PHD Finger Protein 10 (PHF10) Antibody

Este producto es parte de PHF - PHD finger protein
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357.5€ (100 µg)

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935106861
info@markelab.com
name
PHD Finger Protein 10 (PHF10) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx036576
tested applications
ELISA, WB, IHC

Description

Rabbit Polyclonal against the PHF10 protein.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
PHD Finger Protein 10 (PHF10)
Host
Rabbit
Reactivity
Human
Recommended Dilution
ELISA: 1/20000 - 1/80000, WB: 1/500 - 1/2000, IHC: 1/100 - 1/200. Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Purification
Purified by antigen affinity column chromatography.
Size 1
100 µg
Size 2
1 mg
Form
Lyophilized
Tested Applications
ELISA, WB, IHC
Buffer
Prior to lyophilization: 1% BSA and 0.02% NaN3.
Availability
Shipped within 7-15 working days.
Storage
Store at -20 °C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
Alias
BAF45A,SMARCG4,XAP135,BRG1-associated factor 45a
Background
Antibody anti-PHF10
Status
RUO
Note
Concentration: Lyophilized form: Not applicable.  After reconstitution: 1 mg/ml. - 

Descripción

PHF10 is a chromatin-remodeling protein that acts as a subunit of the BAF (SWI/SNF) complex, which regulates transcription by altering nucleosome positioning and chromatin accessibility. Through its PHD domain, PHF10 interacts with histone modifications, particularly methylated and acetylated histones, facilitating recruitment of chromatin remodeling factors to target loci. PHF10 plays a crucial role in processes such as cellular differentiation, proliferation, and DNA repair by modulating transcriptional programs in a cell-specific manner. It is highly expressed in neural and embryonic tissues, where it contributes to neural development and stem cell maintenance. Dysregulation of PHF10 is implicated in neurodevelopmental disorders, immune dysfunction, and cancers, particularly melanoma and glioblastoma, where aberrant chromatin remodeling leads to altered gene expression. Knockout studies reveal impaired cellular differentiation, reduced chromatin accessibility, and defective transcriptional regulation, underscoring its role in epigenetic control, development, and disease progression.

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