HAMSTER ANTI MOUSE CD79b Azide Free

Price:
889 EUR
1066 USD
737 GBP
known as: HAMSTER ANTI MOUSE CD79b Azide Free
Catalog number: genta-ABS0452
Product Quantity: 1 mg
Category:
Supplier: AbD

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Gene target: cd79b

Related genes to: HAMSTER ANTI MOUSE CD79b Azide Free

Symbol : cd79b NIH gene
chromosome : Un
description : CD79b molecule, immunoglobulin-associated beta
type of gene : protein-coding
Modification date : 2015-11-14

Related Pathways to: HAMSTER ANTI MOUSE CD79b Azide Free

Gene about :CD79B
Pathway :Hs B Cell Receptor Signaling Pathway
CD79B

Related product to: HAMSTER ANTI MOUSE CD79b Azide Free

Related Articles about: HAMSTER ANTI MOUSE CD79b Azide Free

Anti-CD22 and anti-CD79b antibody-drug conjugates preferentially target proliferating B cells.

CD22 and CD79b are cell-surface receptors expressed on B-cell-derived malignancies such as non-Hodgkin's lymphoma (NHL). An anti-mitotic agent, monomethyl auristatin E, was conjugated to anti-CD22 and anti-CD79b antibodies to develop target-specific therapies for NHL. The mechanism of action (MOA) and pharmacological and pharmacokinetic (PK) profiles of these antibody-drug conjugates (ADCs) were investigated in cynomolgus monkeys. - Source :PubMed

MYD88, CD79B, and CARD11 gene mutations in CD5-positive diffuse large B-cell lymphoma.

CD5-positive (CD5(+) ) diffuse large B-cell lymphoma (DLBCL) is characterized by frequent central nervous system recurrence and a predominant activated B-cell-like nature. Primary DLBCL in sanctuary sites (DLBCL-SS) also demonstrates these features, and >70% of patients harbor myeloid differentiation primary response 88 (MYD88) (L265P) and CD79B mutations. The objective of the current study was to elucidate a possible relationship between CD5(+) DLBCL and DLBCL-SS. - Source :PubMed

Nodal marginal zone lymphoma: mutation status analyses of CD79A, CD79B, and MYD88 reveal no specific recurrent lesions.

- Source :PubMed

Mutational status of EZH2 and CD79B hot spots in mature B-cell non-Hodgkin's lymphomas: novel CD79B variations have been revealed.

We aimed to determine the hot spot mutational frequencies of Enhancer of Zeste homolog 2 (EZH2) and cluster of differentiation 79B (CD79B) genes in a cohort of mature B-cell non-Hodgkin's lymphomas. - Source :PubMed

Frequent MYD88 L265P and CD79B Mutations in Primary Breast Diffuse Large B-Cell Lymphoma.

Primary breast diffuse large B-cell lymphoma (PB-DLBCL) is a rare disease comprising <3% of extranodal lymphomas. It frequently reveals an activated B-cell (ABC)-like phenotype. ABC-like DLBCL was reported to have gain-of-function mutations in MYD88, CD79B, CARD11, and TNFAIP3, resulting in constitutive activation of the NFκB pathway. Because of the rare occurrence of PB-DLBCL, the frequency of MYD88 and CD79B mutations is still unknown. We used Sanger sequencing to study these mutations from 46 breast DLBCL cases and also investigated the associated clinicopathologic factors. MYD88 L265P was confirmed by allele-specific polymerase chain reaction and compared with the Sanger sequencing results. MYD88 L265P and CD79B mutations were detected in 27/46 (58.7%) and 11/33 (33.3%) cases, respectively. Twenty-eight of 46 cases met the criteria for PB-DLBCL, and the latter 18 cases were further classified as clinical breast DLBCL (CLB-DLBCL). The frequency of MYD88 L265P and CD79B mutations was 16/28 (57.1%) and 9/23 (39.1%), respectively, in PB-DLBCL and 11/18 (61.1%) and 2/10 (20%), respectively, in CLB-DLBCL. When the cutoff value was set at ΔCt≤1, the result of allele-specific polymerase chain reaction for MYD88 corresponded to those of the Sanger sequence at 92.6% sensitivity and 100% specificity. According to Choi's algorithm, 16/27 (59.3%) demonstrated an ABC-like phenotype in PB-DLBCL, and 15/18 (83.3%) demonstrated an ABC-like phenotype in CLB-DLBCL. In conclusion, MYD88 L265P and CD79B mutations were frequently detected in PB-DLBCL, and they may be key molecules associated with PB-DLBCL lymphomagenesis. Further analysis will be required to clarify the mechanism of its pathogenesis. - Source :PubMed

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