Histone-C-Ab ELISA Kit

Name: Histone-C-Ab ELISA Kit
SKU: DEIABL345
Rating: 5 (1 reviews)

Regulatory status: For research use only, not for use in diagnostic procedures.

COA

SDS

Datasheet

Summary

Sample

serum

Species Reactivity

Human

Intended Use

Histone-C-Ab ELISA is a solid phase enzyme immunoassay with human native histones H1, H2A, H2B, H3, H4 isolated from the eukaryotic celline HeLa for the quantitative and qualitative detection of antibodies against histones in human serum.
The assay is a tool in the differential diagnosis of systemic lupus erythematosus (SLE).

Contents of Kit

Sample Buffer (5x): 1 x 20ml
Wash Buffer (50x): 1 x 20ml
Negative Control: 1 x 1.5ml
Positive Control: 1 x 1.5ml
Cut-off Calibrator: 1 x 1.5ml
Calibrators: 6 x 1.5ml
Conjugate, IgG: 1 x 15ml
TMB Substrate: 1 x 15ml
Stop Solution: 1 x 15ml
Microtiter plate 12 x 8 well strips

Storage

2-8°C

Precision

Detection Range

0 - 300 U/mL, cut-off 15 U/mL

Sensitivity

1.0 U/ml

General Description

Histone-C-Ab ELISA is a solid phase enzyme immunoassay with human native histones H1, H2A, H2B, H3, H4 isolated from the eukaryotic celline HeLa for the quantitative detection of antibodies against histones in human serum. The assay is a tool in the differential diagnosis of systemic lupus erythematosus (SLE). Histones are small basic proteins of 11 to 21 kDa constituting a set of interacting proteins that organize and constrain the topology of DNA in most eukaryotic cells into a particle called nucleosome. In this particle the four histones H2A, H2B, H3 and H4 form an octamer (H2A, H2B, H3, H4)2 around which 146 bp of dsDNA is wrapped by 1 3/4 turns. Histone H1 interacts with the nucleosome and together with linked-DNA connects neighboring nucleosomes. Antibodies against histones occur in patients with SLE with a frequency of 50 %, during active phases of SLE with an even higher frequency (80%). They are not specific for SLE, especially when not associated with anti-dsDNA antibodies. They are also found in other inflammatory rheumatoid diseases, like rheumatoid arthritis (low titers and mainly against H1), or systemic sclerosis and juvenile chronic arthritis. Moreover these antibodies are found in primary biliary cirrhosis (up to 70%) and autoimmune hepatitis (up to 35%), too. Anti-histone antibodies, in the absence of antibodies to dsDNA, do play an important role in the diagnosis of drug-induced LE being found in 95% of cases. These drugs are inducing joint and skin symptoms, as well as the different anti-histone specificities, while never renal manifestations. Anti-histone antibodies in drug-induced LE are temporary and disappear within a few months after withdrawal of the inducing drug.

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

Loss of histone lysine methyltransferase EZH2 confers resistance to tyrosine kinase inhibitors in non-small cell lung cancer

CANCER LETTERS

Authors: Quan, Chuntao; Chen, Yuchen; Wang, Xiaomu; Yang, Dong; Wang, Qing; Huang, Yixue; Petersen, Robert B.; Liu, Xinran; Zheng, Ling; Li, Yangkai; Huang, Kun

Abstract

Tyrosine kinase inhibitor (TKI) treatment is the first-line therapy for non-small cell lung cancer (NSCLC) caused by activating mutations of epidermal growth factor receptor (EGFR). However, acquired resistance to EGFR-TKI occurs almost inevitably. Aberrant activation of proto-oncogene MET has been known to confer EGFR-TKI resistance; however, the mechanisms involved remains unclear. Recent evidence implicates epigenetic hetero-geneity as playing roles in cancer drug resistance, whereas links involving epigenetic heterogeneity and MET in NSCLC remain poorly understood. We found that expression of EZH2, a histone methyltransferase, was negatively correlated with MET activation and EGFR-TKI resistance in NSCLC cells and clinical samples, suggesting the potential for EZH2 to be used as a biomarker for EGFR-TKI sensitivity. Knockdown or inhibition of EZH2 up regulated MET expression and phosphorylation, and elevated proliferation and EGFR-TKI resistance of cells in vitro. Meanwhile, inhibition of MET or PI3K/AKT enhanced EZH2 levels and restored sensitivity to EGFR-TKI. These findings indicate a "MET-AKT-EZH2" feedback loop regulating EGFR-TKI-resistance. Furthermore, combination therapy of PI3K/AKT inhibition and EGFR-TKI, which interrupts the loop, enhanced tumor-suppressive effects in an EGFR-TKI-resistant xenograft model, indicating a potential approach against drug resistance in NSCLC.

Broad genic repression domains signify enhanced silencing of oncogenes

NATURE COMMUNICATIONS

Authors: Zhao, Dongyu; Zhang, Lili; Zhang, Min; Xia, Bo; Lv, Jie; Gao, Xinlei; Wang, Guangyu; Meng, Qingshu; Yi, Yang; Zhu, Sen; Tomoiaga, Alin S.; Lee, Min Gyu; Cooke, John P.; Cao, Qi; Chen, Kaifu

Abstract

Cancers result from a set of genetic and epigenetic alterations. Most known oncogenes were identified by gain-of-function mutations in cancer, yet little is known about their epigenetic features. Through integrative analysis of 11,596 epigenomic profiles and mutations from >8200 tumor-normal pairs, we discover broad genic repression domains (BGRD) on chromatin as an epigenetic signature for oncogenes. A BGRD is a widespread enrichment domain of the repressive histone modification H3K27me3 and is further enriched with multiple other repressive marks including H3K9me3, H3K9me2, and H3K27me2. Further, BGRD displays widespread enrichment of repressed cis-regulatory elements. Shortening of BGRDs is linked to derepression of transcription. BGRDs at oncogenes tend to be conserved across normal cell types. Putative tumor-promoting genes and lncRNAs defined using BGRDs are experimentally verified as required for cancer phenotypes. Therefore, BGRDs play key roles in epigenetic regulation of cancer and provide a direction for mutation-independent discovery of oncogenes. Epigenetically altered genes can have a key role in cancer pathobiology but epigenetic signatures that distinguish oncogenes are not yet known. Here, the authors identify broad genic repression domains, defined by widespread H3K27me3 modification, as an epigenetic signature to provide mutation-independent information for discovery of potential oncogenes.