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Mouse Anti-PLEKHG5 Recombinant Antibody (5A9) (CBMAB-P2097-YC)

Provided herein is a Mouse monoclonal antibody against Human Pleckstrin Homology And RhoGEF Domain Containing G5. The antibody can be used for immunoassay techniques, such as ELISA, IF, IHC-P, WB.
See all PLEKHG5 antibodies
Published Data
Fig.1 Syx associates with 14-3-3 proteins at its termini.
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Fig.2 Syx associates with the CRB polarity complex, localizes at TJs, and is required for maintaining monolayer patency.
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Fig.3 VEGF and PKD1 regulate Syx binding to Mupp1 and targeting to cell junctions.
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Fig.4 Localization and GEF activity of Syx are required for Syx effects on cell polarity and migration.
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Fig.5 Dia1 opposes ROCK and phenocopies Syx in U251 cell morphology.
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Summary

Host Animal
Mouse
Specificity
Human
Clone
5A9
Antibody Isotype
IgG2a, κ
Application
ELISA, IF, IHC-P, WB

Basic Information

Immunogen
PLEKHG5 (NP_065682, 896-995 aa) partial recombinant protein with GST tag. Immunogen sequence: SAPSRSLSEL CLAVPAPGIR TQGSPQEAGP SWDCRGAPSP GSGPGLVGCL AGEPAGSHRK RCGDLPSGAS PRVQPEPPPG VSAQHRKLTL AQLYRIRTTL
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at-20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 896-995

Target

Full Name
pleckstrin homology domain containing, family G (with RhoGef domain) member 5
Introduction
PLEKHG5 is a protein that activates the nuclear factor kappa B (NFKB1) signaling pathway. Mutations in this gene are associated with autosomal recessive distal spinal muscular atrophy.
Entrez Gene ID
57449
UniProt ID
O94827
Alternative Names
CMTRIC; GEF720; DSMA4; Syx; Tech
Function
Functions as a guanine exchange factor (GEF) for RAB26 and thus regulates autophagy of synaptic vesicles in axon terminal of motoneurons (By similarity).
Involved in the control of neuronal cell differentiation (PubMed:11704860).
Plays a role in angiogenesis through regulation of endothelial cells chemotaxis. Affects also the migration, adhesion, and matrix/bone degradation in macrophages and osteoclasts (PubMed:23777631).
Biological Process
Endothelial cell chemotaxisISS:UniProtKB
Endothelial cell migrationManual Assertion Based On ExperimentIBA:GO_Central
Positive regulation of I-kappaB kinase/NF-kappaB signalingManual Assertion Based On ExperimentHMP:UniProtKB
Regulation of small GTPase mediated signal transductionTAS:Reactome
Rho protein signal transductionManual Assertion Based On ExperimentIBA:GO_Central
Cellular Location
Cytoplasm
Cytoplasm, perinuclear region
Cell membrane
Cell junction
Cell projection, lamellipodium
Predominantly cytoplasmic, however when endothelial cells are stimulated with lysophosphatidic acid, PLEKHG5 is found in perinuclear regions and at the cell membrane. Localizes at cell-cell junctions in quiescent endothelial cells, and relocalizes to cytoplasmic vesicle and the leading edge of lamellipodia in migrating endothelial cells.
Involvement in disease
Distal spinal muscular atrophy, autosomal recessive, 4 (DSMA4):
A neuromuscular disorder. Distal spinal muscular atrophy, also known as distal hereditary motor neuronopathy, represents a heterogeneous group of neuromuscular disorders caused by selective degeneration of motor neurons in the anterior horn of the spinal cord, without sensory deficit in the posterior horn. The overall clinical picture consists of a classical distal muscular atrophy syndrome in the legs without clinical sensory loss. The disease starts with weakness and wasting of distal muscles of the anterior tibial and peroneal compartments of the legs. Later on, weakness and atrophy may expand to the proximal muscles of the lower limbs and/or to the distal upper limbs. DSMA4 is characterized by childhood onset, generalized muscle weakness and atrophy with denervation and normal sensation. Bulbar symptoms and pyramidal signs are absent.
Charcot-Marie-Tooth disease, recessive, intermediate type, C (CMTRIC):
A form of Charcot-Marie-Tooth disease, a disorder of the peripheral nervous system, characterized by progressive weakness and atrophy, initially of the peroneal muscles and later of the distal muscles of the arms. Recessive intermediate forms of Charcot-Marie-Tooth disease are characterized by clinical and pathologic features intermediate between demyelinating and axonal peripheral neuropathies, and motor median nerve conduction velocities ranging from 25 to 45 m/sec.
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For research use only. Not intended for any clinical use.

Custom Antibody Labeling

We also offer labeled antibodies developed using our catalog antibody products and nonfluorescent conjugates (HRP, AP, Biotin, etc.) or fluorescent conjugates (Alexa Fluor, FITC, TRITC, Rhodamine, Texas Red, R-PE, APC, Qdot Probes, Pacific Dyes, etc.).

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