KAZALD1

Last update 08 May 2025

Basic Info

Synonyms

FKSG28, FKSG40, Kazal type serine peptidase inhibitor domain 1

+ [2]

Introduction

Involved in the proliferation of osteoblasts during bone formation and bone regeneration. Promotes matrix assembly (By similarity).

100 Clinical Results associated with KAZALD1

100 Translational Medicine associated with KAZALD1

0 Patents (Medical) associated with KAZALD1

Literatures (Medical) associated with KAZALD1

01 Mar 2025·Developmental Biology

Comparative analysis of neural crest development in the chick and mouse

Article

Author: Kulesa, P M ; McLennan, R ; McKinney, M C ; Scott, A ; Pushel, I ; Gogol, M M ; Morrison, J A ; Krumlauf, R

A core framework of the gene regulatory network (GRN) governing neural crest (NC) cell development has been generated by integrating separate inputs from diverse model organisms rather than direct comparison. This has limited insights into the diversity of genes in the NC cell GRN and extent of conservation of newly identified transcriptional signatures in cell differentiation and invasion. Here, we address this by leveraging the strengths and accessibility of the avian embryo to precise developmental staging by egg incubation and use an integrated analysis of chick (HH13) and mouse (E9.5) embryo tissue samples collected during NC cell migration into pharyngeal arches 1-2 (PA1 and PA2). We successfully identify a cluster of NC cells containing both mouse and chick cells that share expression of Lmo4, Tfap2B, Sox10, and Twist1, and distinct genes that lack known conserved roles in NC. Importantly, we discovered a cluster of cells exhibiting a conserved transcriptional signature associated with the NC cell migratory wavefront in both mouse and chick, including KAZALD1, BAMBI, DES, and GPC3. We confirm their expression is restricted to leader mouse NCs by multiplexed FISH. Together, these data offer novel insights into the transcriptional programs that underlie NC cell migration and establish the foundation for future comparative functional analyses.

01 Oct 2024·Gene

Multi-omics analysis of renal vein serum with Ischemia-Reperfusion injury

Article

Author: Wang, Xinning ; Zhang, Tianwei ; Jiao, Wei ; Liu, Yunbo ; Xu, Shang ; Guo, Yize ; Liu, Zhilong ; Yan, Yongchao

BACKGROUNDAcute kidney injury (AKI) is frequently caused by renal ischemia-reperfusion injury (IRI). Identifying potential renal IRI disease biomarkers would be useful for evaluating AKI severity.OBJECTIVEWe used proteomics and metabolomics to investigate the differences in renal venous blood between ischemic and healthy kidneys in an animal model by identifying differentially expressed proteins (DEPs) and differentially expressed protein metabolites (DEMs).METHODSNine pairs of renal venous blood samples were collected before and at 20, 40, and 60 min post ischemia. The ischemia time of Group A, B and C was 20,40 and 60 min. The proteome and metabolome of renal venous blood were evaluated to establish the differences between renal venous blood before and after ischemia.RESULTSWe identified 79 common DEPs in all samples of Group A, 80 in Group B, and 131 in Group C. Further common DEPs among all three groups were Tyrosineprotein kinase, GPR15LG, KAZALD1, ADH1B. We also identified 81, 64, and 83 common DEMs in each group respectively, in which 30 DEMs were further common to all groups. Bioinformatic analysis of the DEPs and DEMs was conducted.CONCLUSIONThis study demonstrated that different pathological processes occur during short- and long-term renal IRI. Tyrosine protein kinase, GPR15LG, Kazal-type serine peptidase inhibitor domain 1, and all-trans-retinol dehydrogenase are potential biomarkers of renal IRI.

01 Dec 2022·Clinical Epigenetics

DNA methylation analysis of normal colon organoids from familial adenomatous polyposis patients reveals novel insight into colon cancer development

Article

Author: Li, Li ; Dampier, Christopher H ; Powell, Steven M ; Weisenberger, Daniel ; Eaton, Stephen ; Ali, Mourad Wagdy ; Casey, Graham ; Devall, Matthew A

AbstractBackgroundFamilial adenomatous polyposis (FAP) is an inherited colorectal cancer (CRC) syndrome resulting from germ line mutations in theadenomatous polyposis coli(APC) gene. While FAP accounts for less than 1% of all CRC cases, loss ofAPCexpression is seen in > 80% of non-hereditary CRCs. To better understand molecular mechanisms underlying APC-driven CRC, we performed an epigenome-wide analysis of colon organoids derived from normal-appearing colons of FAP patients versus healthy subjects to identify differentially methylated regions (DMRs) that may precede the onset of CRC.ResultsWe identified 358 DMRs when comparing colon organoids of FAP patients to those of healthy subjects (FDR < 0.05, |mean beta difference| = 5%). Of these, nearly 50% of DMRs were also differentially methylated in at least one of three CRC tumor and normal adjacent tissue (NAT) cohorts (TCGA-COAD, GSE193535 and ColoCare). Moreover, 27 of the DMRs mapped to CRC genome-wide association study (GWAS) loci. We provide evidence suggesting that some of these DMRs led to significant differences in gene expression of adjacent genes using quantitative PCR. For example, we identified significantly greater expression of five genes:Kazal-type serine peptidase inhibitor domain 1(KAZALD1,P = 0.032),F-Box and leucine-rich repeat protein 8(FBXL8, P = 0.036),TRIM31 antisense RNA 1(TRIM31-AS1,P = 0.036),Fas apoptotic inhibitory molecule 2(FAIM2,P = 0.049) and (Collagen beta (1–0)galactosyltransferase 2(COLGALT2,P = 0.049). Importantly, bothFBXL8andTRIM31-AS1were also significantly differentially expressed in TCGA-COAD tumor versus matched NAT, supporting a role for these genes in CRC tumor development.ConclusionsWe performed the first DNA methylome-wide analysis of normal colon organoids derived from FAP patients compared to those of healthy subjects. Our results reveal that normal colon organoids from FAP patients exhibit extensive epigenetic differences compared to those of healthy subjects that appear similar to those exhibited in CRC tumor. Our analyses therefore identify DMRs and candidate target genes that are potentially important in CRC tumor development in FAP, with potential implications for non-hereditary CRC.

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KAZALD1

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