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PHF6 is a member of the plant homeodomain (PHD)-like finger (PHF) family. Additionally we are shipping PHF6 Proteins (7) and PHF6 Kits (4) and many more products for this protein.
Showing 10 out of 43 products:
Human Polyclonal PHF6 Primary Antibody for ICC, IF - ABIN261177
Meacham, Lawton, Soto-Feliciano, Pritchard, Joughin, Ehrenberger, Fenouille, Zuber, Williams, Young, Hemann: A genome-scale in vivo loss-of-function screen identifies Phf6 as a lineage-specific regulator of leukemia cell growth. in Genes & development 2015
Human Polyclonal PHF6 Primary Antibody for ICC, IF - ABIN4345225
Pontén, Jirström, Uhlen: The Human Protein Atlas--a tool for pathology. in The Journal of pathology 2008
The mutations of the gene encoding plant homeodomain (PHD (show PDC Antibodies))-like finger protein 6 (PHF6) contribute to the pathogenesis of the X-linked intellectual disability disorder Borjeson-Forssman-Lehmann syndrome.
PHF6 localizes to the sub-nucleolar fibrillar center where it binds to rDNA-coding sequences. PHF6 mediates the overall levels of ribosome biogenesis within a cell.
Our results suggest that PHF6 may function as an oncogenic factor in several types of cancer. We also hypothesize that PHF6 may also play its role in a tissue-specific manner. Our findings suggest further investigations regarding the exact role of PHF6 in tumor types.
Female phenotypes of Borjeson-Forssman-Lehmann syndrome patients with PHF6 mutations
Our RBBP4 (show RBBP4 Antibodies)-PHF6 complex structure provides insights into the molecular basis of PHF6-NuRD complex interaction and implicates a role for PHF6 in chromatin structure modulation and gene regulation.
Phf6 is a "lineage-specific" cancer gene that plays opposing roles in developmentally distinct hematopoietic malignancies.
The PHF6 tumor suppressor gene was targeted in acute lymphoblastic leukemia by microRNA-128-3p.
Our report confirms that PHF6 loss in females results in a recognizable phenotype overlapping with Coffin-Siris syndrome and distinct from Borjeson-Forssman-Lehmann syndrome.
Recurrent microdeletion was detected in Xq26.3, causing loss of PHF6 expression, a potential tumor suppressor gene, and the miR (show MLXIP Antibodies)-424, which is involved in the development of acute myeloid leukemia (show BCL11A Antibodies).
The findings show that de novo mutations in PHF6 in females result in a recognisable phenotype which overlap with Borjeson-Forssman-Lehmann syndrome but also has additional distinct features, thus adding a new facet to this disorder.
active maintenance of a precise chromatin landscape is essential for sustaining proper leukemia cell identity and that loss of a single factor (PHF6) can cause focal changes in chromatin accessibility and nucleosome positioning that render cells susceptible to lineage transition
These results place miR (show MLXIP Antibodies)-128 upstream of PHF6 in a pathway vital for cortical lamination as well as for the development of neuronal morphology and intrinsic excitability.
As part of a cell-intrinsic transcriptional pathway, PHF6 regulates neuronal migration in the brain.
Strongest Phf6 gene expression and nuclear localisation of Phf6 protein were observed in the developing central nervous system, the anterior pituitary gland, the primordia of facial structures and the limb buds.
This gene is a member of the plant homeodomain (PHD)-like finger (PHF) family. It encodes a protein with two PHD-type zinc finger domains, indicating a potential role in transcriptional regulation, that localizes to the nucleolus. Mutations affecting the coding region of this gene or the splicing of the transcript have been associated with Borjeson-Forssman-Lehmann syndrome (BFLS), a disorder characterized by mental retardation, epilepsy, hypogonadism, hypometabolism, obesity, swelling of subcutaneous tissue of the face, narrow palpebral fissures, and large ears. Alternate splicing results in multiple transcript variants, encoding different isoforms.
PHD finger protein 6
, PHD-like zinc finger protein
, centromere protein 31