Docking Protein 9 (DOCK9) Antibody

Este producto es parte de DOCK - Dedicator of Cytokinesis
Product Graph
637€ (100 µl)

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935106861
info@markelab.com
name
Docking Protein 9 (DOCK9) Antibody
category
Primary Antibodies
provider
Abbexa
reference
abx112014
tested applications
ELISA, WB, IHC, IF/ICC

Description

Dedicator Of Cytokinesis 9 Antibody is a Rabbit Polyclonal antibody against Dedicator Of Cytokinesis 9.

Documents del producto

Instrucciones
Data sheet
Descargar

Product specifications

Category
Primary Antibodies
Immunogen Target
Docking Protein 9 (DOCK9)
Host
Rabbit
Reactivity
Human, Mouse, Rat
Recommended Dilution
Optimal dilutions/concentrations should be determined by the end user.
Clonality
Polyclonal
Conjugation
Unconjugated
Isotype
IgG
Purification
Antigen Affinity Chromatography.
Size 1
100 µl
Form
Liquid
Tested Applications
ELISA, WB, IHC, IF/ICC
Buffer
PBS, pH 7.3, containing 0.02% Sodium Azide and 50% Glycerol.
Availability
Shipped within 5-10 working days.
Storage
Aliquot and store at -20°C. Avoid repeated freeze/thaw cycles.
Dry Ice
No
UniProt ID
Q9BZ29
Gene ID
23348
NCBI Accession
NM_015296.2
OMIM
607325
Alias
ZIZ1,ZIZIMIN1,DOCK9, KIAA1058
Background
Antibody anti-DOCK9
Status
RUO

Descripción

DOCK9, also known as Zizimin1, functions as a GEF for Cdc42, regulating actin remodeling, filopodia formation, and cell polarity. It is widely expressed in tissues, including the brain, where it controls neurite outgrowth, axonal guidance, and synaptic development. DOCK9 interacts with membrane phosphoinositides like PIP3 for activation, linking signaling pathways to cytoskeletal changes. It plays roles in epithelial cell migration and endothelial barrier stability. Dysregulation of DOCK9 is linked to neurological defects and cancer progression through disrupted cytoskeletal control and altered cell adhesion. Knockdown studies reveal impaired filopodia formation, cell spreading, and neuronal development.
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Guanine nucleotide-exchange factor(GEF) that activates CDC42 by exchanging bound GDP for free GTP. Overexpression induces filopodia formation.
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