Ask about this productRelated genes to: HOXB7 antibody
- Gene:
- HOXB7 NIH gene
- Name:
- homeobox B7
- Previous symbol:
- HOX2, HOX2C
- Synonyms:
- -
- Chromosome:
- 17q21.32
- Locus Type:
- gene with protein product
- Date approved:
- 1990-06-15
- Date modifiied:
- 2016-11-09
Related products to: HOXB7 antibody
Related articles to: HOXB7 antibody
- Congenital anomalies of the kidney and urinary tract (CAKUTs) represent the leading cause of pediatric chronic kidney disease, yet the molecular mechanisms underlying these malformations remain incompletely understood. While genetic studies have identified numerous CAKUT-associated genes, conventional knockout approaches often result in embryonic lethality or fail to reveal tissue-specific gene functions. This review aims to synthesize findings from conditional knockout mouse studies that have elucidated the spatiotemporal requirements of key signaling pathways during kidney development. - Source: PubMed
Publication date: 2026/03/18
Kelam NelaTodorović PetarBajt PatricijaPavlović NikolaRakić TomislavVukojević KatarinaRacetin Anita - Laryngeal cancer, a prevalent malignant tumor, frequently leads to mortality through the development of second primary lung cancer (SPLC). To investigate the potential mechanisms underlying SPLC development in laryngeal cancer patients, we conducted an integrated multi-omics analysis. We obtained laryngeal cancer (GSE51985) and lung cancer (GSE102287) datasets from the gene expression omnibus and identified differentially expressed genes using the "limma" package. Our analysis revealed 9 shared genes, with UBE2C, POLQ, RAD51, and HOXB7 being up-regulated and EDNRB, GPD1L, F10, SORBS2, and CXCL12 down-regulated in both cancers. Functional enrichment analysis indicated these genes were primarily involved in pathways in cancer and the cell cycle. We further constructed transcription factor (TF)-miRNA-gene interaction networks, identifying 120 TFs and 246 miRNAs coordinating these shared genes. Metabolic analysis linked CXCL12 to inositol phosphate metabolism, and single-cell RNA sequencing from datasets GSE150321 and GSE127471 demonstrated that intermediate monocytes in lung cancer were highly active in this metabolic pathway. Additionally, immune cell infiltration analysis using CIBERSORT revealed a higher proportion of macrophages in both cancer types compared to non-tumor tissues. In conclusion, our study suggests that shared genetic alterations, regulated by specific TFs and miRNAs, alongside an altered immune microenvironment and CXCL12-mediated inositol phosphate metabolism likely driven by intermediate monocytes, contribute to the development of SPLC following laryngeal cancer. - Source: PubMed
Xu FengfengHuang TengfeiXu QianhuiZhang MeiqingChen Shiyan - Cervical cancer (CC) represents the fourth most commonly diagnosed cancer and main cause of cancer mortality among women globally. We aim to investigate the mechanism of HOXB7 in CC cell progression, providing novel therapeutic implications for CC. Levels of HOXB7, miR-552-3p and IFITM1 in CC cells and tissues were measured by RT-qPCR and WB. After transfection of HOXB7 siRNA into CC cells, cell proliferation, invasion and migration were detected by CCK-8 method and transwell. The bindings of HOXB7 to miR-552-3p promoter and miR-552-3p to IFITM1 were analyzed. Effect of miR-552-3p and IFITM1 on the biological function of CC cells was detected in combined experiments. Results showed that the expression of HOXB7 and miR-552-3p was increased and the expression of IFITM1 was decreased. Cell proliferation, invasion and migration were reduced upon knockdown of HOXB7. Mechanically, HOXB7 bound and upregulated miR-552-3p expression, promoted the targeted binding of miR-552-3p to IFITM1, and reduced IFITM1 expression. miR-552-3p overexpression or IFITM1 downregulation reduced the inhibitory action of HOXB7 silencing on the proliferation, invasion and migration of CC cells. In conclusion, HOXB7 promotes the progression of CC cells via the miR-552-3p/IFITM1 axis. - Source: PubMed
Publication date: 2026/02/02
Zhang JingShen JuanYuan Li - Our studies have established that ureteric bud (UB) prorenin receptor (PRR/ATP6AP2), an accessory subunit of the vacuolar H-ATPase (V-ATPase), is critical for normal UB branching. Here, we tested the hypothesis that V-ATPase activity, acidosis, and UB cell intracellular pH (pH) regulate UB branching morphogenesis during kidney development. The effect of specific V-ATPase inhibitor Bafilomycin, hypercapnic (high CO), and metabolic (low [Formula: see text]) acidosis on UB branching was determined in whole intact E12.5 mouse kidneys grown ex vivo by time-lapse photomicroscopy. The effect of Bafilomycin on UB cell migration in vitro was examined using a transwell migration assay ( = 3 wells/treatment group). The presence of V-ATPase and Na-H exchanger (NHE) activity in UB cells was investigated by measurements of intracellular pH (pH). The ability of UB cells to regulate cell pH in vitro was determined by measurements of Na-dependent and Na-independent pH recovery from acid loads. The mean number of UB cells that migrated through the membrane after 24-h culture was reduced with Bafilomycin compared with control. Treatment with Bafilomycin, hypercapnic acidosis (induced by high CO), or metabolic acidosis (induced by low [Formula: see text] concentration) in the culture media caused a marked reduction in the number of UB tips compared with control. We conclude that intact V-ATPase activity is essential for normal UB branching during kidney development. V-ATPase-dependent reduction in UB cell pH is likely a cause of decreasing UB branching by inhibiting directional movements of UB cells. Disruption of normal kidney development results in a spectrum of congenital anomalies of the kidney and urinary tract (CAKUT), the major cause of end-stage kidney disease in children. We demonstrate that acidosis, kidney cell intracellular pH, and activity of V-ATPase pump are essential for normal kidney development. - Source: PubMed
Publication date: 2026/01/16
Yosypiv Ihor VLiu HongbingNakhoul Nazih L - This study aimed to elucidate the regulatory role of c-Myc-associated miR-196a-5p in the progression of triple-negative breast cancer (TNBC). We further explored its target genes to investigate possible mechanisms of action. - Source: PubMed
Publication date: 2025/12/05
Song Xin-YuYang LeLi Hui-LingXu Hao-YiXu Xiao-LiYan KangLiu Yuan-JingMierzhakenmu ZuliyaerXu RuiDong Chao