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Merck
모든 사진(3)

주요 문서

C8093

Sigma-Aldrich

Anti-Connexin 43 Antibody

mouse monoclonal, CXN-6

동의어(들):

Mouse monoclonal antibody

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About This Item

MDL number:
UNSPSC 코드:
12352203
NACRES:
NA.41

제품명

Monoclonal Anti-Connexin-43 antibody produced in mouse, clone CXN-6, ascites fluid

생물학적 소스

mouse

Quality Level

결합

unconjugated

항체 형태

ascites fluid

항체 생산 유형

primary antibodies

클론

CXN-6, monoclonal

분자량

antigen 43 kDa

포함

15 mM sodium azide

종 반응성

rat, hamster, bovine, mouse, human

기술

immunocytochemistry: suitable
immunohistochemistry (formalin-fixed, paraffin-embedded sections): suitable
immunohistochemistry (frozen sections): suitable
indirect ELISA: suitable
microarray: suitable
western blot: 1:8,000-1:16.000 using mouse whole brain extract

동형

IgM

UniProt 수납 번호

배송 상태

dry ice

저장 온도

−20°C

타겟 번역 후 변형

unmodified

유전자 정보

관련 카테고리

일반 설명

Monoclonal Anti-Connexin-43 (mouse IgM isotype) is derived from the CXN-6 hybridoma produced by the fusion of mouse myeloma cells and splenocytes from an immunized mouse. Connexin 43 (Cx43) is also known as GJA1 (gap junction protein alpha 1). The structure of connexin molecules includes a cytoplasmic N-terminal region, four transmembrane domains, two extracellular loops and a C-terminal cytoplasmic tail of varying length.
The 43 kDa connexin protein (connexin-43, Cx43) belongs to the a-type (group II) subfamily of connexin proteins. It is expressed in most tissues, even though the pattern of expression may differ in various cell types. For example, in the brain it is found in astrocytes, ependyma and leptomeninges but not in neurons, oligodendrocytes and pinealocytes; in the liver it is present in Ito cells but not hepatocytes.

특이성

Monoclonal Anti-Connexin-43 reacts specifically with connexin-43. Reactivity has been observed with human, bovine, hamster, rat, and mouse connexin-43.

면역원

synthetic connexin-43 peptide (362-381).

애플리케이션

Monoclonal Anti-Connexin-43 antibody produced in mouse has been used in:
  • fluorescent immunostaining
  • western blotting
  • immunocytochemistry
  • preparation of immuno-affinity columns

생화학적/생리학적 작용

Mutations in connexin 43 (Cx43) gene result in pleiotropic phenotype of oculodentodigital dysplasia. Connexin 43 participates in the multiplication and differentiation of mature T cells. It also participates in the secretion and manufacturing of cytokines. It helps to release lactate from glycolytic pancreatic ductal adenocarcinoma cells.

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

13 - Non Combustible Solids

WGK

WGK 1

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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문서 라이브러리 방문

Daniel J Jagger et al.
The Journal of neuroscience : the official journal of the Society for Neuroscience, 34(48), 15851-15860 (2014-11-28)
The loss of auditory hair cells triggers repair responses within the population of nonsensory supporting cells. When hair cells are irreversibly lost from the mammalian cochlea, supporting cells expand to fill the resulting lesions in the sensory epithelium, an initial
Multimodal tumor suppression by miR-302 cluster in melanoma and colon cancer
Maadi H, et al.
The International Journal of Biochemistry & Cell Biology, 81, 121-132 (2016)
Up-regulation of gap junction in peripheral blood T lymphocytes contributes to the inflammatory response in essential hypertension
Ni X, et al.
Testing, 12(9) (2017)
Identification of ischemia-regulated phosphorylation sites in connexin43: A possible target for the antiarrhythmic peptide analogue rotigaptide (ZP123)
Axelsen LN, et al.
Journal of Molecular and Cellular Cardiology, 40(6), 790-798 (2006)
Connexin 43 (GJA1) mutations cause the pleiotropic phenotype of oculodentodigital dysplasia.
Paznekas W A, et al.
American Journal of Human Genetics, 72(2), 408-418 (2003)

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