CHRND sirna

CHRND siRNA (Mouse)

Cat. Num. AAA8219434

• Gene Names: Chrnd; Acrd; Achr-4; L10076
• Reactivity: Mouse
• Applications: RNA Interference (RNAi)
• Purity: > 97%
• Synonyms: CHRND; CHRND siRNA (Mouse); ACRD; Acetylcholine receptor subunit delta; CHRND sirna

• Host: Synthetic
• Reactivity: Mouse
• Specificity: CHRND siRNA (Mouse) 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: 520

• Applicable Applications for CHRND 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 mouse CHRND 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 CHRND sirna

siRNA to inhibit CHRND expression using RNA interference

NCBI and Uniprot Product Information

• NCBI GI #: 110225335
• NCBI GeneID: 11447
• NCBI Accession #: NP_067611.2
• NCBI GenBank Nucleotide #: NM_021600.3
• UniProt Accession #: P02716; Q61267
• Molecular Weight: 59,143 Da
• NCBI Official Full Name: acetylcholine receptor subunit delta
• NCBI Official Synonym Full Names: cholinergic receptor, nicotinic, delta polypeptide
• NCBI Official Symbol: Chrnd
• NCBI Official Synonym Symbols: Acrd; Achr-4; L10076
• NCBI Protein Information: acetylcholine receptor subunit delta
• UniProt Protein Name: Acetylcholine receptor subunit delta
• Protein Family: Acetylcholine receptor
• UniProt Gene Name: Chrnd
• UniProt Synonym Gene Names: Acrd
• UniProt Entry Name: ACHD_MOUSE

NCBI Description

This gene encodes the delta subunit of the muscle-derived nicotinic acetylcholine receptor, a pentameric neurotransmitter receptor and member of the ligand-gated ion channel superfamily. The delta subunit together with the alpha subunit forms the ligand-binding site. [provided by RefSeq, Nov 2012]

Uniprot Description

nAChRD: After binding acetylcholine, the AChR responds by an extensive change in conformation that affects all subunits and leads to opening of an ion-conducting channel across the plasma membrane. Defects in CHRND are a cause of multiple pterygium syndrome lethal type (MUPSL). Multiple pterygia are found infrequently in children with arthrogryposis and in fetuses with fetal akinesia syndrome. In lethal multiple pterygium syndrome there is intrauterine growth retardation, multiple pterygia, and flexion contractures causing severe arthrogryposis and fetal akinesia. Subcutaneous edema can be severe, causing fetal hydrops with cystic hygroma and lung hypoplasia. Oligohydramnios and facial anomalies are frequent. Defects in CHRND are a cause of congenital myasthenic syndrome slow-channel type (SCCMS). SCCMS is the most common congenital myasthenic syndrome. Congenital myasthenic syndromes are characterized by muscle weakness affecting the axial and limb muscles (with hypotonia in early-onset forms), the ocular muscles (leading to ptosis and ophthalmoplegia), and the facial and bulbar musculature (affecting sucking and swallowing, and leading to dysphonia). The symptoms fluctuate and worsen with physical effort. SCCMS is caused by kinetic abnormalities of the AChR, resulting in prolonged endplate currents and prolonged AChR channel opening episodes. Defects in CHRND are a cause of congenital myasthenic syndrome fast-channel type (FCCMS). FCCMS is a congenital myasthenic syndrome characterized by kinetic abnormalities of the AChR. In most cases, FCCMS is due to mutations that decrease activity of the AChR by slowing the rate of opening of the receptor channel, speeding the rate of closure of the channel, or decreasing the number of openings of the channel during ACh occupancy. The result is failure to achieve threshold depolarization of the endplate and consequent failure to fire an action potential. Belongs to the ligand-gated ion channel (TC 1.A.9) family. Acetylcholine receptor (TC 1.A.9.1) subfamily. Delta/CHRND sub-subfamily.

Protein type: Membrane protein, multi-pass; Membrane protein, integral; Channel, ligand-gated

Cellular Component: nicotinic acetylcholine-gated receptor-channel complex; postsynaptic membrane; membrane; integral to membrane; plasma membrane; synapse; cell junction

Molecular Function: protein binding; ion channel activity; acetylcholine binding; nicotinic acetylcholine-activated cation-selective channel activity; ligand-gated ion channel activity; extracellular ligand-gated ion channel activity

Biological Process: skeletal muscle contraction; regulation of membrane potential; transport; ion transport; skeletal muscle growth; musculoskeletal movement; cation transport