HINT1 Knockout Cell Lysate

Name: HINT1 Knockout Cell Lysate
SKU: DAG-KO040
Rating: 5 (1 reviews)

HINT1 Knockout Cell Lysate from HeLa cell line for anti-HINT1 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 HINT1 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

HINT1; histidine triad nucleotide binding protein 1; HINT; NMAN; PKCI-1; PRKCNH1; histidine triad nucleotide-binding protein 1; protein kinase C inhibitor 1; adenosine 5'-monophosphoramidase; protein kinase C-interacting protein 1

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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References

Aneuploid acute myeloid leukemia exhibits a signature of genomic alterations in the cell cycle and protein degradation machinery

CANCER

Authors: Simonetti, Giorgia; Padella, Antonella; do Valle, Italo Faria; Fontana, Maria Chiara; Fonzi, Eugenio; Bruno, Samantha; Baldazzi, Carmen; Guadagnuolo, Viviana; Manfrini, Marco; Ferrari, Anna; Paolini, Stefania; Papayannidis, Cristina; Marconi, Giovanni; Franchini, Eugenia; Zuffa, Elisa; Laginestra, Maria Antonella; Zanotti, Federica; Astolfi, Annalisa; Iacobucci, Ilaria; Bernardi, Simona; Sazzini, Marco; Ficarra, Elisa; Maria Hernandez, Jesus; Vandenberghe, Peter; Cools, Jan; Bullinger, Lars; Ottaviani, Emanuela; Testoni, Nicoletta; Cavo, Michele; Haferlach, Torsten; Castellani, Gastone; Remondini, Daniel; Martinelli, Giovanni

Abstract

Background Aneuploidy occurs in more than 20% of acute myeloid leukemia (AML) cases and correlates with an adverse prognosis. Methods To understand the molecular bases of aneuploid acute myeloid leukemia (A-AML), this study examined the genomic profile in 42 A-AML cases and 35 euploid acute myeloid leukemia (E-AML) cases. Results A-AML was characterized by increased genomic complexity based on exonic variants (an average of 26 somatic mutations per sample vs 15 for E-AML). The integration of exome, copy number, and gene expression data revealed alterations in genes involved in DNA repair (eg, SLX4IP, RINT1, HINT1, and ATR) and the cell cycle (eg, MCM2, MCM4, MCM5, MCM7, MCM8, MCM10, UBE2C, USP37, CK2, CK3, CK4, BUB1B, NUSAP1, and E2F) in A-AML, which was associated with a 3-gene signature defined by PLK1 and CDC20 upregulation and RAD50 downregulation and with structural or functional silencing of the p53 transcriptional program. Moreover, A-AML was enriched for alterations in the protein ubiquitination and degradation pathway (eg, increased levels of UHRF1 and UBE2C and decreased UBA3 expression), response to reactive oxygen species, energy metabolism, and biosynthetic processes, which may help in facing the unbalanced protein load. E-AML was associated with BCOR/BCORL1 mutations and HOX gene overexpression. Conclusions These findings indicate that aneuploidy-related and leukemia-specific alterations cooperate to tolerate an abnormal chromosome number in AML, and they point to the mitotic and protein degradation machineries as potential therapeutic targets. (C) 2018 The Authors. Cancer published by Wiley Periodicals, Inc. on behalf of American Cancer Society. This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

HINT1 is involved in the behavioral abnormalities induced by social isolation rearing

NEUROSCIENCE LETTERS

Authors: Dang, Yong-hui; Liu, Peng; Ma, Rui; Chu, Zheng; Liu, You-ping; Wang, Jia-bei; Ma, Xian-cang; Gao, Cheng-ge

Abstract

Social isolation (SI) rearing has been demonstrated to induce behavioral abnormalities like anxiety, impulsivity, aggression, and learning and memory deficits which are relevant to core symptoms in patients with some certain neuropsychiatric disorders. But the underlying pathophysiological mechanisms remain unclear. Recent studies have revealed HINT1 has close relation with diverse neuropsychiatric diseases. In this present study, the SI rearing mice exhibited depression-like and aggressive behavior. Besides, HINT1 protein levels decreased in PFC but increased in HIP. Based on the data obtained, we concluded that HINT1 is involved in the behavioral abnormalities induced by social isolation and exerts distinct roles in different encephalic regions. (C) 2015 Published by Elsevier Ireland Ltd.