Ohm wrote:

Quote:

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incomplete list

- = downregulation
+ = upregulation


a-SMA [-], a1-antitrypsin [+],ADA2 (CCL5 migration to site of injury) [-], AKT [-], AMPK [+], arachidonic acid (upregulated by CCL2, CCL3, CCL4, CCL5, CCL7 [-],CCL8)[-}, ARG1 [-], ASC proteins (via NLRP3 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-1β)[-], 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) [-], 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, IL-5, TFN-y, TGF-b) [-], cyclin D1 (via CCL5 downreg) [-], cyclin E (via CCL5 downreg) [-],cytochrome c (via CCL5 downreg)[-], ECM [-], EGF (in cancer via downreg fibroblasts) [-], 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+],Gsdmd [-] , inositol monophosphate (IP-1) IP-1 implicated in bi-polar disorder)), HbA1c (correlated with CCL5), HDL (high density lipoprotein) [+], HGF, IFN-g [+], HIF-1a [-], IFNy (BACH2 upregulation)[-], IL-1b (via caspase-1 downreg)[-], IL-1Ra [+], IL-2 [-], IL-4, IL-6 (via CCL5) [-], IL-8, IL-10 [-], IL-13 [-], IL-16 [-], IL-17a [-], 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)[-], MCP-1 [-], MCP-2, MDSC (via downreg CCL5) [-], MEK [-], 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) [-], p27 (tumor suppressor) [+], PCNA [-], p-CREB [+], PI3k[-], PDK1 (via PI3K)[-] PD-L1(via downreg Nf-kb/MapK/JAK2) [-], PDGF-B (upreg from ADA2) [-], PKA-Ca [+], PKB/AT (CCL3,CCL5 blockade)[-], PKC (-), PKR (via TNF-a downreg) -[-], PLC (CCL5 blockade)[-], PPARy [+], Prostaglandin D2 (formed from arachidonic acid) [-], Pyk2 (via RAFTK) [-], RAFTK (downreg of bradykinin, CCL5) [-], RAS (via downreg Src) [-], ROS (via CCL5)[-], sFas (via Nf-kB)[-], SHP1[-], SHP2[-], SOCS3 [-], SORT1 (neurotensin receptor-3) (MAP and PI3K dependent) [-], SREBP-1a [-], SREBP-2 [-], Src (via downregulation of Pyk2) [-], STAT3 [-], STAT5 [-], SYK (via CCL4) [-], TGF-b [-], TIMP-1 [-], TIMP-2 [-], TIMP-3 [-], TNF-a (via IL-10, MEK downreg)[-], TNFSF14, TRPM4 (via CA-2+ downreg) [-], VCAM-1 (via TNF-a, IL-1 downreg) [-], VEGF [-], ZAP70 (via CCL5) [-]

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To quote Casey Stengel: Amazin, amazin, amazin. The fact that this molecule has escaped the world's attention is a kind of holocaust by default.