Human CSNK1D blocking peptide

Name: Human CSNK1D blocking peptide
SKU: CDBP0684
Rating: 5 (1 reviews)

Synthetic Human CSNK1D blocking peptide for Apuri, BL, ELISA

COA

SDS

Datasheet

Summary

Product Overview

Blocking/Immunizing peptide for anti-Casein Kinase 1, delta antibody

Target

Casein Kinase 1, delta

Nature

Synthetic

Tag/Conjugate

Unconjugated

Application Notes

For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not for human or animal consumption.

Format

Lyophilized powder

Preservative

None

Storage

Shipped at ambient temperature, store at -20°C.

Entrez Gene ID

1453

Antigen Description

This gene is a member of the casein kinase I (CKI) gene family whose members have been implicated in the control of cytoplasmic and nuclear processes, including DNA replication and repair. The encoded protein may also be involved in the regulation of apoptosis, circadian rhythm, microtubule dynamics, chromosome segregation, and p53-mediated effects on growth. The encoded protein is highly similar to the mouse and rat CK1 delta homologs. Three transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Feb 2014]

Function

ATP binding; glycoprotein binding; peptide binding; phosphoprotein binding; protein binding; protein kinase activity; protein kinase activity; protein kinase activity; protein serine/threonine kinase activity; tau-protein kinase activity;

Synonyms

CSNK1D; casein kinase 1, delta; ASPS; HCKID; FASPS2; CKIdelta; casein kinase I isoform delta; CKId; CKI-delta; tau-protein kinase CSNK1D;

Citations

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Documents

pdf COA

pdf SDS

pdf Datasheet

QA & Reviews

Customer Reviews

References

An evaluation of polymorphisms in casein kinase 1 delta and epsilon genes in major psychiatric disorders

NEUROSCIENCE LETTERS

Authors: Matsunaga, Shinji; Ikeda, Masashi; Kishi, Taro; Fukuo, Yasuhisa; Aleksic, Branko; Yoshimura, Reiji; Okochi, Tomo; Yamanouchi, Yoshio; Kinoshita, Yoko; Kawashima, Kunihiro; Umene-Nakano, Wakako; Inada, Toshiya; Kunugi, Hiroshi; Kato, Tadafumi; Yoshikawa, Takeo; Ujike, Hiroshi; Nakamura, Jun; Ozaki, Norio; Kitajima, Tsuyoshi; Iwata, Nakao

Abstract

Disturbances of the circadian rhythm are involved in the pathophysiology of bipolar disorder (BD), schizophrenia (SCZ) and major depressive disorder (MDD). Specifically, because clock gene dysfunction is good candidate for enhancing the susceptibility to these psychiatric disorders, we selected two circadian rhythm-related genes (CSNK1D and CSNK1E) and investigated genetic associations of the genes with these three disorders. None of the SNPs showed a significant association with MDD, but a SNP (rs2075984) in CSNK1E and SNP (rs6502097) in CSNK1D were associated with SCZ (P=0.0091. uncorrected) and BD (P=0.030, uncorrected), respectively. To confirm these findings, we analyzed an independent dataset (maximum N=3815) but found a lack of association (P=0.63 for rs2075984 and P=0.61 for rs6502097). The final meta-analysis showed no association between these SNPs with SCZ (P=0.21) and BD (P=0.53). These results do not support that genetic variation in CSNK1D and CSNK1E is a susceptibility factor for major psychiatric disorders in the Japanese population. (C) 2012 Elsevier Ireland Ltd. All rights reserved.

Genomewide Histone H3 Lysine 9 Acetylation Profiling in CD4+T Cells Revealed Endoplasmic Reticulum Stress Deficiency in Patients with Acute-on-chronic Liver Failure

SCANDINAVIAN JOURNAL OF IMMUNOLOGY

Authors: Jin, L.; Wang, K.; Liu, H.; Chen, T.; Yang, Y.; Ma, X.; Wang, J.; Li, Y.; Du, D.; Zhao, Y.; He, Y.

Abstract

Acute-on-chronic liver failure (ACLF) displayed sepsis-like' immune paralysis. Little is known about the role of CD4+ T lymphocytes, the primary regulator of innate and adopted immune system, played in ACLF. Acetylation of histone H3 lysine 9 (H3K9ac), a key epigenetic modification, tightly controls gene transcription. Whether and how does H3K9ac modification regulate CD4+ T cells in ACLF remains unclear. PBMCs were isolated from patients with ACLF, immune tolerance of chronic hepatitis B (CHB-T) and immune active of chronic hepatitis B (CHB-A). Then, CD4+ T lymphocytes were purified by magnetic microbeads, and the purity was confirmed by flow cytometry. H3K9ac variations were analysed in CD4+ T cells using chromatin immunoprecipitation microarray and then confirmed by quantitative PCR. Whole-genome H3K9 acetylation analyses were conducted by bioinformatics. A total of 70 genes were differently modified in H3K9ac between CHB-A and ACLF groups, while 44 genes were differently modified in H3K9ac between CHB-T and ACLF groups. Clustering algorithm analysis showed patients with ACLF displayed sepsis-like' immune paralysis. Functional analysis showed endoplasmic reticulum (ER) stress, or downstream pathway-related genes, such as BIP, ATF4, PER1, CSNK1D, IRF3, BNIP1, AKT1 and UBC, were differentially modified in ACLF. We profiled H3K9 acetyl modification in CD4+ T lymphocytes from HBV-infected patients with three different immune states, that is ACLF, immune tolerance and immune active phases. ACLF displayed sepsis-like' immune paralysis. ER stress in CD4+ T lymphocytes attributed to ACLF. This study provides some useful clues for revealing the mechanisms underlying ACLF.