The Plekhg5 Polyclonal Antibody (PACO11300) is a valuable tool for research involving Plekhg5, a protein associated with autophagy and cell membrane trafficking. This antibody, raised in rabbits, is highly specific to human samples and has been validated for use in various applications, including Western blot and immunofluorescence.Plekhg5 is known to play a key role in autophagy, a cellular process responsible for degrading and recycling damaged organelles and proteins. Dysregulation of autophagy has been implicated in various diseases, including neurodegenerative disorders and cancer. By targeting Plekhg5, researchers can investigate the mechanisms underlying autophagy and its potential therapeutic implications.
Moreover, Plekhg5 has been shown to be involved in cell membrane trafficking, a process critical for cell communication and signaling. Understanding the function of Plekhg5 in this context can provide insights into cellular processes and pathways involved in disease development and progression.Overall, the Plekhg5 Polyclonal Antibody (PACO11300) is a valuable tool for researchers interested in studying autophagy, cell membrane trafficking, and related processes in the context of human health and disease. Its high specificity and versatility make it an ideal choice for a wide range of research applications in cell biology and molecular medicine.
pleckstrin homology domain containing, family G (with RhoGef domain) member 5;PLEKHG5;DSMA4;GEF720;KIAA0720;RP4-650H14.3 ;
UniProt Protein Function:
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: 1p36.31Cellular Component: cytoplasm; cytosol; endocytic vesicle; intercellular junction; lamellipodiumMolecular Function: guanyl-nucleotide exchange factor activity; Rho guanyl-nucleotide exchange factor activity; signal transducer activityBiological Process: positive regulation of apoptosis; positive regulation of I-kappaB kinase/NF-kappaB cascade; regulation of small GTPase mediated signal transductionDisease: Charcot-marie-tooth Disease, Recessive Intermediate C; Spinal Muscular Atrophy, Distal, Autosomal Recessive, 4
UniProt Protein Details:
NCBI Summary:
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]
