MOUSE ANTI HUMAN CD38 Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: MOUSE ANTI HUMAN CD38 Azide Free
Catalog number: genta-ABS0307
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd38

Related genes to: MOUSE ANTI HUMAN CD38 Azide Free

Symbol : cd38 NIH gene
chromosome : Un
description : CD38 molecule
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: MOUSE ANTI HUMAN CD38 Azide Free

Gene about :CD38
Pathway :Hs Oxytocin signaling
CD38

Related product to: MOUSE ANTI HUMAN CD38 Azide Free

Related Articles about: MOUSE ANTI HUMAN CD38 Azide Free

The Expression of CD38 ADP-ribosyl Cyclase Ectoenzyme in Immune Cells of Cardiac Surgical Patients.

This study was aimed at following the changes in the expression of CD38 ADP-ribosyl cyclase ectoenzyme on peripheral blood immune cells of patients undergoing cardiac surgical operations. - Source :PubMed

Leukotriene signaling via ALOX5 and cysteinyl leukotriene receptor 1 is dispensable for in vitro growth of CD34(+)CD38(-) stem and progenitor cells in chronic myeloid leukemia.

Tyrosine kinase inhibitors targeting the BCR-ABL oncoprotein in chronic myeloid leukemia (CML) are remarkably effective inducing deep molecular remission in most patients. However, they are less effective to eradicate the leukemic stem cells (LSC), resulting in disease persistence. Therefore, there is great need to develop novel therapeutic strategies to specifically target the LSC. In an experimental mouse CML model system, the leukotriene pathway, and specifically, the expression ALOX5, encoding 5-lipoxygenase (5-LO), has been reported as a critical regulator of the LSC. Based on these results, the 5-LO inhibitor zileuton has been introduced in clinical trials as a therapeutic option to target the LSC although its effect on primary human CML LSC has not been studied. We have here by using multiplex single cell PCR analyzed the expression of the mediators of the leukotriene pathway in bone marrow (BM) BCR-ABL(+)CD34(+)CD38(-) cells at diagnosis, and found low or undetectable expression of ALOX5. In line with this, zileuton did not exert significant overall growth inhibition in the long-term culture-initiating cell (LTC-IC) and colony (CFU-C) assays of BM CD34(+)CD38(-) cells from 7 CML patients. The majority of the single leukemic BCR-ABL(+)CD34(+)CD38(-) cells expressed cysteinyl leukotriene receptors CYSLT1 and CYSLT2. However, montelukast, an inhibitor of CYSLT1, also failed to significantly suppress CFU-C and LTC-IC growth. These findings indicate that targeting ALOX5 or CYSLT1 signaling with leukotriene antagonists, introduced into the clinical practice primarily as prophylaxis and treatment for asthma, may not be a promising pharmacological strategy to eradicate persisting LSC in CML patients. - Source :PubMed

Re: Low CD38 Identifies Progenitor-Like Inflammation-Associated Luminal Cells that Can Initiate Human Prostate Cancer and Predict Poor Outcome.

- Source :PubMed

Identification of the ectoenzyme CD38 as a marker of committed preadipocytes.

Characterization of the adipocyte cellular lineage is required for a better understanding of white adipose tissue homeostasis and expansion. While several studies have focused on the phenotype of the most immature adipocyte progenitors, very few tools exist to identify committed cells. In haematopoiesis, the CD38 ectoenzyme is largely used to delineate various stages of stem cell lineage commitment. We hypothesize that this marker could be used to identify committed preadipocytes. - Source :PubMed

T cells bearing anti-CD19 and/or anti-CD38 chimeric antigen receptors effectively abrogate primary double-hit lymphoma cells.

Patients with B cell lymphomas bearing MYC translocation combined with translocation involving other genes, such as BCL2, BCL3, or BCL6, defined as double-hit lymphoma (DHL), have a poor prognosis. Recent studies expanded the concept to include double-expressing lymphoma (DEL) that co-overexpresses MYC protein with either of those proteins. Accordingly, we defined cytogenetic DHL and DEL as primary DHL. An adoptive T cell immunotherapy with a chimeric antigen receptor (CAR) has been clinically shown to exhibit cytotoxicity in refractory neoplasias. We revealed the marked cytotoxicity of anti-CD19- and/or anti-CD38-CAR T cells against primary DHL cells from patients. CD19- and/or CD38-specific T cells were co-cultured with cytogenetic DHL (n = 3) or DEL (n = 2) cells from five patients for 3 days. We examined whether T cells retrovirally transduced with each vector showed cytotoxicity against DHL cells. Anti-CD19- and/or anti-CD38-CAR T cells were co-cultured with primary DHL cells at an E:T ratio of 1:2 for 3 days. Anti-CD19- and anti-CD38-CAR T cells completely abrogated these DHL cells, respectively. Anti-CD19-CAR T cells synergistically exerted collaborative cytotoxicity against these primary DHL cells with anti-CD38-CAR T cells. Therefore, refractory DHL cells can be efficiently abrogated by the clinical use of T cells with anti-CD19- and/or anti-CD38-CAR. - Source :PubMed

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