WBmore details Unsuitable for:
ICC,IHC-P or IP
Mouse, Rat, Human
Synthetic peptide within Human EGR2 aa 1-100. The exact sequence is proprietary.
LnCaP, HepG2, MCF7, and SH SY5Y cell lysates.
Our RabMAb® technology is a patented hybridoma-based technology for making rabbit monoclonal antibodies. For details on our patents, please refer to RabMab® patents
We are constantly working hard to ensure we provide our customers with best in class antibodies. As a result of this work we are pleased to now offer this antibody in purified format. We are in the process of updating our datasheets. The purified format is designated 'PUR' on our product labels. If you have any questions regarding this update, please contact our Scientific Support team.
This product is a recombinant rabbit monoclonal antibody.
Shipped at 4°C. Store at +4°C short term (1-2 weeks). Upon delivery aliquot. Store at -20°C. Stable for 12 months at -20°C.
Sequence-specific DNA-binding transcription factor. Binds to two specific DNA sites located in the promoter region of HOXA4.
Involvement in disease
Defects in EGR2 are a cause of congenital hypomyelination neuropathy (CHN) [MIM:605253]. Inheritance can be autosomal dominant or recessive. Recessive CHN is also known as Charcot-Marie-Tooth disease type 4E (CMT4E). CHN is characterized clinically by early onset of hypotonia, areflexia, distal muscle weakness, and very slow nerve conduction velocities. Defects in EGR2 are a cause of Charcot-Marie-Tooth disease type 1D (CMT1D) [MIM:607678]. CMT1D is a form of Charcot-Marie-Tooth disease, the most common inherited disorder of the peripheral nervous system. Charcot-Marie-Tooth disease is classified in two main groups on the basis of electrophysiologic properties and histopathology: primary peripheral demyelinating neuropathy or CMT1, and primary peripheral axonal neuropathy or CMT2. Neuropathies of the CMT1 group are characterized by severely reduced nerve conduction velocities (less than 38 m/sec), segmental demyelination and remyelination with onion bulb formations on nerve biopsy, slowly progressive distal muscle atrophy and weakness, absent deep tendon reflexes, and hollow feet. Defects in EGR2 are a cause of Dejerine-Sottas syndrome (DSS) [MIM:145900]; also known as Dejerine-Sottas neuropathy (DSN) or hereditary motor and sensory neuropathy III (HMSN3). DSS is a severe degenerating neuropathy of the demyelinating Charcot-Marie-Tooth disease category, with onset by age 2 years. DSS is characterized by motor and sensory neuropathy with very slow nerve conduction velocities, increased cerebrospinal fluid protein concentrations, hypertrophic nerve changes, delayed age of walking as well as areflexia. There are both autosomal dominant and autosomal recessive forms of Dejerine-Sottas syndrome.
Belongs to the EGR C2H2-type zinc-finger protein family. Contains 3 C2H2-type zinc fingers.
Ubiquitinated by WWP2 leading to proteasomal degradation.
Liu F et al. Increased T-helper 17 cell differentiation mediated by exosome-mediated microRNA-451 redistribution in gastric cancer infiltrated T cells. Cancer Sci109:65-73 (2018).
Read more (PubMed: 29059496) »
Miyamoto Y et al. BIG1/Arfgef1 and Arf1 regulate the initiation of myelination by Schwann cells in mice. Sci Adv4:eaar4471 (2018).
Read more (PubMed: 29740613) »