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Merck
모든 사진(2)

주요 문서

SAB1407805

Sigma-Aldrich

Anti-FANCM antibody produced in mouse

purified immunoglobulin, buffered aqueous solution

동의어(들):

FAAP250, KIAA1596, MGC176453

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크기 선택

50 μG
₩824,891

₩824,891


예상 입고일2025년 6월 16일세부사항

기존과 동일한 품질을 인하된 가격으로 - 어려운 예산 상황을 머크와 함께 극복하세요


크기 선택

보기 변경
50 μG
₩824,891

About This Item

UNSPSC 코드:
12352203
NACRES:
NA.43

₩824,891


예상 입고일2025년 6월 16일세부사항

기존과 동일한 품질을 인하된 가격으로 - 어려운 예산 상황을 머크와 함께 극복하세요

생물학적 소스

mouse

Quality Level

결합

unconjugated

항체 형태

purified immunoglobulin

항체 생산 유형

primary antibodies

클론

polyclonal

양식

buffered aqueous solution

분자량

antigen ~75.6 kDa

종 반응성

human

기술

indirect immunofluorescence: suitable
western blot: 1 μg/mL

NCBI 수납 번호

UniProt 수납 번호

배송 상태

dry ice

저장 온도

−20°C

타겟 번역 후 변형

unmodified

유전자 정보

human ... FANCM(57697)

일반 설명

The Fanconi anemia complementation group (FANC) currently includes FANCA, FANCB, FANCC, FANCD1 (also called BRCA2), FANCD2, FANCE, FANCF, FANCG, FANCI, FANCJ (also called BRIP1), FANCL, FANCM and FANCN (also called PALB2). The previously defined group FANCH is the same as FANCA. Fanconi anemia is a genetically heterogeneous recessive disorder characterized by cytogenetic instability, hypersensitivity to DNA crosslinking agents, increased chromosomal breakage, and defective DNA repair. The members of the Fanconi anemia complementation group do not share sequence similarity; they are related by their assembly into a common nuclear protein complex. This gene encodes the protein for complementation group M. (provided by RefSeq)

면역원

FANCM (AAH36056.1, 1 a.a. ~ 669 a.a) full-length human protein.

Sequence
MSGRQRTLFQTWGSSISRSSGTPGCSSGTERPQSPGSSKAPLPAAAEAQLESDDDVLLVAAYEAERQLCLENGGFCTSAGALWIYPTNCPVRDYQLHISRAALFCNTLVCLPTGLGKTFIAAVVMYNFYRWFPSGKVVFMAPTKPLVTQQIEACYQVMGIPQSHMAEMTGSTQASTRKEIWCSKRVLFLTPQVMVNDLSRGACPAAEIKCLVIDEAHKALGNYAYCQVVRELVKYTNHFRILALSATPGSDIKAVQQVITNLLIGQIELRSEDSPDILTYSHERKVEKLIVPLGEELAAIQKTYIQILESFARSLIQRNVLMRRDIPNLTKYQIILARDQFRKNPSPNIVGIQQGIIEGEFAICISLYHGYELLQQMGMRSLYFFLCGIMDGTKGMTRSKNELGRNEDFMKLYNHLECMFARTRSTSANGISAIQQGDKNKKFVYSHPKLKKLEEVVIEHFKSWNAENTTEKKRDETRVMIFSSFRDSVQEIAEMLSQHQPIIRVMTFVGHASGKSTKGFTQKEQLEVVKQFRDGGYNTLVSTCVGEEGLDIGEVDLIICFDSQKSPIRLVQRMGRTGRKRQGRIVIILSEGREERIYNQSQSNKRSIYKAISSNRQVLHFYQRSPRMVPDGINPKLHKMFITHGVYEPEKPSRNLQRKSSIFSYRDGK

물리적 형태

Solution in phosphate buffered saline, pH 7.4

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Storage Class Code

10 - Combustible liquids

WGK

WGK 1

Flash Point (°F)

Not applicable

Flash Point (°C)

Not applicable


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문서 라이브러리 방문

Veselin Andreev et al.
DNA repair, 74, 38-50 (2019-01-05)
Chromatin regulators play crucial roles in the DNA damage response. While the chromatin changes needed for double-strand break repair and nucleotide excision repair have been intensely studied, the chromatin requirements of interstrand crosslink (ICL) repair have remained largely unexplored. Here
Laura Kasak et al.
American journal of human genetics, 103(2), 200-212 (2018-08-04)
Infertility affects around 7% of men worldwide. Idiopathic non-obstructive azoospermia (NOA) is defined as the absence of spermatozoa in the ejaculate due to failed spermatogenesis. There is a high probability that NOA is caused by rare genetic defects. In this
Jing Zhang et al.
Nature communications, 11(1), 3951-3951 (2020-08-10)
Duplication of mammalian genomes requires replisomes to overcome numerous impediments during passage through open (eu) and condensed (hetero) chromatin. Typically, studies of replication stress characterize mixed populations of challenged and unchallenged replication forks, averaged across S phase, and model a
Jing Huang et al.
Cell reports, 27(6), 1794-1808 (2019-05-09)
Eukaryotic replisomes are driven by the mini chromosome maintenance (MCM [M]) helicase complex, an offset ring locked around the template for leading strand synthesis by CDC45 (C) and GINS (G) proteins. Although the CDC45 MCM GINS (CMG) structure implies that
Daniel González-Acosta et al.
The EMBO journal, 40(14), e106355-e106355 (2021-06-16)
DNA interstrand crosslinks (ICLs) induced by endogenous aldehydes or chemotherapeutic agents interfere with essential processes such as replication and transcription. ICL recognition and repair by the Fanconi Anemia pathway require the formation of an X-shaped DNA structure that may arise

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