KIF22 promotes bladder cancer progression by activating the expression of CDCA3

Bladder most cancers is a typical malignant tumor of the urinary system and is related to a excessive morbidity and mortality, as a result of issue within the correct prognosis of sufferers with early‑stage bladder most cancers and the dearth of efficient therapies for sufferers with superior bladder most cancers. Thus, novel therapeutic targets are urgently required for this illness.
Kinesin member of the family 22 (KIF22) is a kinesin‑like DNA binding protein belonging to kinesin household, and is concerned within the regulation of mitosis. KIF22 has additionally been reported to advertise the development of a number of kinds of most cancers, akin to breast most cancers and melanoma. The current examine demonstrates the excessive expression of KIF22 in human bladder most cancers tissues.
KIF22 was discovered to be related to scientific options, together with scientific stage (P=0.003) and recurrence (P=0.016), and to be related to the prognosis of sufferers with bladder most cancers. Moreover, it was discovered that KIF22 silencing inhibited the proliferation of bladder most cancers cells in vitro and tumor development in mice. Moreover, it was famous that KIF22 transcriptionally activated cell division cycle‑related protein Three expression, which was additionally confirmed in tumors in mice.
Taken collectively, the current examine investigated the molecular mechanisms underlying the promotion of bladder most cancers by KIF22 and supply a novel therapeutic goal for the therapy of bladder most cancers. Introduction.

KIF22 promotes progress of esophageal squamous cell carcinoma cells and is negatively regulated by miR-122

Esophageal squamous cell carcinoma (ESCC) will increase at quick fee of all most cancers varieties in China, which urges the investigations of its potential mechanism. On this analysis, a extremely expressed kinesin superfamily protein 22 (KIF22) was based each in ESCC tissues and most cancers cell strains.
The next experiments identified that down-regulation of KIF22 remarkably restrained the malignant development of ESCC cells. Moreover, KIF22 knockdown promoted ESCC cells apoptosis and arrested cells in G0/G1 section, whereas KIF22 additionally regulated the expression of cell cycle- and EMT-related proteins. Earlier analysis revealed that the aberrant expressions of microRNAs (miRNAs) are associated to tumors growth.
Based mostly on the predict end result, KIF22 was thought of because the goal of miR-122, which was demonstrated by luciferase reporter assay. miR-122 inhibitor might considerably reverse the operate of KIF22 knockdown, together with cell proliferation, migration and invasion. Moreover, down-expressed miR-122 altered the operate of KIF22 knockdown on cell cycle- and EMT-related proteins. In a phrase, this work illustrated the regulatory operate of KIF22/miR-122 axis in ESSC and offered potential targets for potential targets for ESSC therapy.

Impact of KIF22 on selling proliferation and migration of gastric most cancers cells through MAPK-ERK pathways.

Gastric most cancers (GC) is likely one of the most globally prevalent cancers on this planet. The pathogenesis of GC has not been totally elucidated, and there nonetheless lacks efficient focused therapeutics. The affect of altered kinesin superfamily protein 22 (KIF22) expression in GC development remains to be unclearly. The intention of this examine was to research the KIF22 results on GC and associated mechanisms.
Gastric carcinoma tissues and matching non-cancerous tissues had been collected from sufferers with GC who’ve accepted a radical gastrectomy in Lanzhou College Second Hospital from Might 2013 to December 2014. The expression of KIF22 was examined in GC of 67 sufferers and 20 para-carcinoma tissues by immunochemical staining. The connection between the expression of KIF22 and clinicopathologic traits was subsequent investigated within the remaining 52 sufferers aside from 15 sufferers who didn’t full follow-up for five years.
Cell viability was carried out through 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) check and colony formation assay within the MGC-803 and BGC-823 GC cells. Cell scratch and trans-well invasion assay was carried out to evaluate migration means within the MGC-803 and BGC-823 GC cells. Gene set enrichment evaluation (GSEA) pathway enrichment evaluation was carried out to discover the potential capabilities. Cell cycle was detected by move cytometry.
As well as, the 2 GC cell strains had been used to elucidate the underlying mechanism of KIF22 in GC in vitro through assessing the results on mitogen-activated protein kinase and extracellular regulated protein kinases (MAPK/ERK) sign transduction pathway-related expressions by Western blotting assays. The variations had been in contrast by t assessments, one-way evaluation of variance, and Chi-squared assessments.
The examine confirmed that KIF22 was up-regulated in GC, and KIF22 excessive expression was considerably associated to differentiation diploma (χ = 12.842, P = 0.002) and poorly total survivals. GSEA pathway enrichment evaluation confirmed that KIF22 was correlated with the cell cycle.
Silence of KIF22 decreased the power of the proliferation and migration in gastric cells, induced G1/S section cell cycle arrest through regulating the MAPK-ERK pathways.KIF22 protein stage was negatively correlated with prognosis. KIF22 knockdown may inhibit proliferation and metastasis of GC cells through the MAPK-ERK signaling pathway.

KIF22 coordinates CAR and EGFR dynamics to advertise most cancers cell proliferation

The coxsackievirus and adenovirus receptor (CAR) is a transmembrane receptor that performs a key function in cell-cell adhesion. CAR is present in regular epithelial cells and is elevated in abundance in numerous human tumors, together with lung carcinomas.
We investigated the potential mechanisms by which CAR contributes to most cancers cell progress and located that depletion of CAR in human lung most cancers cells lowered anchorage-independent progress, epidermal progress issue (EGF)-dependent proliferation, and tumor progress in vivo. EGF induced the phosphorylation of CAR and its subsequent relocalization to cell junctions by way of the activation of the kinase PKCδ. EGF promoted the binding of CAR to the chromokinesin KIF22.
KIF22-dependent regulation of microtubule dynamics led to delayed EGFR internalization, enhanced EGFR signaling, and coordination of CAR dynamics at cell-cell junctions. These information counsel a job for KIF22 within the coordination of membrane receptors and supply potential new therapeutic methods to fight lung tumor progress.

Recurrent dominant mutations affecting two adjoining residues within the motor area of the monomeric kinesin KIF22 lead to skeletal dysplasia and joint laxity

Spondyloepimetaphyseal dysplasia with joint laxity, leptodactylic kind (lepto-SEMDJL, aka SEMDJL, Corridor kind), is an autosomal dominant skeletal dysfunction that, regardless of being comparatively widespread amongst skeletal dysplasias, has eluded molecular elucidation to this point.
We used whole-exome sequencing of 5 unrelated people with lepto-SEMDJL to establish mutations in KIF22 as the reason for this skeletal situation. Missense mutations affecting one in all two adjoining amino acids within the motor area of KIF22 had been current in 20 familial instances from eight households and in 12 different sporadic instances.

Kinesin-Like Protein KIF22 (KIF22) Antibody

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Kinesin-Like Protein KIF22 (KIF22) Antibody

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KIF22 antibody

70R-1616 100 ug
EUR 377
Description: Rabbit polyclonal KIF22 antibody raised against the C terminal of KIF22

KIF22 antibody

70R-18117 50 ul
EUR 435
Description: Rabbit polyclonal KIF22 antibody

KIF22 Antibody

37684-100ul 100ul
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KIF22 antibody

10R-1635 100 ug
EUR 512
Description: Mouse monoclonal KIF22 antibody

KIF22 Antibody

1-CSB-PA619894LA01HU
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  • 100ug
  • 50ug
  • Form: Liquid
  • Buffer: Preservative: 0.03% Proclin 300
    Constituents: 50% Glycerol, 0.01M PBS, pH 7.4 >95%, Protein G purified
Description: A polyclonal antibody against KIF22. Recognizes KIF22 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC, IF; Recommended dilution: IHC:1:200-1:500, IF:1:50-1:200

KIF22 Antibody

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  • Form: Liquid
  • Buffer: -20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol Antigen affinity purification
Description: A polyclonal antibody against KIF22. Recognizes KIF22 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC;ELISA:1:1000-1:2000, WB:1:200-1:1000, IHC:1:50-1:200

KIF22 Antibody

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  • Form: Liquid
  • Buffer: -20°C, pH7.4 PBS, 0.05% NaN3, 40% Glycerol Antigen affinity purification
Description: A polyclonal antibody against KIF22. Recognizes KIF22 from Human. This antibody is Unconjugated. Tested in the following application: ELISA, IHC;ELISA:1:2000-1:10000, IHC:1:50-1:200

KIF22 antibody

70R-5549 50 ug
EUR 467
Description: Rabbit polyclonal KIF22 antibody raised against the N terminal of KIF22

KIF22 Antibody

1-CSB-PA012325GA01HU
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  • Form: Liquid
  • Buffer: PBS with 0.02% Sodium Azide, 50% Glycerol, pH 7.3. -20℃, Avoid freeze / thaw cycles. Antigen Affinity Purified
Description: A polyclonal antibody against KIF22. Recognizes KIF22 from Human, Mouse, Rat. This antibody is Unconjugated. Tested in the following application: ELISA, WB, IHC

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anti-KIF22

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EUR 363
Description: Mouse polyclonal to KIF22

Kinesin-Like Protein KIF22 (KIF22) Antibody (HRP)

20-abx336267
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Kinesin-Like Protein KIF22 (KIF22) Antibody (FITC)

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KIF22 Rabbit pAb

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KIF22 Rabbit pAb

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KIF22 Rabbit pAb

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KIF22 Blocking Peptide

33R-4798 100 ug
EUR 180
Description: A synthetic peptide for use as a blocking control in assays to test for specificity of KIF22 antibody, catalog no. 70R-1616

KIF22 Blocking Peptide

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Description: A synthetic peptide for use as a blocking control in assays to test for specificity of KIF22 antibody, catalog no. 70R-5549

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KIF22 Polyclonal Antibody

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anti- KIF22 antibody

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EUR 548.75
  • Immunogen: kinesin family member 22
  • Uniprot ID: Q14807
  • Gene ID: 3835
  • Research Area: Cell Division and Proliferation, Metabolism, Developmental biology
Description: Antibody raised against KIF22
The skeletal and connective tissue phenotype produced by these particular mutations level to capabilities of KIF22 past these beforehand ascribed capabilities involving chromosome segregation. Though we’ve discovered Kif22 to be strongly upregulated on the progress plate, the exact pathogenetic mechanisms stay to be elucidated.

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