KIF15 Antibody [M12M19]

Catalog No.: F4980

Application: Reactivity: Human

Lane 1: HEK-293, Lane 2: Hela, Lane 3: HepG2, Lane 4: K562

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代表番号: 045-509-1970|電子メール：sales@selleck.co.jp

使用情報

Dilution
WB1:2000-1:10000 IHC1:50-1:500

Application
WB, IHC, ELISA

Source
Rabbit Monoclonal Antibody

Reactivity
Human

Storage Buffer
PBS, pH 7.2+50% Glycerol+0.05% BSA+0.01% NaN3

Storage (from the date of receipt)
-20°C (avoid freeze-thaw cycles), 2 years

Predicted MW Observed MW
160 kDa 160 kDa
^*なぜ予測分子量と実際の分子量が異なるのか？下記の原因により、実際の分子量が予測と異なる：タンパク質の翻訳後修飾（リン酸化/糖鎖付加），スプライシングバリアント，イソフォーム，相対的な電荷，ポリマー。

Datasheet & SDS

生物学的記述

Specificity
KIF15 Antibody [M12M19] detects endogenous levels of total KIF15 protein.

Clone
M12M19

Synonym(s)
Kinesin-like protein KIF15; Kinesin-like protein 2; Kinesin-like protein 7; Serologically defined breast cancer antigen NY-BR-62; KIF15; KLP2; KNSL7

Background
KIF15 (kinesin‑12; KLP2/KNSL7) is a plus‑end‑directed kinesin motor protein that functions within the mitotic spindle and in interphase intracellular trafficking, acting as both a microtubule‑sliding motor and a microtubule‑cross‑linking factor. KIF15 localizes to spindle microtubules and can partially compensate for the kinesin‑5 motor Eg5 by promoting centrosome separation and bipolar spindle assembly, particularly when Eg5 is inhibited, operating within a broader mitotic spindle‑force network rather than as a standalone driver. KIF15 binds antiparallel microtubule overlaps and, together with microtubule‑bundling proteins, stabilizes these regions so that KIF15‑driven sliding efficiently generates outward forces that help maintain spindle architecture and k‑fiber coherence. KIF15 is recruited into signaling and trafficking pathways through interactions with PI3K‑C2α and RAB11A, enabling it to regulate integrin‑β1 recycling and focal adhesion turnover in cancer cells by directing endosomal transport of integrins to the plasma membrane, thereby influencing cell migration and invasion. KIF15 activity is tuned by post‑translational modifications such as acetylation and phosphorylation, including SIRT1‑dependent acetylation‑linked phosphorylation events that modulate motor function and its association with integrin‑recycling machinery, while its C‑terminal domain also participates in controlling localization and autoinhibition. Its overexpression or dysregulated activity is implicated in aberrant cell division and tumor cell dissemination, particularly in pancreatic and other metastatic cancers.

Background

KIF15 (kinesin‑12; KLP2/KNSL7) is a plus‑end‑directed kinesin motor protein that functions within the mitotic spindle and in interphase intracellular trafficking, acting as both a microtubule‑sliding motor and a microtubule‑cross‑linking factor. KIF15 localizes to spindle microtubules and can partially compensate for the kinesin‑5 motor Eg5 by promoting centrosome separation and bipolar spindle assembly, particularly when Eg5 is inhibited, operating within a broader mitotic spindle‑force network rather than as a standalone driver. KIF15 binds antiparallel microtubule overlaps and, together with microtubule‑bundling proteins, stabilizes these regions so that KIF15‑driven sliding efficiently generates outward forces that help maintain spindle architecture and k‑fiber coherence. KIF15 is recruited into signaling and trafficking pathways through interactions with PI3K‑C2α and RAB11A, enabling it to regulate integrin‑β1 recycling and focal adhesion turnover in cancer cells by directing endosomal transport of integrins to the plasma membrane, thereby influencing cell migration and invasion. KIF15 activity is tuned by post‑translational modifications such as acetylation and phosphorylation, including SIRT1‑dependent acetylation‑linked phosphorylation events that modulate motor function and its association with integrin‑recycling machinery, while its C‑terminal domain also participates in controlling localization and autoinhibition. Its overexpression or dysregulated activity is implicated in aberrant cell division and tumor cell dissemination, particularly in pancreatic and other metastatic cancers.

References
[1] He Z, et al. Cell Death Dis. 2022 Oct 25;13(10):896. [2] Salazar BM, et al. Mol Biol Cell. 2024 Jun 1;35(6):ar84.

PVDFメンブレン孔径参考表

Protein Size (kDa)	PVDF Transfer Membrane Pore Size (μm)
< 10	0.22
10-20	0.22
20-30	0.45
30-45	0.45
45-70	0.45
80-100	0.45
100-140	0.45
> 140	0.45

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Protein Size (kDa)	Separating Gel Percentage
4-40	20%
12-45	15%
10-70	12.5%
15-100	10%
25-100	8%
60-210	5%