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Merck

MABC60

Sigma-Aldrich

Anti-KiSS-1 Antibody, clone 8H4.1

clone 8H4.1, from mouse

別名:

Metastasis-suppressor KiSS-1, Kisspeptin-1, Metastin, Kisspeptin-542, Kisspeptin-143, Kisspeptin-134, Kisspeptin-10

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About This Item

UNSPSCコード:
12352203
eCl@ss:
32160702
NACRES:
NA.41

由来生物

mouse

品質水準

抗体製品の状態

purified antibody

抗体製品タイプ

primary antibodies

クローン

8H4.1, monoclonal

化学種の反応性

human, rat

テクニック

immunohistochemistry: suitable
western blot: suitable

アイソタイプ

IgG1κ

NCBIアクセッション番号

UniProtアクセッション番号

輸送温度

wet ice

ターゲットの翻訳後修飾

unmodified

遺伝子情報

human ... KISS1(3814)

詳細

Metastasis-suppressor KiSS-1 (KiSS-1; or Kisspeptin-1) is one of several endogenous ligands for the orphan G-protein coupled receptor GPR54. KiSS-1 functions as a suppressor of metastasis in various types of cancers, by inhibiting migration and proliferation in affected cells. This effect may be produced by the activation of multiple signaling pathways: Ligand-bound GPR54 activates IP3 and PKC signaling via a PLC pathway; and ERK 1 and ERK 2 by a cPLA2, which may lead to increased calcium signaling and gene transcription, respectively. More recently, however, KiSS-1/GPR54 signaling has been implicated in puberty and development. KiSS-1/GPR54 may regulate signaling of GnRH neurons during puberty and may influence the release of FH and LSH hormones. KISS-1 is highly expressed in the CNS, testis, pancreas, intestine, ovary, and placenta.

免疫原

Recombinant protein corresponding to human KiSS-1.

アプリケーション

Anti-KiSS-1 Antibody, clone 8H4.1 is an antibody against KiSS-1 for use in IHC, Western Blotting.
Immunohistochemistry Analysis: 1:1,000 dilution from a representative lot detected KiSS-1 in human pancreas and rat testis tissues.

品質

Evaluated by Immunohistochemistry in human placenta tissue.

Immunohistochemistry Analysis: 1:1,000 dilution of this antibody detected KiSS-1 in human placenta tissue.

ターゲットの説明

15 kDa calculated

物理的形状

Format: Purified

その他情報

Concentration: Please refer to the Certificate of Analysis for the lot-specific concentration.

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保管分類コード

12 - Non Combustible Liquids

WGK

WGK 1

引火点(°F)

Not applicable

引火点(℃)

Not applicable


適用法令

試験研究用途を考慮した関連法令を主に挙げております。化学物質以外については、一部の情報のみ提供しています。 製品を安全かつ合法的に使用することは、使用者の義務です。最新情報により修正される場合があります。WEBの反映には時間を要することがあるため、適宜SDSをご参照ください。

Jan Code

MABC60:


試験成績書(COA)

製品のロット番号・バッチ番号を入力して、試験成績書(COA) を検索できます。ロット番号・バッチ番号は、製品ラベルに「Lot」または「Batch」に続いて記載されています。

以前この製品を購入いただいたことがある場合

文書ライブラリで、最近購入した製品の文書を検索できます。

文書ライブラリにアクセスする

Phoebe Ohene-Marfo et al.
International journal of molecular sciences, 25(5) (2024-03-13)
Chronic inflammation is a key player in metabolic dysfunction-associated fatty liver disease (MAFLD) progression. Necroptosis, an inflammatory cell death pathway, is elevated in MAFLD patients and mouse models, yet its role is unclear due to the diverse mouse models and
Franco Juan Cruz Dolcetti et al.
Aging, 14(21), 8615-8632 (2022-11-04)
The process of aging is the result of progressive loss of homeostasis and functional body impairment, including the central nervous system, where the hypothalamus plays a key role in regulating aging mechanisms. The consequences of aging include a chronic proinflammatory
Megan L Greenwald-Yarnell et al.
Endocrinology, 157(4), 1555-1565 (2016-02-11)
A variety of data suggest that estrogen action on kisspeptin (Kiss1)-containing arcuate nucleus neurons (which coexpress Kiss1, neurokinin B (the product of Tac2) and dynorphin (KNDy) neurons restrains reproductive onset and function, but roles for estrogen action in these Kiss1
Yang Li et al.
PloS one, 17(6), e0259609-e0259609 (2022-06-16)
Polycystic ovary syndrome often starts in puberty, and its pathogenesis is not clear. This study aimed to explore the pathogenesis of pubertal polycystic ovary syndrome (PCOS) and assess the therapeutic effect of electroacupuncture on pubertal PCOS. Dihydrotestosterone (DHT) was used
Ting Zhang et al.
Nature, 606(7914), 594-602 (2022-05-26)
Only a small proportion of patients with cancer show lasting responses to immune checkpoint blockade (ICB)-based monotherapies. The RNA-editing enzyme ADAR1 is an emerging determinant of resistance to ICB therapy and prevents ICB responsiveness by repressing immunogenic double-stranded RNAs (dsRNAs)

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