추천 제품
생물학적 소스
rabbit
Quality Level
결합
unconjugated
항체 형태
affinity isolated antibody
항체 생산 유형
primary antibodies
클론
polyclonal
양식
lyophilized powder
종 반응성
rat
기술
western blot: 1:200 using rat DRG lysates
UniProt 수납 번호
배송 상태
wet ice
저장 온도
−20°C
타겟 번역 후 변형
unmodified
유전자 정보
human ... SCN11A(11280)
mouse ... Scn11a(24046)
rat ... Scn11a(29701)
일반 설명
Sodium Channel NaV1.9 is a threshold channel, that is expressed in dorsal root ganglion neurons , peripheral nociceptive neurons and visceral afferents. It is also called as SNS and NaN. It is encoded by SCN11A (sodium voltage-gated channel subunit 11) and is located on human chromosome 3p22.
면역원
peptide CNGDLSSLDVAKVKVHND corresponding to residues 1748-1765 of rat Nav1.9. This sequence has 15/18 residues identical in mouse and 14/18 residues identical in human.
생화학적/생리학적 작용
Sodium Channel NaV1.9 participates in pain at the time of inflammation. Downregulation of Nav1.9 is observed in Hirschsprung′s disease.
물리적 형태
Lyophilized from phosphate buffered saline, pH 7.4, with 1% bovine serum albumin, and 0.05% sodium azide.
면책조항
Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.
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Storage Class Code
11 - Combustible Solids
WGK
WGK 2
Flash Point (°F)
Not applicable
Flash Point (°C)
Not applicable
Biology and management of histologic transformation of indolent lymphoma
Freedman AS, et al.
Hematology / the Education Program of the American Society of Hematology. American Society of Hematology. Education Program, 314-20 (2005)
Decreased Nav1.9 channel expression in Hirschsprung's disease
O'Donnell AM, et al.
Journal of Pediatric Surgery, 51(9), 1458-1461 (2016)
Congenital insensitivity to pain: Fracturing without apparent skeletal pathobiology caused by an autosomal dominant, second mutation in SCN11A encoding voltage-gated sodium channel 1.9
Phatarakijnirund V, et al.
Bone, 84, 289-298 (2016)
Sodium channel NaV1.9 mutations associated with insensitivity to pain dampen neuronal excitability
Huang J, et al.
The Journal of Clinical Investigation, 127(7), 2805-2814 (2017)
Patrick Delmas et al.
Trends in neurosciences, 26(2), 55-57 (2003-01-22)
Voltage-gated Na(+) channels play key roles in generating and propagating action potentials. Their gating is believed to rely exclusively on changes in membrane potential. However, recent data from Blum, Kafitz and Konnerth provide direct evidence that the opening of Na(v)1.9
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