KIF15 Antibody [M12M19] | Primary Antibodies

Application: Reactivity: Human

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

Usage Information

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

Application
WB, IHC, ELISA

Reactivity
Human

Source
Rabbit Monoclonal Antibody

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
^*Why do the predicted and actual molecular weights differ? The following reasons may explain differences between the predicted and actual protein molecular weight. Post-translational modifications(e.g., phosphorylation, glycosylation); Splice variants and isoforms; Relative charge; Multimerization.

Datasheet & SDS

Biological Description

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

Reference Table for Selecting PVDF Membrane Pore Size Specifications

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%