Human Bcl10 blocking peptide (CDBP0578)

Synthetic Human Bcl10 blocking peptide for BL, WB

Product Overview
BcL10 ( N - term ) peptide ( human )
Target
Bcl10
Nature
Synthetic
Species Reactivity
Human
Tag/Conjugate
Unconjugated
Procedure
None
Concentration
0.2 mg/ml
Size
100 μg
Buffer
PBS with 0.1% BSA 0.02% sodium azide pH7.2
Preservative
0.02% Sodium Azide
Storage
Upon Receipt - Keep as concentrated solution. Aliquot and store at -20℃ or below. Avoid freeze-thaw cycles.
UniProt ID
Antigen Description
This gene was identified by its translocation in a case of mucosa-associated lymphoid tissue (MALT) lymphoma. The protein encoded by this gene contains a caspase recruitment domain (CARD), and has been shown to induce apoptosis and to activate NF-kappaB. This protein is reported to interact with other CARD domain containing proteins including CARD9, 10, 11 and 14, which are thought to function as upstream regulators in NF-kappaB signaling. This protein is found to form a complex with MALT1, a protein encoded by another gene known to be translocated in MALT lymphoma. MALT1 and this protein are thought to synergize in the activation of NF-kappaB, and the deregulation of either of them may contribute to the same pathogenetic process that leads to the malignancy.
Function
NF-kappaB binding; enzyme binding; contributes_to kinase activator activity; kinase binding; protease binding; protein C-terminus binding; protein binding; protein kinase B binding; protein kinase binding; protein self-association; transcription coactivat
Synonyms
BCL10; B-cell CLL/lymphoma 10; B-cell lymphoma/leukemia 10; c E10; CARD containing molecule enhancing NF kB; CARD containing apoptotic signaling protein; CARD containing proapoptotic protein; CARD like apoptotic protein; CARMEN; caspase recruiting domain containing protein; CIPER; CLAP; mE10; hCLAP; cCARMEN; cellular-E10; cellular homolog of vCARMEN; CARD-containing proapoptotic protein; CARD containing molecule enhancing NF-kB; CARD-containing apoptotic signaling protein; caspase-recruiting domain-containing protein; CARD-containing molecule enhancing NF-kappa-B; mammalian CARD-containing adapter molecule E10; CED-3/ICH-1 prodomain homologous E10-like regulator; c-E10;

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References


BCL10 is recruited to sites of DNA damage to facilitate DNA double-strand break repair

CELL CYCLE

Authors: Ismail, Ismail Hassan; Dronyk, Ashley; Hu, Xiuying; Hendzel, Michael J.; Shaw, Andrew R.

Recent studies have found BCL10 can localize to the nucleus and that this is linked to tumor aggression and poorer prognosis. These studies suggest that BCL10 localization plays a novel role in the nucleus that may contribute to cellular transformation and carcinogenesis. In this study, we show that BCL10 functions as part of the DNA damage response (DDR). We found that BCL10 facilitates the rapid recruitment of RPA, BRCA1 and RAD51 to sites of DNA damage. Furthermore, we also found that ATM phosphorylates BCL10 in response to DNA damage. Functionally, BCL10 promoted DNA double-strand breaks repair, enhancing cell survival after DNA damage. Taken together our results suggest a novel role for BCL10 in the repair of DNA lesions.

Whole exome sequencing identifies novel mutations of epigenetic regulators in chemorefractory pediatric acute myeloid leukemia

LEUKEMIA RESEARCH

Authors: Zhan, Di; Zhang, Yingchi; Xiao, Peifang; Zheng, Xinchang; Ruan, Min; Zhang, Jingliao; Chen, Aili; Zou, Yao; Chen, Yumei; Huang, Gang; Hu, Shaoyan; Wang, Qian-fei; Zhu, Xiaofan

Genomic alterations underlying chemotherapy resistance remains poorly characterized in pediatric acute myeloid leukemia (AML). In this study, we used whole exome sequencing to identify gene mutations associated with chemo-resistance in 44 pediatric AML patients. We identified previously unreported mutations involving epigenetic regulators such as KDM5C, SRIT6, CHD4, and PRPF6 in pediatric AML patients. Despite low prevalence in general pediatric AML, mutations involving epigenetic regulators including splicing factors, were collectively enriched as a group in primary chemo-resistance AML patients. In addition, clonal evolution analysis of secondary chemo-resistance AML patients reveals dominant clone at diagnosis could survive several course of intensified chemotherapy. And gain of new mutations in genes such as MVP, TCF3, SS18, and BCL10, may contribute to chemo-resistance at relapse. These results provide novel insights into the genetic basis of treatment failure in pediatric AML.

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