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anti-Mouse (Murine) HELLS Antibodies:
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Lsh Is Essential for Maintaining Global DNA Methylation Levels in Amphibia and Fish and Interacts Directly with Dnmt1.
Lsh assists epigenetic gene repression upon binding to the Oct4 promoter region.
These results suggest that Lsh exerts epigenetic regulation at key regulators of neural stem cell fate ensuring adequate neural stem/progenitor cells self-renewal and maintenance during development.
fibroblasts derived from chromatin remodeling ATPase LSH (HELLS)-null mouse embryos, which lack DNA methylation from centromeric repeats, transposons and a number of gene promoters, are capable of reestablishing DNA methylation and silencing of misregulated genes upon re-expression of LSH.
Data suggest that HELLS controls cytosine methylation in a nuclear compartment that is in part defined by lamin B1 attachment regions.
histone H3 lysine 4 methylation modification was assessed in murine embryonic fibroblasts (MEFs) derived from the DNA methylation mutant Lsh(-/-) mice.
These results indicate that in the absence of HELLS, proliferation of spermatogonia is reduced and germ cell differentiation arrested at the midpachytene stage, implicating an essential role for HELLS during male meiosis.
LSH is essential for developmentally programmed de novo DNA methylation at the promoters of protein coding genes and recruitment of G9a/GLP complex to a subset of genomic loci.
Data show that hypomethylation in Lsh-/- cells is associated with efficient transcriptional elongation and splicing.
model in which Lsh is recruited by intact heterochromatin structure and then assists in maintaining heterochromatin organization by establishing CpG methylation patterns
PASG mutant mice display signs of growth retardation and premature aging, including low birth weight, failure to thrive, graying and loss of hair, reduced skin fat deposition, osteoporosis, kyphosis, cachexia, and premature death.
Lsh has a critical and previously unidentified role in epigenetic gene silencing and maintenance of genomic stability during female meiosis.
Lsh is part of a physiological feedback loop that reinforces DNA methylation and silencing of polycomb repressive complex targets
DNA hypomethylation caused by Lsh depletion is linked to transcriptional upregulation of retroviral elements and oncogenes such as PU.1 which in turn may promote the development of erythroleukemia in mice
HELLS and CDCA7 comprise a bipartite nucleosome remodeling complex; immunodeficiency-centromeric instability-facial anomalies syndrome has a defective HELLS and CDCA7 bipartite nucleosome remodeling complex
This study elucidates the molecular basis of the c-Myc/EGLN1-mediated induction of LSH expression that inhibits ferroptosis
LSH is likely one of the mechanisms of genome instability underlying 5-hydroxymethylcytosine loss in cancer.
High mRNA levels of HELLS is independent predictor of poor outcome in Renal Cell Carcinoma patients.
LSH promoted cancer progression in part by regulating expression of fumarate hydratase (FH).
Mutations in HELLS cause immunodeficiency-centromeric instability-facial anomalies syndrome type 4.
Mutations of HELLS gene is associated with stomach and colorectal cancers.
Upregulation of HELLS and UHRF1 is essential for the tumor phenotype. Also, these epigenetic regulators are important for the regulation of SYK.
just as E2F3, HELLS is overexpressed in human tumours including prostate cancer, indicating that either factor may contribute to the malignant progression of tumours
E2F1 plays a crucial role in transcriptional control of the human Lsh gene and the decrease of Lsh expression in senescent cells is related to the repression of E2F1
Data provide strong evidence that CEP55 and HELLS may be used in conjunction with FOXM1 as a biomarker set for early cancer detection and indicators of malignant conversion and progression.
LSH serves as a recruiting factor for DNA methyltransferases and histone deacetylases to establish transcriptionally repressive chromatin which is perhaps further stabilized by DNA methylation at targeted loci
These results suggest differences in cellular consequences of hypomethylation mediated by PASG during development compared to that in somatic cells.
Lsh overexpression delays cell senescence by silencing p16(INK4a) in human fibroblasts.
This gene encodes a lymphoid-specific helicase. Other helicases function in processes involving DNA strand separation, including replication, repair, recombination, and transcription. This protein is thought to be involved with cellular proliferation and may play a role in leukemogenesis. Alternatively spliced transcript variants have been described, but their biological validity has not been determined.
, helicase, lymphoid specific
, lymphoid-specific helicase-like
, lymphocyte-specific helicase
, proliferation-associated SNF2-like protein
, TBC1D12: TBC1 domain family, member 12
, SWI/SNF2-related matrix-associated actin-dependent regulator of chromatin subfamily A member 6
, SWI/SNF2-related, matrix-associated, actin-dependent regulator of chromatin, subfamily A, member 6
, lymphoid-specific helicase