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Search results for: BCL10

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#35750252   2022/06/21 To Up

BCL10 loss-of-function novel mutation leading to atypical severe combined immunodeficiency.

Severe combined immunodeficiency (SCID) is characterized by severe, early-onset infection in infants. B-cell lymphoma/leukemia (BCL) 10 defects causing SCID have been reported previously in two patients.
Salem Al-Tamemi, Zaid Alhinai, Najwa Al-Rahbi, Raghad Al-Abdawani, Laila Al-Yazidi, Jalila Al-Shekaili, Mahmood Al-Kindi, Almundher Al-Maawali

1290 related Products with: BCL10 loss-of-function novel mutation leading to atypical severe combined immunodeficiency.

1 kit(96 Wells)100 100 extractions 1 g430 tests961 kit(96 Wells)1 module200 ug

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#35727133   2022/06/21 To Up

A nucleation barrier spring-loads the CBM signalosome for binary activation.

Immune cells activate in binary, switch-like fashion via large protein assemblies known as signalosomes, but the molecular mechanism of the switch is not yet understood. Here, we employed an in-cell biophysical approach to dissect the assembly mechanism of the CARD-BCL10-MALT1 (CBM) signalosome, which governs NF-κB activation in both innate and adaptive immunity. We found that the switch consists of a sequence-encoded and deeply conserved nucleation barrier to ordered polymerization by the adaptor protein BCL10. The particular structure of the BCL10 polymers did not matter for activity. Using optogenetic tools and single-cell transcriptional reporters, we discovered that endogenous BCL10 is functionally supersaturated even in unstimulated human cells, and this results in a predetermined response to stimulation upon nucleation by activated CARD multimers. Our findings may inform on the progressive nature of age-associated inflammation, and suggest that signalosome structure has evolved via selection for kinetic rather than equilibrium properties of the proteins.
Alejandro Rodriguez Gama, Tayla Miller, Jeffrey J Lange, Jay R Unruh, Randal Halfmann

1083 related Products with: A nucleation barrier spring-loads the CBM signalosome for binary activation.

100 ml100.00 ul 1 G1 ml100ug20 ug2 mg 1 G100μg

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#35600392   2022/05/06 To Up

SOCS3 Acts as an Onco-immunological Biomarker With Value in Assessing the Tumor Microenvironment, Pathological Staging, Histological Subtypes, Therapeutic Effect, and Prognoses of Several Types of Cancer.

The suppressor of cytokine signaling () family contains eight members, including and , and has been shown to inhibit cytokine signal transduction in various signaling pathways. Although several studies have currently shown the correlations between and several types of cancer, no pan-cancer analysis is available to date. We used various computational tools to explore the expression and pathogenic roles of in several types of cancer, assessing its potential role in the pathogenesis of cancer, in tumor immune infiltration, tumor progression, immune evasion, therapeutic response, and prognostic. The results showed that was downregulated in most The Cancer Genome Atlas (TCGA) cancer datasets but was highly expressed in brain tumors, breast cancer, esophageal cancer, colorectal cancer, and lymphoma. High expression in glioblastoma multiforme (GBM) and brain lower-grade glioma (LGG) were verified through immunohistochemical experiments. GEPIA and Kaplan-Meier Plotter were used, and this bioinformatics analysis showed that high expression was associated with a poor prognosis in the majority of cancers, including LGG and GBM. Our analysis also indicated that may be involved in tumor immune evasion immune cell infiltration or T-cell exclusion across different types of cancer. In addition, methylation was negatively correlated with expression levels, worse prognoses, and dysfunctional T-cell phenotypes in various types of cancer. Next, different analytical methods were used to select genes related to gene alterations and carcinogenic characteristics, such as , , , , , , , , and , and several biological functions were identified between them. We found that was involved in cancer development primarily through the signaling pathway and cytokine receptor activity. Furthermore, expression levels were associated with immunotherapy or chemotherapy for numerous types of cancer. In conclusion, this study showed that is an immune-oncogenic molecule that may possess value as a biomarker for diagnosis, treatment, and prognosis of several types of cancer in the future.
Lirui Dai, Yiran Tao, Zimin Shi, Wulong Liang, Weihua Hu, Zhe Xing, Shaolong Zhou, Xuyang Guo, Xudong Fu, Xinjun Wang

1074 related Products with: SOCS3 Acts as an Onco-immunological Biomarker With Value in Assessing the Tumor Microenvironment, Pathological Staging, Histological Subtypes, Therapeutic Effect, and Prognoses of Several Types of Cancer.



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#35540095   2022/04/25 To Up

CARD9-Mediated Signaling and Cardiovascular Diseases.


Xuanyou Liu, Bimei Jiang, Hong Hao, Zhenguo Liu

1953 related Products with: CARD9-Mediated Signaling and Cardiovascular Diseases.

95 Tests / Kit1.5x10(6) cells100ug2 Pieces/Box1 g250 Tests / Kit100 96 wells (1 kit)100ug200 200ul

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#35411950   2022/04/12 To Up

USP7 sustains an active epigenetic program via stabilizing MLL2 and WDR5 in diffuse large B-cell lymphoma.

Activated B-cell-like (ABC)-diffuse large B-cell lymphoma (ABC-DLBCL) is a common subtype of non-Hodgkin's lymphoma with poor prognosis. The survival of ABC-DLBCL relies on constitutive activation of BCR signaling, but the underlying molecular mechanism is not fully addressed. By mining The Cancer Genome Atlas database, we found that the expression of ubiquitin-specific protease 7 (USP7) is significantly elevated in three cancer types including DLBCL. Interestingly, unlike germinal center B-cell-like (GCB)-DLBCL, ABC-DLBCL shows upregulated expression of USP7. Inhibiting the enzymatic activity of USP7 (P22077) has a drastic effect on ABC-DLBCL, but not GCB-DLBCL cells. Compared to GCB-DLBCL, ABC-DLBCL cells show transcriptional upregulation of multiple components of BCR-signaling. USP7 inhibition significantly reduces the expression of upregulated components of BCR signaling. Mechanistically, USP7 inhibition greatly reduces the methylation of histone 3 on lysine 4 (H3K4me2), which is an epigenetic marker for active enhancers. USP7 inhibition greatly reduces the protein level of WDR5 and MLL2, key components of lysine-specific methyltransferase complex (complex of proteins associated with Set1 [COMPASS]). In ABC-DLBCL cells, USP7 stabilizes WDR5 and MLL2. In patients, the expression of USP7 is significantly associated with components of BCR signaling (LYN, SYK, BTK, PLCG2, PRKCB, MALT1, BCL10, and CARD11) and targets of BCR signaling (MYC and IRF4). In summary, we demonstrated an essential role of USP7 in ABC-DLBCL by organizing an oncogenic epigenetic program via stabilization of WDR5 and MLL2. Targeting USP7 might be a novel and efficient approach to treat patients with ABC-DLBCL and it might be better than targeting individual components such as BTK in BCR signaling.
Yuanyuan Wu, Hongyan Gu, Yuhua Bao, Ting Lin, Zhenyu Wang, Donghua Gu, Haoliang Shen, Hua Xian, Yihui Fan, Renfang Mao

1495 related Products with: USP7 sustains an active epigenetic program via stabilizing MLL2 and WDR5 in diffuse large B-cell lymphoma.

100ug Lyophilized100 ug/vial100ug Lyophilized100ug Lyophilized2 Pieces/Box

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#35406738   2022/03/31 To Up

CARD19 Interacts with Mitochondrial Contact Site and Cristae Organizing System Constituent Proteins and Regulates Cristae Morphology.

CARD19 is a mitochondrial protein of unknown function. While CARD19 was originally reported to regulate TCR-dependent NF-κB activation via interaction with BCL10, this function is not recapitulated ex vivo in primary murine CD8 T cells. Here, we employ a combination of SIM, TEM, and confocal microscopy, along with proteinase K protection assays and proteomics approaches, to identify interacting partners of CARD19 in macrophages. Our data show that CARD19 is specifically localized to the outer mitochondrial membrane. Through deletion of functional domains, we demonstrate that both the distal C-terminus and transmembrane domain are required for mitochondrial targeting, whereas the CARD is not. Importantly, mass spectrometry analysis of 3×Myc-CARD19 immunoprecipitates reveals that CARD19 interacts with the components of the mitochondrial intermembrane bridge (MIB), consisting of mitochondrial contact site and cristae organizing system (MICOS) components MIC19, MIC25, and MIC60, and MICOS-interacting proteins SAMM50 and MTX2. These CARD19 interactions are in part dependent on a properly folded CARD. Consistent with previously reported phenotypes upon siRNA silencing of MICOS subunits, absence of CARD19 correlates with irregular cristae morphology. Based on these data, we propose that CARD19 is a previously unknown interacting partner of the MIB and the MIC19-MIC25-MIC60 MICOS subcomplex that regulates cristae morphology.
Kariana E Rios, Ming Zhou, Nathaniel M Lott, Chelsi R Beauregard, Dennis P McDaniel, Thomas P Conrads, Brian C Schaefer

2187 related Products with: CARD19 Interacts with Mitochondrial Contact Site and Cristae Organizing System Constituent Proteins and Regulates Cristae Morphology.

100ul2.5 mg50 mg25 mg96T100ul50 ug 10 mg1000 tests100ug500 mg25 mg

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#35406516   2022/03/29 To Up

Extranodal Marginal Zone Lymphoma: Pathogenesis, Diagnosis and Treatment.

Extranodal Marginal Zone Lymphoma (EMZL lymphoma) is an indolent B-cell lymphoma with a median age at diagnosis of about 60 years. It accounts for 7-8% of all B-cell lymphomas. It can occur in various extranodal sites, including stomach, lung, ocular adnexa, and skin; furthermore, the disseminated disease can be found in 25-50% of cases. Several infectious agents, such as () in the case of gastric Mucosa Associated Lymphoid Tissue (MALT) Lymphoma, can drive the pathogenesis of this cancer, through the autoantigenic stimulation of T cells, but there may also be other factors participating such autoimmune diseases. Initial staging should include total body computed tomography, bone marrow aspirate, and endoscopic investigation if indicated. Fluorescence in situ hybridization (FISH), should be performed to detect the presence of specific chromosomal translocations involving the and genes, which leads to the activation of the signaling pathway. Depending on the location and dissemination of the disease, different therapeutic choices may include targeted therapy against the etiopathogenetic agent, radiotherapy, immunochemotherapy, and biological drugs. The purpose of this review is to illustrate the complex biology and the diagnosis of this disease and to better define new treatment strategies.
Alice Di Rocco, Luigi Petrucci, Giovanni Manfredi Assanto, Maurizio Martelli, Alessandro Pulsoni

1936 related Products with: Extranodal Marginal Zone Lymphoma: Pathogenesis, Diagnosis and Treatment.

1 ml100ug1 g 6 ml Ready-to-use 96 wells (1 kit)100ugeach200ul

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#35403148   2021/07/03 To Up

Pancreatic-type Mixed Acinar-neuroendocrine Carcinoma of the Stomach: A Case Report and Literature Review.

Pancreatic-type mixed acinar-neuroendocrine carcinoma (PMANEC) in the stomach is very rare. We report a case of PMANEC that was initially misdiagnosed as a gastric neuroendocrine tumor.
James Saller, Brooke Hough, Domenico Coppola

1104 related Products with: Pancreatic-type Mixed Acinar-neuroendocrine Carcinoma of the Stomach: A Case Report and Literature Review.



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#35352485   // To Up

Identification and validation of a seven-gene prognostic marker in colon cancer based on single-cell transcriptome analysis.

Colon cancer (CC) is one of the most commonly diagnosed tumours worldwide. Single-cell RNA sequencing (scRNA-seq) can accurately reflect the heterogeneity within and between tumour cells and identify important genes associated with cancer development and growth. In this study, scRNA-seq was used to identify reliable prognostic biomarkers in CC. ScRNA-seq data of CC before and after 5-fluorouracil treatment were first downloaded from the Gene Expression Omnibus database. The data were pre-processed, and dimensionality reduction was performed using principal component analysis and t-distributed stochastic neighbour embedding algorithms. Additionally, the transcriptome data, somatic variant data, and clinical reports of patients with CC were obtained from The Cancer Genome Atlas database. Seven key genes were identified using Cox regression analysis and the least absolute shrinkage and selection operator method to establish signatures associated with CC prognoses. The identified signatures were validated on independent datasets, and somatic mutations and potential oncogenic pathways were further explored. Based on these features, gene signatures, and other clinical variables, a more effective predictive model nomogram for patients with CC was constructed, and a decision curve analysis was performed to assess the utility of the nomogram. A prognostic signature consisting of seven prognostic-related genes, including CAV2, EREG, NGFRAP1, WBSCR22, SPINT2, CCDC28A, and BCL10, was constructed and validated. The proficiency and credibility of the signature were verified in both internal and external datasets, and the results showed that the seven-gene signature could effectively predict the prognosis of patients with CC under various clinical conditions. A nomogram was then constructed based on features such as the RiskScore, patients' age, neoplasm stage, and tumor (T), nodes (N), and metastases (M) classification, and the nomogram had good clinical utility. Higher RiskScores were associated with a higher tumour mutational burden, which was confirmed to be a prognostic risk factor. Gene set enrichment analysis showed that high-score groups were enriched in 'cytoplasmic DNA sensing', 'Extracellular matrix receptor interactions', and 'focal adhesion', and low-score groups were enriched in 'natural killer cell-mediated cytotoxicity', and 'T-cell receptor signalling pathways', among other pathways. A robust seven-gene marker for CC was identified based on scRNA-seq data and was validated in multiple independent cohort studies. These findings provide a new potential marker to predict the prognosis of patients with CC.
Yang Zhou, Yang Guo, Yuanhe Wang

2264 related Products with: Identification and validation of a seven-gene prognostic marker in colon cancer based on single-cell transcriptome analysis.



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