(Total Views: 737)
Posted On: 02/19/2024 12:36:36 AM
Post# of 148899
Quite a few of those chemokines are in my work in progress leronlimab regulator list.
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)[-], CCL13 (MCP-4)[-], CCL14 (HCC-1)[-], CCL16 (HCC-4)[-], 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) [-], collagen[-], CREB [+], CTLA-4, CX3CL1 (fractalkine) (NF-kB /TNF-a downregulation)[-], CXCL1 [-], 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 [-], 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 [-], IFN-a (via downreg GM-CSF) [-], IFN-g [+],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).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-kb (via PI3K/AKT downreg) [-], NFAT (via CA2+ downreg) [-], NLRP1 [-] NLRP3 (via IL-36, ATP, ROS downreg) [-], Nox1 (via CCL5) [-], p21 (tumor suppressor) (via downreg of PI3K/AKT)[+], p27 (tumor suppressor) [+], 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 (-), 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) [-], RAS (via downreg Src) [-], Reg3a [-], ROS (via CCL5)[-], S100A4 (via downreg of CCL5) [-], 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 [-], STAT5 [-], SYK (via CCL4) [-], TGF-b [-], TIMP-1 [-], TIMP-2 [-], TIMP-3 [-], TNF-a (via IL-10, MEK downreg)[-], 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) [-]
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)[-], CCL13 (MCP-4)[-], CCL14 (HCC-1)[-], CCL16 (HCC-4)[-], 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) [-], collagen[-], CREB [+], CTLA-4, CX3CL1 (fractalkine) (NF-kB /TNF-a downregulation)[-], CXCL1 [-], 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 [-], 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 [-], IFN-a (via downreg GM-CSF) [-], IFN-g [+],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).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-kb (via PI3K/AKT downreg) [-], NFAT (via CA2+ downreg) [-], NLRP1 [-] NLRP3 (via IL-36, ATP, ROS downreg) [-], Nox1 (via CCL5) [-], p21 (tumor suppressor) (via downreg of PI3K/AKT)[+], p27 (tumor suppressor) [+], 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 (-), 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) [-], RAS (via downreg Src) [-], Reg3a [-], ROS (via CCL5)[-], S100A4 (via downreg of CCL5) [-], 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 [-], STAT5 [-], SYK (via CCL4) [-], TGF-b [-], TIMP-1 [-], TIMP-2 [-], TIMP-3 [-], TNF-a (via IL-10, MEK downreg)[-], 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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