PLEKHG5 sirna

PLEKHG5 siRNA (Human)

Cat. Num. AAA8225543

• Gene Names: PLEKHG5; Syx; Tech; DSMA4; CMTRIC; GEF720
• Reactivity: Human
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: PLEKHG5; PLEKHG5 siRNA (Human); KIAA0720; Pleckstrin homology domain-containing family G member 5; PH domain-containing family G member 5; Guanine nucleotide exchange factor 720; GEF720; PLEKHG5 sirna

• Host: Synthetic
• Reactivity: Human
• Specificity: PLEKHG5 siRNA (Human) is a target-specific 19-23 nt siRNA oligo duplexes designed to knock down gene expression.
• Purity/Purification: > 97%
• Form/Format: Lyophilized powder
• Sequence Length: 1062

• Applicable Applications for PLEKHG5 sirna: RNA Interference (RNAi)
• Quality Control: Oligonucleotide synthesis is monitored base by base through trityl analysis to ensure appropriate coupling efficiency. The oligo is subsequently purified by affinity-solid phase extraction. The annealed RNA duplex is further analyzed by mass spectrometry to verify the exact composition of the duplex. Each lot is compared to the previous lot by mass spectrometry to ensure maximum lot-to-lot consistency.
• Directions for Use: We recommends transfection with 100 nM siRNA 48 to 72 hours prior to cell lysis. Before resuspending, briefly centrifuge the tube to ensure the lyophilized siRNA is at the bottom of the tube. Resuspend the siRNA oligos to an appropriate concentration with DEPC water. For each vial, suitable for 250 transfections in 24 well plate (20 pmol for each well).
• Components: We offer pre-designed sets of 3 different target-specific siRNA oligo duplexes of human PLEKHG5 gene. Each vial contains 5 nmol of lyophilized siRNA. The duplexes can be transfected individually or pooled together to achieve knockdown of the target gene, which is most commonly assessed by qPCR or western blot. Our siRNA oligos are also chemically modified (2'-OMe) at no extra charge for increased stability and enhanced knockdown in vitro and in vivo.
• Preparation and Storage: Shipped at 4 degree C. Store at -20 degree C for one year.

Related Product Information for PLEKHG5 sirna

siRNA to inhibit PLEKHG5 expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 111154078
• NCBI GeneID: 57449
• NCBI Accession #: NP_001036128.1
• NCBI GenBank Nucleotide #: NM_001042663.1
• UniProt Accession #: O94827; Q5SY17; Q5T8W5; Q5T8W9; Q6ZNM0; Q7Z436; Q86YD8; B3KU07; B7Z2M3; B7Z5X2; F5GZ21; F5H1I0
• Molecular Weight: 118,479 Da
• NCBI Official Full Name: pleckstrin homology domain-containing family G member 5 isoform c
• NCBI Official Synonym Full Names: pleckstrin homology domain containing, family G (with RhoGef domain) member 5
• NCBI Official Symbol: PLEKHG5
• NCBI Official Synonym Symbols: Syx; Tech; DSMA4; CMTRIC; GEF720
• NCBI Protein Information: pleckstrin homology domain-containing family G member 5
• UniProt Protein Name: Pleckstrin homology domain-containing family G member 5
• Protein Family: Pleckstrin homology domain-containing family
• UniProt Gene Name: PLEKHG5
• UniProt Synonym Gene Names: KIAA0720; PH domain-containing family G member 5; GEF720
• UniProt Entry Name: PKHG5_HUMAN

NCBI Description

This gene encodes 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. Multiple transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, May 2012]

Uniprot Description

PLEKHG5: Activates the NF-kappa-B signaling pathway and RHOA. Appears to be involved in the control of neuronal cell differentiation. Defects in PLEKHG5 are the cause of distal spinal muscular atrophy autosomal recessive type 4 (DSMA4). 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. 5 isoforms of the human protein are produced by alternative splicing.

Chromosomal Location of Human Ortholog: 1p36.31

Cellular Component: perinuclear region of cytoplasm; endocytic vesicle; lamellipodium; cytoplasm; plasma membrane; intercellular junction; cytosol

Molecular Function: Rho guanyl-nucleotide exchange factor activity; signal transducer activity

Biological Process: regulation of small GTPase mediated signal transduction; positive regulation of I-kappaB kinase/NF-kappaB cascade; nerve growth factor receptor signaling pathway; positive regulation of apoptosis; small GTPase mediated signal transduction

Disease: Spinal Muscular Atrophy, Distal, Autosomal Recessive, 4; Charcot-marie-tooth Disease, Recessive Intermediate C