Anti-CHD1L polyclonal antibody (DPABH-05285)

Specifications


Host Species
Rabbit
Antibody Isotype
IgG
Species Reactivity
Human
Immunogen
Recombinant fragment, corresponding to a region within internal sequence amino acids 274-598 of Human CHD1L (Uniprot ID: Q86WJ1).
Conjugate
Unconjugated

Applications


Application Notes
WB: 1/500 - 1/3000;
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
CHD1L; chromodomain helicase DNA binding protein 1-like; ALC1; CHDL; chromodomain-helicase-DNA-binding protein 1-like; amplified in liver cancer 1
Entrez Gene ID
UniProt ID

Citations


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References


CHD1L is associated with poor survival and promotes the proliferation and metastasis of intrahepatic cholangiocarcinoma

ONCOLOGY REPORTS

Authors: Li, Shimiao; Chai, Yi; Ding, Yanbao; Yuan, Tinghao; Wu, Changwen; Huang, Changwen

Chromodomain helicase/ATPase DNA-binding protein 1-like gene (CHD1L) is a new oncogene which has been confirmed to be crucial to the progression of many solid tumors. In the present study, the expression of CHD1L was found to be upregulated in intrahepatic cholangiocarcinoma (ICC), which was significantly associated with histological differentiation (P=0.011), vascular invasion (P=0.002), lymph node metastasis (P=0.008) and TNM stage (P=0.001). Kaplan-Meier survival analysis revealed that ICC patients with positive CHD1L expression had shorter overall and disease-free survival than those with negative CHD1L expression. Functional study found that CHD1L exhibited strong oncogenic roles, including increased cell growth by CCK-8 assay, colony formation by plate colony formation assay, G1/S transition by flow cytometry and tumor formation in nude mice. In addition, RNAi-mediated silencing of CHD1L inhibited ICC invasion and metastasis by wound healing, Transwell migration and Matrigel invasion assays in vitro and in vivo. Collectively, our results show that CHD1L is upregulated and promotes the proliferation and metastasis of ICC cells. CHD1L acts as an oncogene and may be a prognostic factor or therapeutic target for patients with ICC.

A Novel Regulatory Axis, CHD1L-MicroRNA 486-Matrix Metalloproteinase 2, Controls Spermatogonial Stem Cell Properties

MOLECULAR AND CELLULAR BIOLOGY

Authors: Liu, Shan-Shan; Maguire, Eithne Margaret; Bai, Yin-Shan; Huang, Li; Liu, Yurong; Xu, Liping; Fauzi, Iliana; Zhang, Shou-Quan; Xiao, Qingzhong; Ma, Ning-Fang

Spermatogonial stem cells (SSCs) are unipotent germ cells that are at the foundation of spermatogenesis and male fertility. However, the underlying molecular mechanisms governing SSC stemness and growth properties remain elusive. We have recently identified chromodomain helicase/ATPase DNA binding protein 1-like (Chd1l) as a novel regulator for SSC survival and self-renewal, but how these functions are controlled by Chd1l remains to be resolved. Here, we applied high-throughput small RNA sequencing to uncover the microRNA (miRNA) expression profiles controlled by Chd1l and showed that the expression levels of 124 miRNA transcripts were differentially regulated by Chd1l in SSCs. KEGG pathway analysis shows that the miRNAs that are differentially expressed upon Chd1l repression are significantly enriched in the pathways associated with stem cell pluripotency and proliferation. As a proof of concept, we demonstrate that one of the most highly upregulated miRNAs, miR-486, controls SSC stemness gene expression and growth properties. The matrix metalloproteinase 2 (MMP2) gene has been identified as a novel miR-486 target gene in the context of SSC stemness gene regulation and growth properties. Data from cotransfection experiments showed that Chd1l, miR486, and MMP2 work in concert in regulating SSC stemness gene expression and growth properties. Finally, our data also revealed that MMP2 regulates SSC stemness gene expression and growth properties through activating beta-catenin signaling by cleaving N-cadherin and increasing beta-catenin nuclear translocation. Our data demonstrate that Chd1l-miR-486-MMP2 is a novel regulatory axis governing SSC stemness gene expression and growth properties, offering a novel therapeutic opportunity for treating male infertility.

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