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Merck
모든 사진(3)

주요 문서

SCC420

Sigma-Aldrich

B16-OVA MO4 Mouse Melanoma Cell Line

Mouse

동의어(들):

B16-OVA MO4 Cell Line, Melanoma Cell Line, Mouse Melanoma Cells

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About This Item

UNSPSC 코드:
41106514
NACRES:
NA.71
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제품명

B16-OVA MO4 Mouse Melanoma Cell Line,

생물학적 소스

mouse

포장

vial of >1X10⁶ cells

제조업체/상표

Millipore

성장 모드

N/A

기술

cell culture | mammalian: suitable

배송 상태

dry ice

저장 온도

−196°C

일반 설명

The immune system can recognize and destroy tumors. Cytotoxic T lymphocytes (CTLs) kill neoplastic (or virally infected) cells after recognizing antigenic peptides bound to major histocompatibility complex (MHC) class I molecules on their surface. These peptides are derived from antigens that are degraded in the cytosol of the affected cell. Immunizations with killedpathogens or their proteins do not generally elicit CTLs, because exogenous proteins cannot enter the cytosol (to bepresented). However, antigens that are internalized into phagocytic cells can enter the cytosol and be processed for classI presentation. Immunization with a purified antigen attached to an avidly phagocytized particle primes CTLs, which in turnprotect animals from subsequent challenge with tumors transfected with the antigen gene.

애플리케이션

  • Each vial contains >1X106 viable cells.
  • Cells are tested negative for infectious diseases by a Mouse Essential CLEAR panel by Charles River Animal Diagnostic Services.

Cells are verified to be of mouse origin and negative for inter-species contamination from rat, Chinese hamster, Golden Syrian hamster, human and non-human primate (NHP) as assessed by a Contamination CLEAR panel by Charles River Animal Diagnostic Services.
  • Cells are negative for mycoplasma contamination.

Background
The immune system can recognize and destroy tumors. Cytotoxic T lymphocytes (CTLs) kill neoplastic or virally infected cells after recognizing antigenic peptides bound to major histocompatibility complex class I molecules on their surface. These peptides are derived from antigens that are degraded in the cytosol of the affected cell. Immunizations with killed pathogens or their proteins do not generally elicit CTLs, because exogenous proteins cannot enter the cytosol (to be presented). However, antigens that are internalized into phagocytic cells can enter the cytosol and be processed for class I presentation. Immunization with a purified antigen attached to an avidly phagocytized particle primes CTLs, which in turn protect animals from subsequent challenge with tumors transfected with the antigen gene.1

Source
Tumor rejection antigens – TRAs – differ from any other protein synthesized by the cell in that the host is intolerant to them. Thus virtually any foreign protein synthesized by a tumor, including those expressed from foreign antigen genes transfected into tumor cells, should function and behave like TRAs. This hypothesis was tested in a murine tumor model developed by transfecting the chicken ovalbumin gene into the C57BL/6 (H-2b haplotype)-derived murine melanoma cell line B16, followed by selection and isolation of the ovalbumin (OVA)-transfected B16 clone B16-OVA MO4.1
In in vitro challenge, B16-OVA MO4 cells stimulated the OVA+ Kb-specific T-cell hybridoma RF33.70 to produce interleukin-2 whereas untransfected B16 cells did not. Injected intradermally into syngeneic C57Bl/6 mice, both B16 and B16-OVA MO4 grew progressively, metastasized, and killed the animals showing that expression of the ovalbumin antigen alone does not render this tumor sufficiently immunogenic to be rejected. Subcutaneous immunization of C57Bl/6 mice with ovalbumin conjugated to iron beads (OVA-Fe), however, protected B16-OVA MO4 (but not B16) challenged animals both from local tumor growth and death. This approach could be exploited to develop tumor and viral vaccines.1

References
1. Falo LD Jr, Kovacsovics-Bankowski M, Thompson K, Rock KL. Nat. Med. 1995; 1(7):649-653.
2. Fidler IJ. Cancer Res. 1975; 35(1):218-224.


Note: Mouse xenotropic retrovirus Bxv-1 proviral DNA is detected in B16-OVA MO4 cells, BXV-1 is a Biosafety Level 2 (BSL-2) pathogen.

특징 및 장점

B16-OVA MO4 cell line is a model for cancer immunotherapy, expressing ovalbumin (OVA) in order to facilitate strong immune responses to tumor antigens.

저장 및 안정성

Cells should be stored in liquid nitrogen until use. The cells can be cultured for at least 10 passages after initial thawing without significantly affecting the cell marker expression and functionality.

기타 정보

This product is intended for sale and sold solely to academic institutions for internal academic research use per the terms of the “Academic Use Agreement” as detailed in the product documentation.

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.

Storage Class Code

10 - Combustible liquids

WGK

WGK 2

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


시험 성적서(COA)

제품의 로트/배치 번호를 입력하여 시험 성적서(COA)을 검색하십시오. 로트 및 배치 번호는 제품 라벨에 있는 ‘로트’ 또는 ‘배치’라는 용어 뒤에서 찾을 수 있습니다.

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문서 라이브러리 방문

질문

  1. What are the details regarding the B16-OVA line? Specifically:

    What is the suggested selection antibiotic and concentration for culturing? Regarding Ova expression, is it cytosolic, surface, or secreted? Is the cell line derived from B16F10 or a different line? How was the line genetically modified for Ova expression?

    1 답변
    1. For culturing, it is recommended to ue 1 mg/ml Geneticin (G418; Sigma 345810) as the selection antibiotic and concentration.

      The Ova expression in the B16-OVA cell line is related to the presentation of the OVA peptide, SIINFEKL, with its surface class I molecules.

      The cell line was derived from C57BI/6 mice (H-2b haplotype) as B16, followed by transfection with the pAc-new-OVA plasmid.

      The line was genetically modified for Ova expression through transfection with the pAc-new-OVA plasmid.

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