Datasheet

生物学的記述

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

Specificity

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

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.

使用情報

Application

WB, IHC, ELISA

Dilution

WB	IHC
1:2000-1:10000	1:50-1:500

Reactivity

Human

Source

Rabbit Monoclonal Antibody

MW

160 kDa

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

プロトコール

References

https://pubmed.ncbi.nlm.nih.gov/36280663/
https://pubmed.ncbi.nlm.nih.gov/38598297/

Application Data

WB

Validated by Selleck

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