNF-a and ILF downreg)[-],
Jak 1, 2 and 3[-],
LDL (low density lipoprotein)[-],
LFA-1(lymphocyte function–associated antigen-1) [-],
macrophage polarization M2 to M1 shift, MapK (p38 MAPK)[-],
MDSC (via downreg CCL5) [-],
MEK [-],
miR21 (via downreg TFNa) [-],
MMP-1 [-],
MMP-2 (via CCL3 downreg)[-],
MMP-3, MMP-9 (CCL5/PLC pathway) [-],
MMP-12 [-],
MMP-13, mTORc1[-],
N-GSDMD [-],
NETosis[-],
neuropilin-1[-],
NF-H (neurofilament heavy) [+],
NF-kb (via PI3K/AKT downreg) [-],
NFAT (via CA2+ downreg) [-],
NLRP1 [-]
NLRP3 (via IL-36, ATP, ROS downreg) [-],
NOS (nitric oxide synthase) (via downreg NF-kb, MAPK) [-],
NO (nitric oxide) (via downreg NOS) [-],
Nox1 (via CCL5) [-],
p21 (tumor suppressor) (via downreg of PI3K/AKT)[+],
p27 (tumor suppressor) [+],
p50 (via NF-kb downreg) [-],
p53 (via downreg of NF-kb) [+],
p55 (aka CD25) [-],
p-CREB [+],
PCNA [-],
PDK1 (via PI3K)[-]
PD-L1(via downreg Nf-kb/MapK/JAK2) [-],
PDGF-B (upreg from ADA2) [-],
PI3k (via blocking CCL4 activation) [-],
PKA-Ca [+],
PKB/AT (CCL3,CCL5 blockade)[-],
PKC [protein kinase C] [via CA2+ downreg][-],
PKR (via TNF-a downreg) -[-],
PLA2 (via CCL2, CCL3, CCL5, CCL7, TNF-a, IL-1b, IFNy, GM-CSF downreg) [-],
PLC (CCL5 blockade)[-],
PPARy [+],
Prostaglandin D2 (formed from arachidonic acid) [-],
Pyk2 (via RAFTK) [-],
RAFTK (downreg of bradykinin, CCL5) [-],
RAGE [-],
RAS (via downreg Src) [-],
Reg3a [-],
ROS (via CCL5)[-],
S100A4 (via downreg of CCL5) [-],
SCG3 (Secretogranin III)(via downreg CA2+)[-],
sFas (via Nf-kB)[-],
SHP1[-],
SHP2[-],
SOCS3 [-],
SORT1 (neurotensin receptor-3) (MAP and PI3K dependent) [-],
SRC (via downregulation of Pyk2) [-],
SREBP-1a [-],
SREBP-2 [-],
STAT3 [-],
STAT4 (feedback loop, also increases CCR5) [-],
STAT5 [-],
SYK (via CCL4) [-],
TGF-b [-],
TIMP-1 [-],
TIMP-2 [-],
TIMP-3 [-],
TNF-a (via IL-10, MEK downreg)[-],
TNFR2 [-],
TFN-y, TGF-b) [-]
TNFSF14, TRPM4 (via CA-2+ downreg) [-],
TSC2 (via AKT downreg) [+],
TSLP (thymic stromal lymphopoietin) (via IL-1b, IL-4, IL-13, TNF-a downreg)[-],
VCAM-1 (via TNF-a, IL-1 downreg) [-],
VEGF [-],
ZAP70 (via CCL5) [-]
[+] = upregulation
[-] = downregulation
a-SMA [-],
a1-antitrypsin [+],
ADA2 (CCL5 migration to site of injury) [-],
AKT (via blockade of CCL4)[-], AMPK [+],
arachidonic acid (upregulated by CCL2, CCL3, CCL4, CCL5, CCL7 [-],
CCL8)[-],
ARG1 [-],
ASC proteins (via NLRP3 downreg)[-],
ATP (via CCL5 downreg) [-,]
b-arrestin [-],
BACH2 (via decrease of inflammatory TREG reaponse) [+],
Bcl-2 [-],
BDNF [+],
bradykinin[-],
beta- catenin (via downreg CCL5/CCL2) [-],
bFGF (-),
BTK (via SYK) [-],
caspase-1 (via NLRP3/ASC downreg) [-],
capase-3 [-],
capase 9 [-],
C5a, CA-2+[-],
Calcineurin (via downreg CA-2+[-],
cAMP (via CD38)[-],
CCL2 (MCP-1)[-],
CCL3 (MIP-1a)[-],
CCL4 (MIP-1b)[-],
CCL5 (RANTES)[-],
CCL7 (MCP-3)[-],
CCL8 (MCP-2)[-],
CCL11(Eotaxin-1)(low binding affinity) (high binding of CCR3)[-]
CCL13 (MCP-4)[-],
CCL14 (HCC-1)[-],
CCL16 (HCC-4)[-],
CCL18 [-],
CCL20 (LARC MIP3A)(not a CCR5 ligand) (via NF-kB downreg)[-],
CCR1 (via TNF-a and IL-4) [-],
CD25 (aka p55)(IL-2 receptor) [-],
CD69 [+],
CDK2 (via CCL5 downreg) [-],
CDK4 (via CCL5 downreg) [-],
CDK6 (via CCL5 downreg) [-],
CREB [+],
CTLA-4 (via IFN-a downreg)[-],
CX3CL1 (fractalkine) (NF-kB /TNF-a downregulation)[-],
CXCL1 [-],
CXCL8 [-],
CXCR4 (via downreg IL-17a, cyclin D1 (via CCL5 downreg) [-],
cyclin E (via CCL5 downreg) [-],
cytochrome c (via CCL5 downreg)[-],
DNMT1 (vis downreg of STAT3)[-],
ECM [-],
EGF/EGFR (in cancer via downreg fibroblasts, downreg GRP78) [-],
eIF2a (via PKR downreg) [-],
eIF4E [-],
EN-RAGE [-],
Erk 1 and 2[-],
FAK (via CCL5) [-],
FLNa, FOXP3 (downregulation of PKB/Akt pathway)[+],
GLP-1 [+],
GLUT-1 (via CCL5 downreg) [-],
GM-CSF (CSF2)[-],
GPR75 (increased binding of CCL5 to GPR75 due to CCR5 blockade) [effect is downreg CA2[+],
GRP78 (via M2 to M1 machrophage switch, via PI3K/AKT pathway downreg) [-],
Gsdmd [-] ,
inositol monophosphate (IP-1) IP-1 implicated in bi-polar disorder)), HbA1c (correlated with CCL5), HDL (high density lipoprotein) [+],
HGF, HIF-1a (via STAT3 downreg)[-],
HIF-2a (via NF-kb downreg)[-],
ICAM-1(intercellular adhesion molecule-)[-],
IDO (via IFN-y downreg) [-],
IFN-a (via downreg GM-CSF) [-],
IFNy (BACH2 upregulation)[-],
IL-1b (via caspase-1 downreg)[-],
IL-1Ra [+],
IL-2 [-],
IL-4 (-),
IL-5, IL-6 (via CCL5) [-],
IL-8 [-],
IL-10 [?],
IL-13 [-],
IL-16 [-],
IL-17a (via upregulation of CD69 and subsequent downregulation of TH17 cells)[-],
IL-18 (via caspase-1 downreg)[-],
IL-33, IL-36 (via TNF-a and ILF downreg)[-],
Jak 1, 2 and 3[-],
LDL (low density lipoprotein)[-],
LFA-1(lymphocyte function–associated antigen-1) [-],
macrophage polarization M2 to M1 shift, MapK (p38 MAPK)[-],
MDSC (via downreg CCL5) [-],
MEK [-],
miR21 (via downreg TFNa) [-],
MMP-1 [-],
MMP-2 (via CCL3 downreg)[-],
MMP-3, MMP-9 (CCL5/PLC pathway) [-],
MMP-12 [-],
MMP-13, mTORc1[-],
N-GSDMD [-],
NETosis[-],
neuropilin-1[-],
NF-H (neurofilament heavy) [+],
NF-kb (via PI3K/AKT downreg) [-],
NFAT (via CA2+ downreg) [-],
NLRP1 [-]
NLRP3 (via IL-36, ATP, ROS downreg) [-],
NOS (nitric oxide synthase) (via downreg NF-kb, MAPK) [-],
NO (nitric oxide) (via downreg NOS) [-],
Nox1 (via CCL5) [-],
p21 (tumor suppressor) (via downreg of PI3K/AKT)[+],
p27 (tumor suppressor) [+],
p50 (via NF-kb downreg) [-],
p53 (via downreg of NF-kb) [+],
p55 (aka CD25) [-],
p-CREB [+],
PCNA [-],
PDK1 (via PI3K)[-]
PD-L1(via downreg Nf-kb/MapK/JAK2) [-],
PDGF-B (upreg from ADA2) [-],
PI3k (via blocking CCL4 activation) [-],
PKA-Ca [+],
PKB/AT (CCL3,CCL5 blockade)[-],
PKC [protein kinase C] [via CA2+ downreg][-],
PKR (via TNF-a downreg) -[-],
PLA2 (via CCL2, CCL3, CCL5, CCL7, TNF-a, IL-1b, IFNy, GM-CSF downreg) [-],
PLC (CCL5 blockade)[-],
PPARy [+],
Prostaglandin D2 (formed from arachidonic acid) [-],
Pyk2 (via RAFTK) [-],
RAFTK (downreg of bradykinin, CCL5) [-],
RAGE [-],
RAS (via downreg Src) [-],
Reg3a [-],
ROS (via CCL5)[-],
S100A4 (via downreg of CCL5) [-],
SCG3 (Secretogranin III)(via downreg CA2+)[-],
sFas (via Nf-kB)[-],
SHP1[-],
SHP2[-],
SOCS3 [-],
SORT1 (neurotensin receptor-3) (MAP and PI3K dependent) [-],
SRC (via downregulation of Pyk2) [-],
SREBP-1a [-],
SREBP-2 [-],
STAT3 [-],
STAT4 (feedback loop, also increases CCR5) [-],
STAT5 [-],
SYK (via CCL4) [-],
TGF-b [-],
TIMP-1 [-],
TIMP-2 [-],
TIMP-3 [-],
TNF-a (via IL-10, MEK downreg)[-],
TNFR2 [-],
TFN-y, TGF-b) [-]
TNFSF14, TRPM4 (via CA-2+ downreg) [-],
TSC2 (via AKT downreg) [+],
TSLP (thymic stromal lymphopoietin) (via IL-1b, IL-4, IL-13, TNF-a downreg)[-],
VCAM-1 (via TNF-a, IL-1 downreg) [-],
VEGF [-],
ZAP70 (via CCL5) [-]
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