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anti-Human KIF5B Anticorps:
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Human Polyclonal KIF5B Primary Antibody pour ELISA, WB - ABIN184774
Semiz, Park, Nicoloro, Furcinitti, Zhang, Chawla, Leszyk, Czech: Conventional kinesin KIF5B mediates insulin-stimulated GLUT4 movements on microtubules. dans The EMBO journal 2003
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Human Monoclonal KIF5B Primary Antibody pour IF - ABIN535262
Mac?rek, Dráberová, Richterová, Böhm, Dráber: Monoclonal antibodies KN-02 and KN-03 against the heavy chain of kinesin. dans Hybridoma and hybridomics 2003
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Dog (Canine) Polyclonal KIF5B Primary Antibody pour EIA, IHC (fro) - ABIN372810
Wattenberg, Kwilas, Gameiro, Dicker, Hodge: Expanding the use of monoclonal antibody therapy of cancer by using ionising radiation to upregulate antibody targets. dans British journal of cancer 2014
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Cow (Bovine) Polyclonal KIF5B Primary Antibody pour IHC, WB - ABIN2778184
Diefenbach, Diefenbach, Douglas, Cunningham: The ribosome receptor, p180, interacts with kinesin heavy chain, KIF5B. dans Biochemical and biophysical research communications 2004
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X-ray fiber diffraction, fluorescence speckle microscopy, and second-harmonic generation microscopy, as well as cryo-EM, collectively demonstrated that the binding of nucleotide-free kinesin-1 to GDP microtubules changes the conformation of the GDP microtubule to a conformation resembling the GTP microtubule.
this is the first report of a KIF5B-ALK fusion gene in large-cell neuroendocrine carcinoma (LCNEC) . The patient was successfully treated with ALK inhibitors, suggesting that sensitivity to ALK inhibitor may define a specific LCNEC subtype. We propose that screening for ALK rearrangement in patients with LCNEC may assist in selecting potential candidates for targeted therapy.
The KIF5B-MET variant was demonstrated to have an oncogenic function in cancer cells.
the discovery of kinesore, a small molecule that in vitro inhibits kinesin-1 interactions with short linear peptide motifs found in organelle-specific cargo adaptors, yet activates kinesin-1's function of controlling microtubule dynamics in cells, demonstrating that these functions are mechanistically coupled.
HIV-1 did not stimulate widespread FEZ1 phosphorylation but, instead, bound microtubule (MT) affinity-regulating kinase 2 (MARK2) to stimulate FEZ1 phosphorylation on viral cores.
Study demonstrate that the kinesin and kinase domains of KIF5B-RET act together to establish an emergent microtubule and RAB-vesicle-dependent RET-SRC-EGFR-FGFR signaling hub. Study demonstrate that drugs designed to inhibit RET alone work poorly in KIF5B-RET-transformed cells.
In particular, counteracting forces between minus-end-directed kinesin-14 and plus-end-directed kinesin-5 motors have recently been implicated in the regulation of microtubule nucleation.
The studies describing the interplay between kinesin-1 and cytoplasmic dynein in the translocation of microtubules are discussed.
Utilizing novel electron cryomicroscopy methods, the authors solved structures of microtubule-attached, dimeric kinesin bound to an ATP analog. They find that under these conditions, the kinesin dimer can attach to the microtubule with either one or two motor domains.
cargo recognition and concurrent activation of kinesin-1 proceed in hierarchical stepwise fashion driven by a dynamic network of inter- and intra-molecular interactions.
BORC and Arl8 function upstream of two structurally distinct kinesin types: kinesin-1 (KIF5B) and kinesin-3 (KIF1Bbeta and KIF1A).
KIF5B gene rearrangement plays a role in the pathogenesis of papillary thyroid cancer.
compared to those of brain, on MCF7 microtubules, kinesin-1's processivity is significantly reduced although its velocity is only slightly altered
these observations identify a previously unappreciated role for KIF5B in mediating the Nup358 dependent nuclear import of the HIV-1 viral genome during infection.
For Fat3, the Kif5-ID is regulated by alternative splicing, and the timecourse of splicing suggests that the distribution of Fat3 may switch between early and later stages of retinal development. In contrast, P75NTR binding to Kif5B is enhanced by tyrosine phosphorylation and thus has the potential to be dynamically regulated on a more rapid time scale
Data suggest that light-chain subunits/fragments of kinesin-1 inhibit the pathological aggregation of amyloid(beta).
In this work, we performed normal mode analysis with elastic network model using different conformation of kinesin to determine the effect of tail binding.
KIF5B is essential for Ostm1 intracellular dispersion.
differences between the structural kinetics of Eg5 and kinesin-1 yield insights into how these two motors adapt their enzymologies for their distinct functions
data suggest one-step screening platform for KIF5B-RET as well as EGFR, K-RAS, ALK oncogenic mutations be necessary for lung adenocarcinoma patients
Kinesin-1-dependent process plays a role for platelet function by acting into the mechanism underlying alpha-granule and dense granule secretion.
The authors concluded that kinesin-1 proteins KIF5A, -5B, and -5C are important in the anterograde transport of the majority of herpes simplex virus enveloped virions in neuronal axons and kinesin-3 proteins are less important.
kinesin and microtubules can compensate for defects in myosin-Va and actin-based transport in mammals, but endogenous Kif5b does not have an important role in transport of melanocytes due to its inefficient recruitment to melanosomes
High KIF5B expression is associated with Lung Metastasis of Breast Cancer.
It was concluded that selective deletion of Kif5b in adipose tissue exacerbates HFD-induced obesity and its associated metabolic disorders, partly through a decrease in energy expenditure, dysregulation of adipokine secretion, and insulin signaling.
PI3K-dependent formation of a kinesin-1/Slp3/Rab27b complex is critical for the microtubule-dependent movement of secretory granules required for mast cell degranulation.
The KIF5B level was up-regulated during 3T3-L1 adipogenesis. This increase in cytosolic KIF5B was synchronized with the induction of adiponectin. Endogenous KIF5B and adiponectin were partially colocalized at the peri-nuclear and cytosolic regions.
results indicate that NCAM is delivered to the cell surface through a kinesin-1-mediated transport mechanism in a PAK1-dependent manner.
Kif5b expression during mouse kidney development
we showed that the KIF5B-RET fusion gene is oncogenic in lung alveolar epithelial cells in vivo.
nesprin-dependent recruitment of kinesin-1 to the nuclear envelope through the interaction of a conserved LEWD motif with kinesin light chain might be a general mechanism for cell-type-specific nuclear positioning during development.
KIF5B is critical in suppressing chromosomal instability at the early stages of female meiotic cell development and mitotic cell division.
These results suggest that while the KLC binding domain may directly targets Kif5b to the myonuclear membrane, the autoinhibitory peptide may play an indirect role in regulating the kinesin-1-mediated myonuclear positioning
Kif5b is responsible for the localization of alpha-sarcomeric actin, desmin and nestin in differentiating myoblast cells.
identification of the microtubule-associated protein ensconsin (Ens)/microtubule-associated protein 7 (MAP7) and kinesin heavy chain (Khc)/Kif5b as essential, evolutionarily conserved regulators of myonuclear positioning in Drosophila and cultured mammalian myotubes
Nesca directly binds KIF5B, kinesin light-chain and syntaxin-1
Anterograde trafficking via kinesin 5B is essential for both receptor recycling from the phagosome and delivery of Rab11-containing membrane stores to effect broad and functional pseudopods during Fcgamma receptor-mediated phagocytosis.
Impairment of anterograde transport by knockdown of KIF5B or KLC1 delayed stress-granule dissolution.
data reveal that insulin signaling targets the engagement or initiates the movement of glutamate transporter 4-containing membranes on microtubules via KIF5B through a phosphatidylinositol 3-kinase-independent mechanism.
Data show that single kinesins undergo premature dissociation, but not preferential pausing, at the annealed sites.
Microtubule-dependent motor required for normal distribution of mitochondria and lysosomes (By similarity).
conventional kinesin heavy chain
, kinesin 1 (110-120kD)
, kinesin heavy chain
, kinesin-1 heavy chain
, ubiquitous kinesin heavy chain
, kinesin-like protein KHC
, kinesin family member 5B
, kinesin heavy chain member 5B, ubiquitous
, kinesin family member 5A