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Human Polyclonal KLC1 Primary Antibody for FACS, IHC (p) - ABIN652577
Chernajovsky, Brown, Clark: Human kinesin light (beta) chain gene: DNA sequence and functional characterization of its promoter and first exon. in DNA and cell biology 1997
Show all 2 Pubmed References
structural plasticity of the N-terminal capping helix might represent a structural determinant for TPR domain structural versatility in cargo binding
All binary complexes (KLC1:APP (显示 APP 抗体), KLC1:JIP1 (显示 MAPK8IP1 抗体), and APP:JIP1) contain conformations with favorable binding free energies indicating that KLC1 and JIP1 (显示 MAPK8IP1 抗体) may take part in APP (显示 APP 抗体) transport in Alzheimer's disease patients.
BNIP-2 (显示 BNIP2 抗体) is a kinesin-1 adapter involved in vesicular transportation in the cytoplasm and that association with cargos depends on interaction of the CRAL-TRIO (显示 TRIO 抗体) domain with membrane phosphatidylserine.
The G allele and GG genotype of KLC1 rs8702 were significantly over-represented among cataract patients, as compared to healthy controls, and were associated with an odds ratio for cataract development.
Dnm1L (显示 DNM1L 抗体) interacts with KLC1 through the tetratricopeptide repeat domains.
Microtubule-bound kinesin-1 and kinesin-3 motor domains were visualized at multiple steps in their ATPase (显示 DNAH8 抗体) cycles--including their nucleotide-free states--at approximately 7 A resolution using cryo-electron microscopy.
Studies indicate that FEZ1 (fasciculation and elongation protein zeta 1 (显示 LZTS1 抗体)), SCOCO (short coiled-coil protein (显示 SCOC 抗体)) and kinesins (kinesin heavy chain (显示 KIF5A 抗体)) are involved in biological transport process.
The expression levels of KLC1 variant E in brain and lymphocytes were significantly higher in Alzheimer's disease patients.
study provides evidence that the combined effect of three variants within the KLC1 gene may predispose to age-related cataract.
For the binding of cargos shared by KLC1, we propose a different site located within the groove but not involving N343.
Phosphorylation of KLC1 at Thr466 increased in aged brains, and JIP1 (显示 MAPK8IP1 抗体) binding to kinesin-1 decreased, suggesting that APP (显示 APP 抗体) transport is impaired by aging. Authors conclude that phosphorylation of KLC1 at Thr466 regulates the velocity of transport of APP (显示 APP 抗体) by kinesin-1 by modulating its interaction with JIP1b.
In old mice, lack of KLC1 results in retinal pigment epithelium pathogenesis that was strikingly comparable to aspects of age-related macular degeneration.
Alcalpha (显示 CLSTN1 抗体) is efficiently processed in part to minimize the inappropriate peripheral retention of kinesin-1
A small peptide sequence is sufficient for initiating kinesin-1 activation through part of TPR (显示 GRID2 抗体) region of KLC1
Data show that amyloid precursor protein (APP (显示 APP 抗体)) levels are well-correlated with the amount of the light chain of kinesin-1 (KLC1).
KLC1-ALK (显示 ALK 抗体) is the first novel oncogenic fusion identified using only formalin-fixed paraffin-embedded tissue tissues
Phosphorylation of KLC1 at serine 460 modulates binding and trafficking of calsyntenin-1 (显示 CLSTN1 抗体).
changes in the phosphorylation state of KLC1 at Ser517/520 are unlikely to affect motor function.
An essential role of mNUDC for anterograde transport of dynein and dynactin (显示 DCTN1 抗体) by kinesin-1.
Impairment of anterograde transport by knockdown of KIF5B (显示 KIF5B 抗体) or KLC1 delayed stress-granule dissolution.
Conventional kinesin is a tetrameric molecule composed of two heavy chains and two light chains, and transports various cargos along microtubules toward their plus ends. The heavy chains provide the motor activity, while the light chains bind to various cargos. This gene encodes a member of the kinesin light chain family. It associates with kinesin heavy chain through an N-terminal domain, and six tetratricopeptide repeat (TPR) motifs are thought to be involved in binding of cargos such as vesicles, mitochondria, and the Golgi complex. Thus, kinesin light chains function as adapter molecules and not motors per se. Although previously named 'kinesin 2', this gene is not a member of the kinesin-2 / kinesin heavy chain subfamily of kinesin motor proteins. Extensive alternative splicing produces isoforms with different C-termini that are proposed to bind to different cargos\; however, the full-length nature and/or biological validity of most of these variants have not been determined.
, kinesin light chain 1
, kinesin light chain 2
, kinesin light chain 4
, kinesin 2 60/70kDa
, kinesin ii
, KLC 1
, medulloblastoma antigen MU-MB-2.50