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rabbit anti mklp1 polyclonal antibody (Novus Biologicals)

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Novus Biologicals rabbit anti mklp1 polyclonal antibody

Mos −/− eggs have defects in meiotic midbody formation. (A–D) Representative immunofluorescence images of wild-type (A) and Mos −/− eggs (B–D) showing localization of <t>MKLP1</t> (magenta), tubulin (green), and DNA (white). Arrowheads indicate structure features of MKLP1. Wild-type and Mos −/− oocytes were fixed 9–11.5 h after prophase I release. Scale bars: 10 µm. (E) Percentage of wild-type and Mos −/− eggs with normal or defective MKLP1 structure ( n indicates the number of eggs imaged per condition; three or more independent experiments conducted per condition). **** P <0.0001 (two-sided Fisher's exact test).

Rabbit Anti Mklp1 Polyclonal Antibody, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 94/100, based on 10 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/rabbit anti mklp1 polyclonal antibody/product/Novus Biologicals
Average 94 stars, based on 10 article reviews

rabbit anti mklp1 polyclonal antibody - by Bioz Stars, 2026-06

94/100 stars

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1) Product Images from "MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies"

Article Title: MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies

Journal: Journal of Cell Science

doi: 10.1242/jcs.264411

Figure Legend Snippet: Mos −/− eggs have defects in meiotic midbody formation. (A–D) Representative immunofluorescence images of wild-type (A) and Mos −/− eggs (B–D) showing localization of MKLP1 (magenta), tubulin (green), and DNA (white). Arrowheads indicate structure features of MKLP1. Wild-type and Mos −/− oocytes were fixed 9–11.5 h after prophase I release. Scale bars: 10 µm. (E) Percentage of wild-type and Mos −/− eggs with normal or defective MKLP1 structure ( n indicates the number of eggs imaged per condition; three or more independent experiments conducted per condition). **** P <0.0001 (two-sided Fisher's exact test).

Techniques Used: Immunofluorescence

Image Search Results

Journal: Journal of Cell Science

Article Title: MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies

doi: 10.1242/jcs.264411

Figure Lengend Snippet: Mos −/− eggs have defects in meiotic midbody formation. (A–D) Representative immunofluorescence images of wild-type (A) and Mos −/− eggs (B–D) showing localization of MKLP1 (magenta), tubulin (green), and DNA (white). Arrowheads indicate structure features of MKLP1. Wild-type and Mos −/− oocytes were fixed 9–11.5 h after prophase I release. Scale bars: 10 µm. (E) Percentage of wild-type and Mos −/− eggs with normal or defective MKLP1 structure ( n indicates the number of eggs imaged per condition; three or more independent experiments conducted per condition). **** P <0.0001 (two-sided Fisher's exact test).

Article Snippet: The primary antibodies used were: rabbit anti-MKLP1 polyclonal antibody (Novus NBP2-56923; 1:100) and rabbit anti-PRC1 polyclonal antibody (Proteintech 15617-1-AP; 1:100).

Techniques: Immunofluorescence

Multivariate Cox analysis of the three gene signatures: ( A ) unreduced; ( B ) FDR-reduced; ( C ) GO-reduced.

Journal: International Journal of Molecular Sciences

Article Title: Identification of Overexpressed Genes in Malignant Pleural Mesothelioma

doi: 10.3390/ijms22052738

Figure Lengend Snippet: Multivariate Cox analysis of the three gene signatures: ( A ) unreduced; ( B ) FDR-reduced; ( C ) GO-reduced.

Article Snippet: The membranes were blocked with 5% milk TBST and probed overnight at 4 °C with the specific primary antibody: anti-CIT rabbit polyclonal antibody (1:500; Proteintech, Rosemont, IL, USA); anti-CTHRC1 rabbit polyclonal antibody (1:1000; Proteintech, Rosemont, IL, USA); anti-E selectin rabbit polyclonal antibody (1:750; Proteintech, Rosemont, IL, USA); anti-Midkine (MDK) rabbit polyclonal antibody (1:500; Proteintech, Rosemont, IL, USA); anti-SPARC rabbit polyclonal antibody (1:750; Proteintech, Rosemont, IL, USA); anti-TRAF2 rabbit polyclonal antibody (1:1000; Proteintech, Rosemont, IL, USA); anti-UHRF1 rabbit polyclonal antibody (1:1000; Proteintech, Rosemont, IL, USA); anti-DSC3 mouse polyclonal antibody (1:500; Genetex, Irvine, CA, USA); anti-KIF23 rabbit polyclonal antibody (1:500; OriGene, Rockville, MD, USA); anti-PRSS23 rabbit polyclonal antibody (1:500; Abcam, Cambridge, MA, USA); anti-ADAMTS1 rabbit polyclonal antibody (1:500; GeneTex, Irvine, CA, USA); anti-PODXL rabbit polyclonal antibody (1:500; Proteintech, Rosemont, IL, USA); anti-BAG2 rabbit polyclonal antibody (1:1000; Proteintech, Rosemont, IL, USA); anti-TNNT1 rabbit polyclonal antibody (1:1000; Proteintech, Rosemont, IL, USA); anti-MAD2L1 rabbit polyclonal antibody (1:800; Proteintech, Rosemont, IL, USA).

Techniques:

Comparison of effects of acute optogenetic removal of PRC1 and long-term depletion by siRNA. All values are given as mean ± s.e.m. The numbers in the brackets denote the number of measurements and cells, respectively; a single number is the number of cells. Symbols (arrows and equal signs) denote trend of change of parameters; equal sign means no change; two arrows mark stronger effect. Measurements include cells without and with SiR-tubulin. Signal intensities of microtubule-associated proteins were normalized to the mean value of the signal of corresponding control for each treatment. BAC denotes live-cell experiments on HeLa cells expressing a fluorescently tagged protein from a BAC, immuno denotes immunocytochemistry experiments. # Consistent with our previous studies ( <xref ref-type=

Kajtez et al., 2016 ; Polak et al., 2017 )." width="100%" height="100%">

Journal: eLife

Article Title: Optogenetic control of PRC1 reveals its role in chromosome alignment on the spindle by overlap length-dependent forces

doi: 10.7554/eLife.61170

Figure Lengend Snippet: Comparison of effects of acute optogenetic removal of PRC1 and long-term depletion by siRNA. All values are given as mean ± s.e.m. The numbers in the brackets denote the number of measurements and cells, respectively; a single number is the number of cells. Symbols (arrows and equal signs) denote trend of change of parameters; equal sign means no change; two arrows mark stronger effect. Measurements include cells without and with SiR-tubulin. Signal intensities of microtubule-associated proteins were normalized to the mean value of the signal of corresponding control for each treatment. BAC denotes live-cell experiments on HeLa cells expressing a fluorescently tagged protein from a BAC, immuno denotes immunocytochemistry experiments. # Consistent with our previous studies ( Kajtez et al., 2016 ; Polak et al., 2017 ).

Article Snippet: Following primary antibodies were used: mouse anti-PRC1 monoclonal antibody (1:100; C-1; sc-376983, Santa Cruz Biotechnology), rabbit anti-α-tubulin polyclonal antibody (1:100; RRID: AB_10743646 ; SAB4500087; Sigma-Aldrich Corporation, St. Louis, MO, USA), mouse monoclonal anti-Kif4A antibody (1:100; RRID: AB_10707683 ; E-8; sc-365144; Santa Cruz Biotechnology), rabbit polyclonal anti-MKLP1 antibody (1:100; RRID: AB_631959 ; N-19; sc-867, Santa Cruz Biotechnology), mouse monoclonal anti-Eg5 antibody (1:100; RRID: AB_10841907 ; A-1; sc-365681, Santa Cruz Biotechnology), rabbit polyclonal anti-Kif18A antibody (1:100; RRID: AB_2296551 ; A301-080A; Bethyl), rabbit polyclonal anti-Kif4A antibody (1:200; RRID: AB_2280904 ; A301-074A; Bethyl).

Techniques: Comparison, Control, Expressing, Immunocytochemistry

( A ) Spindle (first block, left) in a U2OS cell with stable expression of CENP-A-GFP (not shown), immunostained for endogenous Kif4A (AF-594, green), PRC1 (AF-647, magenta) and stained with DAPI (cyan). Enlargements of the boxed region are shown (right). White arrowhead points to Kif4A outside chromosomes, at the position where PRC1-AF-647 is found, which corresponds to the bridging fiber. Spindle (middle block, top) in a U2OS cell with stable expression of CENP-A-GFP (cyan), immunostained for endogenous Kif18A (AF-594, green) and PRC1 (AF-647, magenta). Enlargements of the boxed region are shown (bottom). White arrowhead points to Kif18A in the bridging fiber where PRC1-AF-647 is found. Spindle (right block, top) of HeLa cell stably expressing MKLP1-GFP (green) and stained for SiR-tubulin (magenta). Enlargements of the boxed region are shown (bottom). White arrowhead points to the MKLP1 in the bridging fiber. Schemes (right) show Kif4A and Kif18A localization on chromosome arms and plus ends of k-fibers, respectively, and Kif4A, Kif18A, and MKLP1 in the bridging fiber. ( B ) Time-lapse images (left block) of unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and GFP-Kif4A (green), and stained with SiR-DNA (cyan) before (Dark, top) and after 12 min of the exposure to the blue light (Light, middle). Enlargements of the boxed regions are shown (bottom rows). Before opto-PRC1 removal (Dark) Kif4A is also found outside chromosomes, at the position of opto-PRC1 labeled bundles (white arrowheads). Note that after 12 min of opto-PRC1 removal (Light), Kif4A signal is found only at the positions of the chromosomes. The intensities in the enlargements are adjusted differently than those of the whole spindle to better point out localization of proteins. Time-lapse images (right block) of unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and EGFP-Kif18A (green) before (Dark, top) and after 12 min of the exposure to the blue light (Light, middle). Enlargements of the boxed regions are shown (bottom). Before opto-PRC1 removal (Dark, bottom left) Kif18A is found in the bridging fiber (white arrowhead). In the enlargement of the boxed region after 12 min of opto-PRC1 removal (Light, bottom right), the signal of the EGFP-Kif18A on the bridging fiber is weaker. ( C ) Normalized bridging fiber Kif4A (left) and Kif18A (right) intensity measured before and after acute and long-term PRC1 removal in cells as in B and A, respectively. Dark; black, Light; cyan, untreated; magenta, PRC1 siRNA; green. ( D ) Timelapse of the spindle in HeLa BAC cell (left) stably expressing MKLP1-GFP (gray) with transient expression of opto-PRC1 (not shown) and iLID-CAAX, and stained with SiR-DNA (not shown) before (0 min, Dark), at the end of continuous exposure (20 min, Light) and 10 min after cessation of exposure to the blue light (30 min, Dark). Note that opto-PRC1 is not shown in order to point out localization of MKLP1-GFP. Image is a maximum projection of three z-planes. Graph (right) shows normalized bridging fiber MKLP1 intensity measured before and after acute and long-term PRC1 removal in cells as in . ( E ) Spindles from HeLa cells stably expressing PRC1-GFP (gray) in untreated (left), Kif4A siRNA (middle), and Kif18A siRNA (right) -treated cell. ( F ) Ratios of overlap and spindle lengths for untreated (black), Kif4A siRNA (magenta), and Kif18A siRNA (green) -treated cells. Gray scattered points show individual measurements. ( G ) Difference in PRC1-labeled overlap and spindle length for Kif4A siRNA (magenta) and Kif18A siRNA (green) treatment when compared to untreated cells. Numbers in brackets; number of measurements and cells, respectively. Statistical analysis: t-test ( C, G ); one-way ANOVA ( F ). All images are smoothed with 0.5-pixel-sigma Gaussian blur, and one z-plane is shown unless stated otherwise. Scale bars: 2 µm.

Journal: eLife

Article Title: Optogenetic control of PRC1 reveals its role in chromosome alignment on the spindle by overlap length-dependent forces

doi: 10.7554/eLife.61170

Figure Lengend Snippet: ( A ) Spindle (first block, left) in a U2OS cell with stable expression of CENP-A-GFP (not shown), immunostained for endogenous Kif4A (AF-594, green), PRC1 (AF-647, magenta) and stained with DAPI (cyan). Enlargements of the boxed region are shown (right). White arrowhead points to Kif4A outside chromosomes, at the position where PRC1-AF-647 is found, which corresponds to the bridging fiber. Spindle (middle block, top) in a U2OS cell with stable expression of CENP-A-GFP (cyan), immunostained for endogenous Kif18A (AF-594, green) and PRC1 (AF-647, magenta). Enlargements of the boxed region are shown (bottom). White arrowhead points to Kif18A in the bridging fiber where PRC1-AF-647 is found. Spindle (right block, top) of HeLa cell stably expressing MKLP1-GFP (green) and stained for SiR-tubulin (magenta). Enlargements of the boxed region are shown (bottom). White arrowhead points to the MKLP1 in the bridging fiber. Schemes (right) show Kif4A and Kif18A localization on chromosome arms and plus ends of k-fibers, respectively, and Kif4A, Kif18A, and MKLP1 in the bridging fiber. ( B ) Time-lapse images (left block) of unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and GFP-Kif4A (green), and stained with SiR-DNA (cyan) before (Dark, top) and after 12 min of the exposure to the blue light (Light, middle). Enlargements of the boxed regions are shown (bottom rows). Before opto-PRC1 removal (Dark) Kif4A is also found outside chromosomes, at the position of opto-PRC1 labeled bundles (white arrowheads). Note that after 12 min of opto-PRC1 removal (Light), Kif4A signal is found only at the positions of the chromosomes. The intensities in the enlargements are adjusted differently than those of the whole spindle to better point out localization of proteins. Time-lapse images (right block) of unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and EGFP-Kif18A (green) before (Dark, top) and after 12 min of the exposure to the blue light (Light, middle). Enlargements of the boxed regions are shown (bottom). Before opto-PRC1 removal (Dark, bottom left) Kif18A is found in the bridging fiber (white arrowhead). In the enlargement of the boxed region after 12 min of opto-PRC1 removal (Light, bottom right), the signal of the EGFP-Kif18A on the bridging fiber is weaker. ( C ) Normalized bridging fiber Kif4A (left) and Kif18A (right) intensity measured before and after acute and long-term PRC1 removal in cells as in B and A, respectively. Dark; black, Light; cyan, untreated; magenta, PRC1 siRNA; green. ( D ) Timelapse of the spindle in HeLa BAC cell (left) stably expressing MKLP1-GFP (gray) with transient expression of opto-PRC1 (not shown) and iLID-CAAX, and stained with SiR-DNA (not shown) before (0 min, Dark), at the end of continuous exposure (20 min, Light) and 10 min after cessation of exposure to the blue light (30 min, Dark). Note that opto-PRC1 is not shown in order to point out localization of MKLP1-GFP. Image is a maximum projection of three z-planes. Graph (right) shows normalized bridging fiber MKLP1 intensity measured before and after acute and long-term PRC1 removal in cells as in . ( E ) Spindles from HeLa cells stably expressing PRC1-GFP (gray) in untreated (left), Kif4A siRNA (middle), and Kif18A siRNA (right) -treated cell. ( F ) Ratios of overlap and spindle lengths for untreated (black), Kif4A siRNA (magenta), and Kif18A siRNA (green) -treated cells. Gray scattered points show individual measurements. ( G ) Difference in PRC1-labeled overlap and spindle length for Kif4A siRNA (magenta) and Kif18A siRNA (green) treatment when compared to untreated cells. Numbers in brackets; number of measurements and cells, respectively. Statistical analysis: t-test ( C, G ); one-way ANOVA ( F ). All images are smoothed with 0.5-pixel-sigma Gaussian blur, and one z-plane is shown unless stated otherwise. Scale bars: 2 µm.

Techniques: Blocking Assay, Expressing, Staining, Stable Transfection, Labeling

( A ) Additional example (left block) of the spindle from the cell in and the same cell type treated with PRC1 siRNA (middle block). Right block: spindle in a U2OS cell with stable expression of CENP-A-GFP (cyan), immunostained for endogenous Kif18A (AF-594, green) and PRC1 (AF-647, magenta), treated with PRC1 siRNA. ( B ) Left: vertically oriented spindle in unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and GFP-Kif4A (green), and stained with SiR-DNA (cyan). Enlargements of the boxed regions (right) show Kif4A localization outside chromosomes, at the position of opto-PRC1 signal. Right: Vertically oriented spindle in unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and EGFP-Kif18A (green). Note that the spindle is slightly tilted. The enlargement of the boxed region shows Kif18A at the position where opto-PRC1 is found (right). Each opto-PRC1 spot, which we interpret as the bridging fiber, also has Kif18A signal, while spots containing Kif18A only we interpret as its signal on plus-ends of k-fibers. ( C ) Images of untreated and PRC1 siRNA-treated spindles in: HeLa cell expressing Kif4A-GFP (gray) from bacterial artificial chromosome (BAC) with the corresponding graph showing normalized Kif4A bridge intensity in those treatments (left); HeLa BAC cell expressing Kif18A-GFP (gray) with the corresponding graph showing normalized Kif18A bridge intensity in those treatments (middle) and HeLa BAC cell expressing MKLP1-GFP (gray) (right). Cells are stained with SiR-tubulin (not shown). ( D ) Spindles in fixed HeLa cells stably expressing MKLP1-GFP (yellow) and immunostained for PRC1 (AF-640, magenta), tubulin (AF-560, green) and stained with DAPI (blue) in untreated (left) and PRC1 siRNA-treated (right) cells (left). All images are sum intensity projections of five z-planes. Graph (right) shows PRC1 intensity in untreated (magenta) and PRC1 siRNA-treated (green) cells. Numbers inside bars; number of cells. ( E ) Spindle in a fixed unlabeled untreated HeLa cell (top left) and HeLa BAC cell expressing MKLP1-GFP (bottom left), immunostained for MKLP1 (AF-594, green), PRC1 (AF-647, magenta) and stained with DAPI (not shown). Images are sum-intensity projections of five z-planes smoothed with 0.5-pixel-Gaussian blur. Graph (right) shows MKLP1 intensity in untreated unlabeled (magenta) and BAC cells (green). The signal intensity of MKLP1 in these cells was 6% higher compared to endogenous MKLP1. ( F ) Time-lapse of HeLa BAC cell expressing MKLP1-GFP (green), depleted for endogenous PRC1, with transient expression of opto-PRC1 (magenta) and iLID-CAAX in time-points as in . Graphs (middle) correspond to membrane-to-membrane intensity profiles of MKLP1-GFP (green) and opto-PRC1 (magenta) acquired by 1 µm wide line across equatorial plane in time-points as in on maximum projection of three z-planes. Schematic representation of performed measurement is given on the right. Graphs (bottom) show individual MKLP1-GFP (left) and opto-PRC1 intensities (right). ( G ) Time-lapse of a cell as in F , which progresses to cytokinesis during time-points as in F . Statistical analysis: t-test.

Journal: eLife

Article Title: Optogenetic control of PRC1 reveals its role in chromosome alignment on the spindle by overlap length-dependent forces

doi: 10.7554/eLife.61170

Figure Lengend Snippet: ( A ) Additional example (left block) of the spindle from the cell in and the same cell type treated with PRC1 siRNA (middle block). Right block: spindle in a U2OS cell with stable expression of CENP-A-GFP (cyan), immunostained for endogenous Kif18A (AF-594, green) and PRC1 (AF-647, magenta), treated with PRC1 siRNA. ( B ) Left: vertically oriented spindle in unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and GFP-Kif4A (green), and stained with SiR-DNA (cyan). Enlargements of the boxed regions (right) show Kif4A localization outside chromosomes, at the position of opto-PRC1 signal. Right: Vertically oriented spindle in unlabeled U2OS cell with transient expression of opto-PRC1 (magenta), iLID-CAAX and EGFP-Kif18A (green). Note that the spindle is slightly tilted. The enlargement of the boxed region shows Kif18A at the position where opto-PRC1 is found (right). Each opto-PRC1 spot, which we interpret as the bridging fiber, also has Kif18A signal, while spots containing Kif18A only we interpret as its signal on plus-ends of k-fibers. ( C ) Images of untreated and PRC1 siRNA-treated spindles in: HeLa cell expressing Kif4A-GFP (gray) from bacterial artificial chromosome (BAC) with the corresponding graph showing normalized Kif4A bridge intensity in those treatments (left); HeLa BAC cell expressing Kif18A-GFP (gray) with the corresponding graph showing normalized Kif18A bridge intensity in those treatments (middle) and HeLa BAC cell expressing MKLP1-GFP (gray) (right). Cells are stained with SiR-tubulin (not shown). ( D ) Spindles in fixed HeLa cells stably expressing MKLP1-GFP (yellow) and immunostained for PRC1 (AF-640, magenta), tubulin (AF-560, green) and stained with DAPI (blue) in untreated (left) and PRC1 siRNA-treated (right) cells (left). All images are sum intensity projections of five z-planes. Graph (right) shows PRC1 intensity in untreated (magenta) and PRC1 siRNA-treated (green) cells. Numbers inside bars; number of cells. ( E ) Spindle in a fixed unlabeled untreated HeLa cell (top left) and HeLa BAC cell expressing MKLP1-GFP (bottom left), immunostained for MKLP1 (AF-594, green), PRC1 (AF-647, magenta) and stained with DAPI (not shown). Images are sum-intensity projections of five z-planes smoothed with 0.5-pixel-Gaussian blur. Graph (right) shows MKLP1 intensity in untreated unlabeled (magenta) and BAC cells (green). The signal intensity of MKLP1 in these cells was 6% higher compared to endogenous MKLP1. ( F ) Time-lapse of HeLa BAC cell expressing MKLP1-GFP (green), depleted for endogenous PRC1, with transient expression of opto-PRC1 (magenta) and iLID-CAAX in time-points as in . Graphs (middle) correspond to membrane-to-membrane intensity profiles of MKLP1-GFP (green) and opto-PRC1 (magenta) acquired by 1 µm wide line across equatorial plane in time-points as in on maximum projection of three z-planes. Schematic representation of performed measurement is given on the right. Graphs (bottom) show individual MKLP1-GFP (left) and opto-PRC1 intensities (right). ( G ) Time-lapse of a cell as in F , which progresses to cytokinesis during time-points as in F . Statistical analysis: t-test.

Techniques: Blocking Assay, Expressing, Staining, Stable Transfection, Membrane

( A ) We propose that the interactions between k-fibers and bridging fibers regulate the movement of bi-oriented chromosomes by forces that depend on the length of the antiparallel overlaps (purple). Shorter overlaps lead to more precise alignment of kinetochores (cyan) than longer ones. ( B ) If a kinetochore pair is displaced away from the equatorial plane toward one pole, the overlap between the k-fiber and the bridging fiber (purple) is shorter on this side and longer on the opposite side. More motors and/or crosslinkers accumulate in the longer overlap, pulling the kinetochore back to the center ( F , pulling force). The efficiency of centering depends on the relative asymmetry in the overlap length on either side. This asymmetry is larger if the overlap is short, which explains why short overlaps lead to better alignment than long ones (see A). ( C ) The overlap length is regulated by Kif4A and Kif18A at the plus ends of bridging microtubules. Kif4A and Eg5 within the bridging fiber possibly slide the microtubules apart, whereas PRC1 stabilizes the overlaps probably together with MKLP1, Eg5, and other crosslinkers.

Journal: eLife

Article Title: Optogenetic control of PRC1 reveals its role in chromosome alignment on the spindle by overlap length-dependent forces

doi: 10.7554/eLife.61170

Figure Lengend Snippet: ( A ) We propose that the interactions between k-fibers and bridging fibers regulate the movement of bi-oriented chromosomes by forces that depend on the length of the antiparallel overlaps (purple). Shorter overlaps lead to more precise alignment of kinetochores (cyan) than longer ones. ( B ) If a kinetochore pair is displaced away from the equatorial plane toward one pole, the overlap between the k-fiber and the bridging fiber (purple) is shorter on this side and longer on the opposite side. More motors and/or crosslinkers accumulate in the longer overlap, pulling the kinetochore back to the center ( F , pulling force). The efficiency of centering depends on the relative asymmetry in the overlap length on either side. This asymmetry is larger if the overlap is short, which explains why short overlaps lead to better alignment than long ones (see A). ( C ) The overlap length is regulated by Kif4A and Kif18A at the plus ends of bridging microtubules. Kif4A and Eg5 within the bridging fiber possibly slide the microtubules apart, whereas PRC1 stabilizes the overlaps probably together with MKLP1, Eg5, and other crosslinkers.

Techniques:

Journal: eLife

Article Title: Optogenetic control of PRC1 reveals its role in chromosome alignment on the spindle by overlap length-dependent forces

doi: 10.7554/eLife.61170

Figure Lengend Snippet:

Techniques: Stable Transfection, Expressing, Transfection, Construct, Recombinant, Plasmid Preparation, Sequencing, Cloning, Software, Staining

Review

Structured Review

Images

1) Product Images from "MOS is a key regulator of meiotic midbody assembly and prevents abnormal divisions in mouse eggs and their polar bodies"

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