Table 2.

Summary of published KLF14 mouse lines.

Mouse line	Targeted region	Source	Diet	Sex studied	Phenotypes	Reference
Whole-body Klf14 knockout	1,035 bp between positions 30907660-30908694 of Chromosome 6 (Genome Build37), including the entire Klf14 open reading frame	KOMP repository	Standard chow and 60% kcal high fat diet (switched at week 8)	Male	No difference in metabolic phenotypes; No difference was observed in whole-body Klf14 KO mice plasma lipoprotein profile, cholesterol, HDL-C. No difference in insulin resistance and adipose gene expression change.	(91)
CRISPR-Cas9 whole-body knockout	A 7-bp frameshift insertion-deletion allele was introduced to the 5' end of the Klf14 gene through CRISPR-Cas9	In house	45% kcal high fat diet (switched at week 18)	Male	Decrease in HDL-C level in Klf14 whole-body knockout mice	(1)
KLF14 null mouse	The loxP sites were added ~1.6 kb upstream of the Klf14 transcriptional start site and 300 bp downstream of the Klf14 3′-UTR separated by a total of 4.9 kb. Male offspring were crossed with Sox2: CRE transgenic females to generate a constitutive null allele	In house	Standard	Phenotypic analysis: female Gene expression analysis: male and female	Placenta is overgrown in Klf14hetKO mice who carry maternal Klf14 allele (Klf14matKO). Fetal size remained unchanged. No morphological change in placenta layers. No abnormal lipid accumulation in Klf14matKO mice.	(94)
Klf14-KO mice	Klf14 exon is disrupted by deleting 8-bp sequence using TALEN, which further disrupted the tenth amino acid and resulted in premature termination.	In house	Standard chow	NA	33.3% of Klf14-KO adult mice developed tumors in lung, spleen, and lymph nodes starting from 11-month-old. No spontaneous tumor was identified in other organs such as the heart, liver, kidney, breast, colon, and thymus. No obvious difference in body weight and serum lipids in KO mice.	(95)
Adipose-specific Klf14 KO (AdnKlf14-KO)	Two LoxP sites were inserted at 3,415 bp upstream and 327 bp downstream of Klf14 through CRISPR-Cas9. Offspring with two loxP sequences segregated on the same chromosome were crossed with Adipoq-Cre mice of the same genetic background	In house	Standard chow	Male and female	HDL-C was reduced in female AdnKlf14-KO mice while triglycerides were increased in males. Glucose tolerance and insulin sensitivity were impaired in both sexes	(1)
Liver-specific Klf14 KO (Klf14-LKO)	Klf14 exon flanked by LoxP sites (specific targeted region unknown), followed by germline transmission and Flp recombinase removal. Offspring were crossed with Alb-Cre transgenic mice (003574 from Jackson Laboratory)	In house	Standard chow	Male	Pooled blood serum was collected and analyzed by HPLC. Total cholesterol and triglyceride levels were comparable between WT and Klf14-LKO mice. HDL-C level was decreased in Klf14-LKO mice. ApoA-1 level was also decreased in hepatic Klf14 KO mice liver.	(92)