GNA13 Knockout Cell Lysate

Name: GNA13 Knockout Cell Lysate
SKU: DAG-KO177
Rating: 5 (1 reviews)

GNA13 Knockout Cell Lysate from HeLa cell line for anti-GNA13 antibody specificity validation.

COA

SDS

Datasheet

Summary

Product Overview

HeLa cell lines were engineered into double-knockout lines by CRISPR technology. The double knockout genotype was verified by PCR followed by sequencing. The GNA13 knockout cell lysate are the cell homogenate in RIPA buffer made from the KO cell lines. A vial of lysate from the parental cell line was also provided as an internal control.

Nature

Cell Lysate

Alternative Names

GNA13; guanine nucleotide binding protein (G protein), alpha 13; G13; guanine nucleotide-binding protein subunit alpha-13; g alpha-13; G-protein subunit alpha-13;

Application Notes

Prior to SDS-PAGE fractionation, boil the lysate for 5 minutes.

Dilution

Lysate samples can be diluted with 2x SDS Sample Buffer.
After dilution, the protein sample should be aliquoted and stored at -20°C for long term storage.

Format

Lyophilized

Concentration

The protein concentration was determined with BCA assay.

Buffer

RIPA buffer

Preservative

None

Storage

Store at -20°C. Avoid repeated freeze-thaw cycles.

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

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Customer Reviews

References

Genetic heterogeneity of diffuse large B-cell lymphoma

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Authors: Zhang, Jenny; Grubor, Vladimir; Love, Cassandra L.; Banerjee, Anjishnu; Richards, Kristy L.; Mieczkowski, Piotr A.; Dunphy, Cherie; Choi, William; Au, Wing Yan; Srivastava, Gopesh; Lugar, Patricia L.; Rizzieri, David A.; Lagoo, Anand S.; Bernal-Mizrachi, Leon; Mann, Karen P.; Flowers, Christopher; Naresh, Kikkeri; Evens, Andrew; Gordon, Leo I.; Czader, Magdalena; Gill, Javed I.; Hsi, Eric D.; Liu, Qingquan; Fan, Alice; Walsh, Katherine; Jima, Dereje; Smith, Lisa L.; Johnson, Amy J.; Byrd, John C.; Luftig, Micah A.; Ni, Ting; Zhu, Jun; Chadburn, Amy; Levy, Shawn; Dunson, David; Dave, Sandeep S.

Abstract

Diffuse large B-cell lymphoma (DLBCL) is the most common form of lymphoma in adults. The disease exhibits a striking heterogeneity in gene expression profiles and clinical outcomes, but its genetic causes remain to be fully defined. Through whole genome and exome sequencing, we characterized the genetic diversity of DLBCL. In all, we sequenced 73 DLBCL primary tumors (34 with matched normal DNA). Separately, we sequenced the exomes of 21 DLBCL cell lines. We identified 322 DLBCL cancer genes that were recurrently mutated in primary DLBCLs. We identified recurrent mutations implicating a number of known and not previously identified genes and pathways in DLBCL including those related to chromatin modification (ARID1A and MEF2B), NF-kappa B (CARD11 and TNFAIP3), PI3 kinase (PIK3CD, PIK3R1, and MTOR), B-cell lineage (IRF8, POU2F2, and GNA13), and WNT signaling (WIF1). We also experimentally validated a mutation in PIK3CD, a gene not previously implicated in lymphomas. The patterns of mutation demonstrated a classic long tail distribution with substantial variation of mutated genes from patient to patient and also between published studies. Thus, our study reveals the tremendous genetic heterogeneity that underlies lymphomas and highlights the need for personalized medicine approaches to treating these patients.

The Identification of Key Genes and Pathways in Glioma by Bioinformatics Analysis

JOURNAL OF IMMUNOLOGY RESEARCH

Authors: Liu, Mingfa; Xu, Zhennan; Du, Zepeng; Wu, Bingli; Jin, Tao; Xu, Ke; Xu, Liyan; Li, Enmin; Xu, Haixiong

Abstract

Glioma is the most common malignant tumor in the central nervous system. This study aims to explore the potential mechanism and identify gene signatures of glioma. The glioma gene expression profile GSE4290 was analyzed for differentially expressed genes (DEGs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were applied for the enriched pathways. A protein-protein interaction (PPI) network was constructed to find the hub genes. Survival analysis was conducted to screen and validate critical genes. In this study, 775 downregulated DEGs were identified. GO analysis demonstrated that the DEGs were enriched in cellular protein modification, regulation of cell communication, and regulation of signaling. KEGG analysis indicated that the DEGs were enriched in the MAPK signaling pathway, endocytosis, oxytocin signaling, and calcium signaling. PPI network and module analysis found 12 hub genes, which were enriched in synaptic vesicle cycling rheumatoid arthritis and collecting duct acid secretion. The four key genes CDK17, GNA13, PHF21A, and MTHFD2 were identified in both generation (GSE4412) and validation (GSE4271) dataset, respectively. Regression analysis showed that CDK13, PHF21A, and MTHFD2 were independent predictors. The results suggested that CDK17, GNA13, PHF21A, and MTHFD2 might play important roles and potentially be valuable in the prognosis and treatment of glioma.