PHD Finger Protein 10 (PHF10) Antibody

357.5€ (100 µg)
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935106861
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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
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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