RAPSN Knockout HEK293 Cell Line

RAPSN Knockout HEK293 Cell Line
Cat.No.:

EDJ-KQ14994

Species:

Human

Cell Name:

HEK293

Gene:

RAPSN

Gene ID:

5913

Size:

1×10⁶cells

RAPSN Knockout Cell Line (HEK293) is an exclusive upgraded CRISPR/Cas9 system-mediated gene knockout cell, with the advantages of Optimized Strategy Design, Efficient Cell Transfection, High-Performance Cas9 Protein and Hassle-Free Cell Selection.
Cat.No. EDJ-KQ14994
Product Name RAPSN Knockout Cell Line (HEK293)
Cell Line HEK293
Cellosaurus ID CVCL_0045
Cell Line Synonyms Hek293, HEK-293, HEK/293, (HEK)293, HEK 293, HEK,293, 293, 293 HEK, 293 Ad5, Graham 293, Graham-293, Human Embryonic Kidney 293
Gene
NCBI Gene ID
Gene Synonyms CMS11|CMS4C|FADS|FADS2|RAPSYN|RNF205
Summary
This gene encodes a member of a family of proteins that are receptor associated proteins of the synapse. The encoded protein contains a conserved cAMP-dependent protein kinase phosphorylation site, and plays a critical role in clustering and anchoring nicotinic acetylcholine receptors at synaptic sites by linking the receptors to the underlying postsynaptic cytoskeleton, possibly by direct association with actin or spectrin. Mutations in this gene may play a role in postsynaptic congenital myasthenic syndromes. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Apr 2011]
Associated Diseases Non-tumor
Morphology Adherent
Passage Ratio 1/5,2days
Complete Culture Medium DMEM + 10% FBS
Freezing Medium 95% Complete culture medium+ 5% DMSO
QC Indels validated by Sanger sequencing; sterility confirmed via microbial testing.
* For research use only. Not intended for use in humans or animals, including clinical, therapeutic, or diagnostic purposes.
LociSTR Info (Sample Cell)
Sample Cell Line: HEK293
STR Info (Cell bank)
Cell Line: HEK293
Allele1Allele2Allele1Allele2
Amelogenin X X
CSF1P0 12 11 12
D2S1338 19 19
D3S1358 15 17 15 17
D5S818 8 8 9
D7S820 11 12 11 12
D8S1179 12 14 12 14
D13S317 12 14 12 14
D16S539 9 13 9 13
D18S51 17 18 17 18
D19S433 15 18 15 18
D21S11 28 30.2 28 30.2
FGA 23 23
Penta D 9 10 9 10
Penta E 7 15 7 15
TH01 7 9.3 7 9.3
TPOX 11 11
vWA 16 19 16 19
D6S1043 11 11
D12S391 19 21 11 15
D2S441 11 15 11 15
* STR authentication data of this cell line matches with that of cell lines sourced from ATCC, DSMZ, JCRB, and RIKEN databases.
Conclusion: The STR identification of this cell is correct.
* Research Use Disclaimer: Content is generated from publicly available research data, bioinformatic resources, and computational analyses for research reference only.

Research Publications

IF=15
Neuron
Our daily life depends on muscle contraction, a process that is controlled by the neuromuscular junction (NMJ). However, the mechanisms of NMJ assembly remain unclear. Here we show that Rapsn, a protein critical for NMJ formation, undergoes liquid-liquid phase separation (LLPS) and condensates into liquid-like assemblies. Such assemblies can recruit acetylcholine receptors (AChRs), cytoskeletal proteins, and signaling proteins for postsynaptic differentiation. Rapsn LLPS requires multivalent binding of tetratricopeptide repeats (TPRs) and is increased by Musk signaling. The capacity of Rapsn to condensate and co-condensate with interaction proteins is compromised by mutations of congenital myasthenic syndromes (CMSs). NMJ formation is impaired in mutant mice carrying a CMS-associated, LLPS-deficient mutation. These results reveal a critical role of Rapsn LLPS in forming a synaptic semi-membraneless compartment for NMJ formation.
This KO model may be useful for: - Investigating the role of RAPSN in phase separation and membraneless condensate formation - Studying molecular mechanisms underlying neuromuscular junction (NMJ) assembly and organization - Functional validation of RAPSN-dependent signaling pathways in synaptic development - Modeling RAPSN-related congenital myasthenic syndromes for disease mechanism studies - Screening for modulators of NMJ formation and synaptic protein condensation

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