Human CXCR4 blocking peptide (CDBP0921)

Synthetic Human CXCR4 blocking peptide for BL

Product Overview
CXCR 4 ( Extracellular ) peptide ( human )
Species Reactivity
0.2 mg/ml
50 μg
PBS with 0.1% BSA 0.02% sodium azide pH7.2
0.02% Sodium Azide
Upon receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene encodes a CXC chemokine receptor specific for stromal cell-derived factor-1. The protein has 7 transmembrane regions and is located on the cell surface. It acts with the CD4 protein to support HIV entry into cells and is also highly expressed in breast cancer cells. Mutations in this gene have been associated with WHIM (warts, hypogammaglobulinemia, infections, and myelokathexis) syndrome. Alternate transcriptional splice variants, encoding different isoforms, have been characterized.
C-X-C chemokine receptor activity; G-protein coupled receptor activity; actin binding; coreceptor activity; myosin light chain binding; protein binding; receptor activity; signal transducer activity; ubiquitin binding; ubiquitin protein ligase binding;
CXCR4; chemokine (C-X-C motif) receptor 4; chemokine (C X C motif), receptor 4 (fusin); C-X-C chemokine receptor type 4; CD184; D2S201E; fusin; HM89; HSY3RR; LESTR; NPY3R; NPYR; NPYY3R; CXC-R4; CXCR-4; CD184 antigen; SDF-1 receptor; neuropeptide Y receptor Y3; seven transmembrane helix receptor; stromal cell-derived factor 1 receptor; lipopolysaccharide-associated protein 3; seven-transmembrane-segment receptor, spleen; leukocyte-derived seven transmembrane domain receptor; leukocyte-derived seven-transmembrane-domain receptor; FB22; LAP3; LCR1; WHIM; NPYRL;


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Mdm4 controls ureteric bud branching via regulation of p53 activity


Authors: Hilliard, Sylvia A.; Li, Yuwen; Dixon, Angelina; El-Dahr, Samir S.

The antagonism between Mdm2 and its close homolog Mdm4 (also known as MdmX) and p53 is vital for embryogenesis and organogenesis. Previously, we demonstrated that targeted disruption of Mdm2 in the Hoxb7 + ureteric bud (Ub) lineage, which gives rise to the renal collecting system, causes renal hypodysplasia culminating in perinatal lethality. In this study, we examine the unique role of Mdm4 in establishing the collecting duct system of the murine kidney. Hoxb7Cre driven loss of Mdm4 in the Ub lineage (Ub(Mdm4-/-)) disrupts branching morphogenesis and triggers UB cell apoptosis. Ub(Mdm4-/-) kidneys exhibit abnormally dilated Ub tips while the medulla is hypoplastic. These structural alterations result in secondary depletion of nephron progenitors and nascent nephrons. As a result, newborn Ub(Mdm4-/-) mice have hypo-dysplastic kidneys. Transcriptional profiling revealed downregulation of the Ret-tyrosine kinase pathway components, Gdnf, Wnt11, Sox8, Etv4 and Cxcr4 in the Ub(Mdm4-/-) mice relative to controls. Moreover, the expression levels of the canonical Wnt signaling members Axin2 and Wnt9b are downregulated. Mdrn4 deletion upregulated p53 activity and p53-target gene expression including Cdkn1 alpha (p21), Gdf15, Ccng1, PERP, and Fas. Germline loss of p53 in Ub(Mdm4-/-) mice largely rescues kidney development and terminal differentiation of the collecting duct. We conclude that Mdm4 plays a unique and vital role in Ub branching morphogenesis and collecting system development.

HMGB1 and its membrane receptors as therapeutic targets in an intravesical substance P-induced bladder pain syndrome mouse model


Authors: Irie, Yuhei; Tsubota, Maho; Maeda, Mariko; Hiramoto, Shiori; Sekiguchi, Fumiko; Ishikura, Hiroyasu; Wake, Hidenori; Nishibori, Masahiro; Kawabata, Atsufumi

HMGBI, a nuclear protein, once released to the extracellular space, promotes somatic and visceral pain signals. We thus analyzed the role of HMGB1 in an intravesical substance P-induced bladder pain syndrome (BPS) mouse model. Intravesical administration of substance P caused referred hyperalgesia/ allodynia in the lower abdomen and hindpaw without producing severe urothelial damage, which was prevented by an anti-HMGB1-neutralizing antibody, thrombomodulin alpha capable of inactivating HMGB1 and antagonists of RAGE or CXCR4. The HMGB1 inactivation or RAGE blockade also reversed the established bladder pain symptoms. HMGB1 and RAGE are thus considered to serve as therapeutic targets for BPS. (C) 2020 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society.

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