Anti-CSNK1D (aa 144-361) polyclonal antibody

Cutaneous squamous cell carcinoma (cSCC) is a common skin cancer with an increasing incidence. As a pre-cancerous condition, actinic keratosis (AK) has an up to 20% risk of progression to cSCC. This study aims to define the potential genes that associated with genesis and progression of cSCC, thereby further identify critical biomarkers for the prevention, early diagnosis, and effective treatment of cSCC. Two datasets GSE42677 and GSE45216 were downloaded from the GEO. Microarray data analysis was applied to explore the differentially expressed genes (DEGs) between cSCC samples and AK samples. Then functional enrichment analysis, protein-protein interaction (PPI) network, and drug-gene interaction analysis were performed to screen key genes. A total of 711 DEGs, including 238 upregulated genes and 473 downregulated genes, were screened out. DEGs mainly involved in pathways as extracellular matrix (ECM)-receptor interaction, hematopoietic cell lineage, phosphatidylinositol 3-kinase (PI3K-Akt) signaling pathway, and focal adhesion. Candidate genes, including upregulated genes as JUN, filamin A (FLNA), casein kinase 1 delta (CSNK1D), and histone cluster 1 H3 family member f (HIST1H3F), and downregulated genes as androgen receptor (AR), heat shock protein family H member 1 (HSPH1), tropomyosin 1 (TPM1), pyruvate kinase, muscle (PKM), LIM domain and actin binding 1 (LIMA1), and synaptopodin (SYNPO) were screened out. In drug-gene interaction analysis, 13 genes and 44 drugs were identified. This study demonstrates that genes JUN, FLNA, AR, HSPH1, and CSNK1D have the potential to function as targets for diagnosis and treatment of cSCC.

Tau abnormal hyperphosphorylation and the formation of neurofibrillary tangles in the Alzheimer's disease (AD) brain is the result of upregulation of tau kinases. In a group of 729 Spanish late-onset AD patients and 670 healthy controls, we examined variations into a set of 20 candidate genes of kinases involved in tau phosphorylation at AD-related sites (PRKACB; CAMK2A; MARK1, 2, 3 and 4; CSNK1D; CDC2; RPS6KB1 and 2; p38 alpha and eta; IB1; JNK1, 2 and 3; MEK1 and 2; ERK1 and 2), to address hypotheses of genetic variation that might influence both AD risk and age at disease onset. There was an increased frequency of RPS6KB2 (intron 2, rs917570) minor allele in patients (50%) versus controls (39%) (OR = 1.52; 95% CI 1.30-1.77; p = 1.24x10(-5) Bonferroni corrected), and the presence of this minor allele was significantly (p = 4.2x10(-5)) associated with a 3-years later onset of AD (mean age 74.1 years) when compared to age at onset of non-minor allele carriers (mean age 71.1 years). In APOE non-epsilon 4 allele carriers, the combined effect of AD-associated risk alleles from the genes of CDC2, RPS6KB1 and 2, p38 alpha, JNK (1, 2 and 3), MEK2, and ERK2 was significantly (p = 0.002) associated with a late-onset (>76 years) of AD. The CDC2 AGC haplotype derived from SNPs in introns 3 (rs2448347), 5 (rs2456772), and 7 (rs1871447) showed a protective effect against AD in APOE non-epsilon 4 allele carriers (permutation p = 1.0x10(-4)) with a frequency of 9% in cases and 15% in controls. Common genetic variation in the tau kinases pathway does underlie individual differences not only in susceptibility to AD but also in disease phenotype (age at disease onset).