Log in

Relevant bibliographies by topics / Hox genes / Journal articles

Journal articles on the topic 'Hox genes'

To see the other types of publications on this topic, follow the link: Hox genes.

Author: Grafiati

Published: 4 June 2021

Last updated: 25 May 2024

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'Hox genes.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

1

Lin, Hou, Chen Zhijuan, Xu Mingyu, Lin Shengguo, and Wang Lu. "Hox genes and study of Hox genes in crustacean." Chinese Journal of Oceanology and Limnology 22, no. 4 (December 2004): 392–98. http://dx.doi.org/10.1007/bf02843634.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Snape, Alison. "Regulating Hox genes." Trends in Genetics 15, no. 1 (January 1999): 14. http://dx.doi.org/10.1016/s0168-9525(98)01676-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Nazarali, A., Y. Kim, and M. Nirenberg. "Hox-1.11 and Hox-4.9 homeobox genes." Proceedings of the National Academy of Sciences 89, no. 7 (April 1, 1992): 2883–87. http://dx.doi.org/10.1073/pnas.89.7.2883.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Hrycaj, Steven M., and Deneen M. Wellik. "Hox genes and evolution." F1000Research 5 (May 10, 2016): 859. http://dx.doi.org/10.12688/f1000research.7663.1.

Full text

Abstract:

Hox proteins are a deeply conserved group of transcription factors originally defined for their critical roles in governing segmental identity along the antero-posterior (AP) axis in Drosophila. Over the last 30 years, numerous data generated in evolutionarily diverse taxa have clearly shown that changes in the expression patterns of these genes are closely associated with the regionalization of the AP axis, suggesting that Hox genes have played a critical role in the evolution of novel body plans within Bilateria. Despite this deep functional conservation and the importance of these genes in AP patterning, key questions remain regarding many aspects of Hox biology. In this commentary, we highlight recent reports that have provided novel insight into the origins of the mammalian Hox cluster, the role of Hox genes in the generation of a limbless body plan, and a novel putative mechanism in which Hox genes may encode specificity along the AP axis. Although the data discussed here offer a fresh perspective, it is clear that there is still much to learn about Hox biology and the roles it has played in the evolution of the Bilaterian body plan.

APA, Harvard, Vancouver, ISO, and other styles

5

Marshall, Heather, Alastair Morrison, Michèle Studer, Heike Pöpperl, and Robb Krumlauf. "Retinoids and Hox genes." FASEB Journal 10, no. 9 (July 1996): 969–78. http://dx.doi.org/10.1096/fasebj.10.9.8801179.

Full text

APA, Harvard, Vancouver, ISO, and other styles

6

Vitiello, Danielle, Pinar Kodaman, and Hugh Taylor. "HOX Genes in Implantation." Seminars in Reproductive Medicine 25, no. 6 (November 2007): 431–36. http://dx.doi.org/10.1055/s-2007-991040.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

Ruddle, F. H., J. L. Bartels, K. L. Bentley, C. Kappen, M. T. Murtha, and J. W. Pendleton. "Evolution of Hox Genes." Annual Review of Genetics 28, no. 1 (December 1994): 423–42. http://dx.doi.org/10.1146/annurev.ge.28.120194.002231.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Botti, Gerardo, Clemente Cillo, Rossella De Cecio, Maria Gabriella Malzone, and Monica Cantile. "Paralogous HOX13 Genes in Human Cancers." Cancers 11, no. 5 (May 20, 2019): 699. http://dx.doi.org/10.3390/cancers11050699.

Full text

Abstract:

Hox genes (HOX in humans), an evolutionary preserved gene family, are key determinants of embryonic development and cell memory gene program. Hox genes are organized in four clusters on four chromosomal loci aligned in 13 paralogous groups based on sequence homology (Hox gene network). During development Hox genes are transcribed, according to the rule of “spatio-temporal collinearity”, with early regulators of anterior body regions located at the 3’ end of each Hox cluster and the later regulators of posterior body regions placed at the distal 5’ end. The onset of 3’ Hox gene activation is determined by Wingless-type MMTV integration site family (Wnt) signaling, whereas 5’ Hox activation is due to paralogous group 13 genes, which act as posterior-inhibitors of more anterior Hox proteins (posterior prevalence). Deregulation of HOX genes is associated with developmental abnormalities and different human diseases. Paralogous HOX13 genes (HOX A13, HOX B13, HOX C13 and HOX D13) also play a relevant role in tumor development and progression. In this review, we will discuss the role of paralogous HOX13 genes regarding their regulatory mechanisms during carcinogenesis and tumor progression and their use as biomarkers for cancer diagnosis and treatment.

APA, Harvard, Vancouver, ISO, and other styles

9

Bogue, C. W., I. Gross, H. Vasavada, D. W. Dynia, C. M. Wilson, and H. C. Jacobs. "Identification of Hox genes in newborn lung and effects of gestational age and retinoic acid on their expression." American Journal of Physiology-Lung Cellular and Molecular Physiology 266, no. 4 (April 1, 1994): L448—L454. http://dx.doi.org/10.1152/ajplung.1994.266.4.l448.

Full text

Abstract:

Hox genes are sequence-specific DNA transcription factors, which are important in embryonic development and are expressed in a number of fetal tissues, including the lung. Additionally, retinoic acid (RA) has been shown to modulate Hox gene expression in a number of cell types. The specific aims of this study were to 1) identify those Hox genes expressed in newborn mouse lung using reverse transcription-polymerase chain reaction (RT-PCR), 2) study the ontogeny of Hox gene expression in fetal mouse and rat lung by Northern analysis using cDNAs for mouse Hox genes, and 3) study the effects of RA on whole lung Hox mRNA levels in cultured fetal rat lung explants. Our data show that 16 different homeobox genes are expressed in newborn mouse lung. This includes seven Hox genes not previously identified in lung, as well as the divergent homeobox gene Hex. Steady-state mRNA levels of Hox A5 (Hox 1.3), B5 (Hox 2.1), B6 (Hox 2.2), and B8 (Hox 2.4) decrease with advancing gestational age in mouse lungs (E14 to adult). Similarly, Hox A5, B5, and B6 follow the same decreasing pattern of expression with advancing gestational age in rat lungs (E15 to adult). RA treatment of E17 rat lung explants in culture resulted in a significant dose- and time-dependent increase in Hox A5, B5, and B6 mRNA levels. The highest mRNA levels were seen in explants treated with 1 x 10(-5) M RA for 4-16 h. We conclude that there are many homeobox genes expressed in developing rodent lung and that their mRNA levels are affected by both gestational age and RA.

APA, Harvard, Vancouver, ISO, and other styles

10

Strathdee, Gordon R., Tessa L. Holyoake, Alyson Sim, Anton Parker, David G. Oscier, Junia V. Melo, Stefan Meyer, et al. "HOX Genes - Candidate Tumor Suppressor Genes in Adult and Childhood Leukemia." Blood 110, no. 11 (November 16, 2007): 2641. http://dx.doi.org/10.1182/blood.v110.11.2641.2641.

Full text

Abstract:

Abstract The role of the HOX gene family in leukemia development has been extensively studied. However, these studies have focused almost exclusively on the potential oncogenic role of HOX gene family members. In contrast to the oncogenic function often attributed to HOX genes, our studies have identified several HOX gene family members as candidate tumor suppressor genes and shown that inactivation of HOX genes, particularly HOXA4, is associated with poor prognosis. We have used multiple quantitative methylation assays to search for epigenetic inactivation of HOX genes in adult and childhood leukemia. In both adult myeloid and lymphoid leukemia two members of the HOXA cluster (HOXA4 and A5) were found to be frequently inactivated by promoter hypermethylation (26–64% of cases were hypermethylated). In contrast, a further 12 HOXA, B and C cluster genes were found to be essentially devoid of hypermethylation (except HOXA6 in CLL, where 34% of samples exhibited hypermethylation). HOXA4 and HOXA5 were also frequently inactivated in childhood ALL and AML (39–79% of samples). However, in contrast to the adult leukemias, all but one of the additional HOX genes analyzed were also found to be targets for hypermethylation in both ALL and AML (4–26% of samples), suggesting that HOX genes are differentially regulated in childhood versus adult leukemia. Hypermethylation of HOX genes (HOXA4, HOXA5 and HOXA6) was associated with loss of expression of the corresponding gene. Expression analysis also suggests that interaction between different HOX genes may be crucial. In normal karyotype AML samples, those expressing of high levels of HOXA9, but not those with low HOXA9 expression, were associated with invariable HOXA4 hypermethylation (p=0.01). Interestingly HOXA4 hypermethylation also correlates with poor prognosis in all types of leukemia tested. Hypermethylation of HOXA4 correlates with progression to blast crisis (p=0.007) and poor response to imatinib in CML (p=0.04), with cytogenetic status in AML (33%, 72% and 100% in good, intermediate and poor prognostic groups respectively, p=0.0004) and with IgVh mutational status (p=0.003) and poor survival in CLL (median survival 159 versus 199 months in hypermethylated and non hypermethylated patients, respectively). Furthermore transfection of a HOXA4 expressing construct into a CML blast crisis cell line results in re-expression of markers of myeloid differentiation, suggesting that loss of HOXA4 is functionally relevant in leukemic cells. These results indicate that aberrant epigenetic regulation of HOXA4, and indeed other frequently inactivated HOX genes such as HOXA5 and HOXA6, may play a key role in the development of multiple types of leukemia. Thus co-ordinated up and down regulation of expression of HOX gene family members may be crucial in the leukemogenic process.

APA, Harvard, Vancouver, ISO, and other styles

11

Akam, Michael. "Hox genes: From master genes to micromanagers." Current Biology 8, no. 19 (September 1998): R676—R678. http://dx.doi.org/10.1016/s0960-9822(98)70433-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Geada, A. M., S. J. Gaunt, M. Azzawi, S. M. Shimeld, J. Pearce, and P. T. Sharpe. "Sequence and embryonic expression of the murine Hox-3.5 gene." Development 116, no. 2 (October 1, 1992): 497–506. http://dx.doi.org/10.1242/dev.116.2.497.

Full text

Abstract:

The murine Hox-3.5 gene has been mapped and linked genomically to a position 18 kb 3′ of its most 5′ locus neighbour, Hox-3.4, on chromosome 15. The sequence of the Hox-3.5 cDNA, together with the position of the gene within the locus, show it to be a paralogue of Hox-2.6, Hox-1.4 and Hox-4.2. The patterns of embryonic expression for the Hox-3.5 gene are examined in terms of three rules, proposed to relate a Hox gene's expression pattern to its position within the locus. The anterior boundaries of Hox-3.5 expression in the hindbrain and prevertebral column lie anterior to those of Hox-3.4 and all other, more 5′-located Hox-3 genes. Within the hindbrain, the Hox-3.5 boundary is seen to lie posterior to that of its paralogue, Hox-2.6, by a distance equal to about the length of one rhombomere. Patterns of Hox-3.5 expression within the oesophagus and spinal cord, but not the testis, are similar to those of other Hox-3 genes, Hox-3.3 and Hox-3.4.

APA, Harvard, Vancouver, ISO, and other styles

13

Morgan, B. A. "Hox genes and embryonic development." Poultry Science 76, no. 1 (January 1997): 96–104. http://dx.doi.org/10.1093/ps/76.1.96.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Kelly, Zoë L., Agnieszka Michael, Simon Butler-Manuel, Hardev S. Pandha, and Richard GL Morgan. "HOX genes in ovarian cancer." Journal of Ovarian Research 4, no. 1 (2011): 16. http://dx.doi.org/10.1186/1757-2215-4-16.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Arendt, Detlev. "Hox genes and body segmentation." Science 361, no. 6409 (September 27, 2018): 1310–11. http://dx.doi.org/10.1126/science.aav0692.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Tabin, Cliff, and Ed Laufer. "Hox genes and serial homology." Nature 361, no. 6414 (February 1993): 692–93. http://dx.doi.org/10.1038/361692a0.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Krumlauf, Robb. "Hox genes, clusters and collinearity." International Journal of Developmental Biology 62, no. 11-12 (2018): 659–63. http://dx.doi.org/10.1387/ijdb.180330rr.

Full text

Abstract:

This year marks the 40th anniversary of the discovery by Ed Lewis of the property of collinearity in the bithorax gene complex in Drosophila. This landmark work illustrated the need to understand regulatory mechanisms that coordinate expression of homeotic gene clusters. Through the efforts of many groups, investigation of the Hox gene family has generated many fundamental findings on the roles and regulation of this conserved gene family in development, disease and evolution. This has led to a number of important conceptual advances in gene regulation and evolutionary biology. This article presents some of the history and advances made through studies on Hox gene clusters.

APA, Harvard, Vancouver, ISO, and other styles

18

Daftary, Gaurang S., and Hugh S. Taylor. "Endocrine Regulation of HOX Genes." Endocrine Reviews 27, no. 4 (April 21, 2006): 331–55. http://dx.doi.org/10.1210/er.2005-0018.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Kmita, Marie, Denis Duboule, and Basile Tarchini. "Hox genes and limb morphogenesis." Developmental Biology 306, no. 1 (June 2007): 288–89. http://dx.doi.org/10.1016/j.ydbio.2007.03.050.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Novikova, E. L., N. I. Bakalenko, A. Y. Nesterenko, and M. A. Kulakova. "Hox genes and animal regeneration." Russian Journal of Developmental Biology 47, no. 4 (July 2016): 173–80. http://dx.doi.org/10.1134/s106236041604007x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Golpon, Heiko A., Mark W. Geraci, Mark D. Moore, Heidi L. Miller, Gary J. Miller, Rubin M. Tuder, and Norbert F. Voelkel. "HOX Genes in Human Lung." American Journal of Pathology 158, no. 3 (March 2001): 955–66. http://dx.doi.org/10.1016/s0002-9440(10)64042-4.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Swinehart, Ilea T., and Deneen M. Wellik. "Hox genes in axial patterning." Developmental Biology 331, no. 2 (July 2009): 519–20. http://dx.doi.org/10.1016/j.ydbio.2009.05.494.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Wright, Christopher V. E. "Hox genes and the hindbrain." Current Biology 3, no. 9 (September 1993): 618–21. http://dx.doi.org/10.1016/0960-9822(93)90013-e.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Krumlauf, Robb. "Hox genes in vertebrate development." Cell 78, no. 2 (July 1994): 191–201. http://dx.doi.org/10.1016/0092-8674(94)90290-9.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Goymer, Patrick. "How old are Hox genes?" Nature Reviews Genetics 8, no. 5 (May 2007): 328. http://dx.doi.org/10.1038/nrg2114.

Full text

APA, Harvard, Vancouver, ISO, and other styles

26

Patterson, Larry T., and S. Steven Potter. "Hox genes and kidney patterning." Current Opinion in Nephrology and Hypertension 12, no. 1 (January 2003): 19–23. http://dx.doi.org/10.1097/00041552-200301000-00004.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Kappen, C. "Hox genes in the lung." American Journal of Respiratory Cell and Molecular Biology 15, no. 2 (August 1996): 156–62. http://dx.doi.org/10.1165/ajrcmb.15.2.8703471.

Full text

APA, Harvard, Vancouver, ISO, and other styles

28

Wellik, Deneen M. "Hox genes and kidney development." Pediatric Nephrology 26, no. 9 (September 2011): 1559–65. http://dx.doi.org/10.1007/s00467-011-1902-1.

Full text

APA, Harvard, Vancouver, ISO, and other styles

29

Soshnikova, Natalia. "Hox genes regulation in vertebrates." Developmental Dynamics 243, no. 1 (September 2, 2013): 49–58. http://dx.doi.org/10.1002/dvdy.24014.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Simon, H. G., and C. J. Tabin. "Analysis of Hox-4.5 and Hox-3.6 expression during newt limb regeneration: differential regulation of paralogous Hox genes suggest different roles for members of different Hox clusters." Development 117, no. 4 (April 1, 1993): 1397–407. http://dx.doi.org/10.1242/dev.117.4.1397.

Full text

Abstract:

Adult urodele amphibians can regenerate their limbs and tail. Based on their roles in other developing systems, Hox genes are strong candidates for genes that play a role in regulating pattern formation during regeneration. There are four homologous clusters of Hox genes in vertebrate genomes. We isolated cDNA clones of two newt homeobox genes from homologous positions within two Hox clusters; Hox-4.5 and Hox-3.6. We used RNase protection on nonamputated (normal) and regenerating newt appendages and tissue to compare their transcriptional patterns. Both genes show increased expression upon amputation with similar kinetics. Hox-4.5 and Hox-3.6 transcription is limited to the mesenchymal cells in the regenerates and is not found in the epithelial tissue. In addition to regenerating appendages, both genes are transcriptionally active in adult kidney of the newt. Striking differences were found in the regulation of Hox-4.5 and Hox-3.6 when they were compared in unamputated limbs and in regenerating forelimbs versus regenerating hindlimbs. Hox-4.5 is expressed in the blastema of regenerating fore- and hindlimbs, but Hox-4.5 transcripts are not detectable in normal limbs. In contrast, Hox-3.6 transcripts are found exclusively in posterior appendages, but are present in normal as well as regenerating hindlimbs and tails. Hox-4.5 is also expressed at a higher level in proximal (mid-humerus) regenerates than in distal ones (mid-radius). When we proximalized the positional memory of a distal blastema with retinoic acid, we find that the early expression level of Hox-4.5 is also proximalized. When the expression of these genes is compared to the expression of two previously reported newt Hox genes, a consistent pattern emerges, which can be interpreted in terms of differential roles for the different Hox clusters in determining regenerative limb morphology.

APA, Harvard, Vancouver, ISO, and other styles

31

Popodi, E., J. C. Kissinger, M. E. Andrews, and R. A. Raff. "Sea urchin Hox genes: insights into the ancestral Hox cluster." Molecular Biology and Evolution 13, no. 8 (October 1, 1996): 1078–86. http://dx.doi.org/10.1093/oxfordjournals.molbev.a025670.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Kuo, Tzu-Lei, Kuang-Hung Cheng, Li-Tzong Chen, and Wen-Chun Hung. "Deciphering The Potential Role of Hox Genes in Pancreatic Cancer." Cancers 11, no. 5 (May 27, 2019): 734. http://dx.doi.org/10.3390/cancers11050734.

Full text

Abstract:

The Hox gene family plays an important role in organogenesis and animal development. Currently, 39 Hox genes that are clustered in four chromosome regions have been identified in humans. Emerging evidence suggests that Hox genes are involved in the development of the pancreas. However, the expression of Hox genes in pancreatic tumor tissues has been investigated in only a few studies. In addition, whether specific Hox genes can promote or suppress cancer metastasis is not clear. In this article, we first review the recent progress in studies on the role of Hox genes in pancreatic cancer. By comparing the expression profiles of pancreatic cancer cells isolated from genetically engineered mice established in our laboratory with three different proliferative and metastatic abilities, we identified novel Hox genes that exhibited tumor-promoting activity in pancreatic cancer. Finally, a potential oncogenic mechanism of the Hox genes was hypothesized.

APA, Harvard, Vancouver, ISO, and other styles

33

He, Rong-Qiao, and Jun-Lan Yao. "Divergences in homeodomains of hox genes and von baer's law." Protein & Peptide Letters 7, no. 2 (April 2000): 123–31. http://dx.doi.org/10.2174/092986650702221206115639.

Full text

Abstract:

Abstract: Divergences among homeodomains coded by Hox clusters of human beings have been analyzed with both methods of dynamic programming [I] and hydropathic mass [2). Homeodomains of the anterior genes (Hox A-1 to -4), including the paralogs of Hox B and Hox D, showed more distinguishable divergences than those of the posterior genes (from Hox A-5 to -13). The homeodomains grew exponentially more divergent in progression from the paralogue group I to 13 along a Hox complex. The divergence of homeodomains of Hox B-1 between C. elegans and human was small, but it became larger between those of the posterior genes. It appears that Hox genes should be involved in Von Baer's law.

APA, Harvard, Vancouver, ISO, and other styles

34

Prince, V. E., L. Joly, M. Ekker, and R. K. Ho. "Zebrafish hox genes: genomic organization and modified colinear expression patterns in the trunk." Development 125, no. 3 (February 1, 1998): 407–20. http://dx.doi.org/10.1242/dev.125.3.407.

Full text

Abstract:

The Hox genes are implicated in conferring regional identity to the anteroposterior axis of the developing embryo. We have characterized the organization and expression of hox genes in the teleost zebrafish (Danio rerio), and compared our findings with those made for the tetrapod vertebrates. We have isolated 32 zebrafish hox genes, primarily via 3′RACE-PCR, and analyzed their linkage relationships using somatic cell hybrids. We find that in comparison to the tetrapods, zebrafish has several additional hox genes, both within and beyond the expected 4 hox clusters (A-D). For example, we have isolated a member of hox paralogue group 8 lying on the hoxa cluster, and a member of hox paralogue group 10 lying on the b cluster, no equivalent genes have been reported for mouse or human. Beyond the 4 clusters (A-D) we have isolated a further 3 hox genes (the hoxx and y genes), which according to their sequence homologies lie in paralogue groups 4, 6, and 9. The hoxx4 and hoxx9 genes occur on the same set of hybrid chromosomes, hinting at the possibility of an additional hox cluster for the zebrafish. Similar to their tetrapod counterparts, zebrafish hox genes (including those with no direct tetrapod equivalent) demonstrate colinear expression along the anteroposterior (AP) axis of the embryo. However, in comparison to the tetrapods, anterior hox expression limits are compacted over a short AP region; some members of adjacent paralogue groups have equivalent limits. It has been proposed that during vertebrate evolution, the anterior limits of Hox gene expression have become dispersed along the AP axis allowing the genes to take on novel patterning roles and thus leading to increased axial complexity. In the teleost zebrafish, axial organization is relatively simple in comparison to that of the tetrapod vertebrates; this may be reflected by the less dispersed expression domains of the zebrafish hox genes.

APA, Harvard, Vancouver, ISO, and other styles

35

Zheng, Chaogu, Ho Ming Terence Lee, and Kenneth Pham. "Nervous system-wide analysis of Hox regulation of terminal neuronal fate specification in Caenorhabditis elegans." PLOS Genetics 18, no. 2 (February 28, 2022): e1010092. http://dx.doi.org/10.1371/journal.pgen.1010092.

Full text

Abstract:

Hox genes encode evolutionarily conserved transcription factors that specify regional identities along the anterior-posterior (A-P) axis. Although some Hox genes are known to regulate the differentiation of certain neurons, to what extent Hox genes are involved in the terminal specification of the entire nervous system is unclear. Here, we systematically mapped the expression of all six Hox genes in C. elegans nervous system and found Hox expression in 97 (32%) of the 302 neurons in adult hermaphrodites. Our results are generally consistent with previous high-throughput expression mapping and single-cell transcriptomic studies. Detailed analysis of the fate markers for these neurons revealed that Hox genes regulate the differentiation of 29 (25%) of the 118 classes of C. elegans neurons. Hox genes not only regulate the specification of terminal neuronal fates through multiple mechanisms but also control subtype diversification along the A-P axis. The widespread involvement of Hox genes in neuronal differentiation indicates their roles in establishing complex nervous systems.

APA, Harvard, Vancouver, ISO, and other styles

36

Bhatlekar, Seema, Jeremy Z. Fields, and Bruce M. Boman. "Role of HOX Genes in Stem Cell Differentiation and Cancer." Stem Cells International 2018 (July 22, 2018): 1–15. http://dx.doi.org/10.1155/2018/3569493.

Full text

Abstract:

HOX genes encode an evolutionarily conserved set of transcription factors that control how the phenotype of an organism becomes organized during development based on its genetic makeup. For example, in bilaterian-type animals, HOX genes are organized in gene clusters that encode anatomic segment identity, that is, whether the embryo will form with bilateral symmetry with a head (anterior), tail (posterior), back (dorsal), and belly (ventral). Although HOX genes are known to regulate stem cell (SC) differentiation and HOX genes are dysregulated in cancer, the mechanisms by which dysregulation of HOX genes in SCs causes cancer development is not fully understood. Therefore, the purpose of this manuscript was (i) to review the role of HOX genes in SC differentiation, particularly in embryonic, adult tissue-specific, and induced pluripotent SC, and (ii) to investigate how dysregulated HOX genes in SCs are responsible for the development of colorectal cancer (CRC) and acute myeloid leukemia (AML). We analyzed HOX gene expression in CRC and AML using information from The Cancer Genome Atlas study. Finally, we reviewed the literature on HOX genes and related therapeutics that might help us understand ways to develop SC-specific therapies that target aberrant HOX gene expression that contributes to cancer development.

APA, Harvard, Vancouver, ISO, and other styles

37

Martinou, Eirini, Giulia Falgari, Izhar Bagwan, and Angeliki M. Angelidi. "A Systematic Review on HOX Genes as Potential Biomarkers in Colorectal Cancer: An Emerging Role of HOXB9." International Journal of Molecular Sciences 22, no. 24 (December 14, 2021): 13429. http://dx.doi.org/10.3390/ijms222413429.

Full text

Abstract:

Emerging evidence shows that Homeobox (HOX) genes are important in carcinogenesis, and their dysregulation has been linked with metastatic potential and poor prognosis. This review (PROSPERO-CRD42020190953) aims to systematically investigate the role of HOX genes as biomarkers in CRC and the impact of their modulation on tumour growth and progression. The MEDLINE, EMBASE, Web of Science and Cochrane databases were searched for eligible studies exploring two research questions: (a) the clinicopathological and prognostic significance of HOX dysregulation in patients with CRC and (b) the functional role of HOX genes in CRC progression. Twenty-five studies enrolling 3003 CRC patients, showed that aberrant expression of HOX proteins was significantly related to tumour depth, nodal invasion, distant metastases, advanced stage and poor prognosis. A post-hoc meta-analysis on HOXB9 showed that its overexpression was significantly associated with the presence of distant metastases (pooled OR 4.14, 95% CI 1.64–10.43, I2 = 0%, p = 0.003). Twenty-two preclinical studies showed that HOX proteins are crucially related to tumour growth and metastatic potential by affecting cell proliferation and altering the expression of epithelial-mesenchymal transition modulators. In conclusion, HOX proteins may play vital roles in CRC progression and are associated with overall survival. HOXB9 may be a critical transcription factor in CRC.

APA, Harvard, Vancouver, ISO, and other styles

38

Conlon, R. A., and J. Rossant. "Exogenous retinoic acid rapidly induces anterior ectopic expression of murine Hox-2 genes in vivo." Development 116, no. 2 (October 1, 1992): 357–68. http://dx.doi.org/10.1242/dev.116.2.357.

Full text

Abstract:

Exogenous retinoic acid (RA) has teratogenic effects on vertebrate embryos and alters Hox-C gene expression in vivo and in vitro. We wish to examine whether RA has a role in the normal regulation of Hox-C genes, and whether altered Hox-C gene expression in response to RA leads to abnormal morphology. The expression of 3′ Hox-2 genes (Hox-2.9, Hox-2.8, Hox-2.6 and Hox-2.1) and a 5′ gene (Hox-2.5) were examined by whole-mount in situ hybridization on embryos 4 hours after maternal administration of teratogenic doses of RA on embryonic day 7 to 9. The expression of the 3′ Hox-2 genes was found to be ectopically induced in anterior regions in a stage-specific manner. The Hox-2.9 and Hox-2.8 genes were induced anteriorly in the neurectoderm in response to RA on day 7 but not at later stages. Expression of Hox-2.6 and Hox-2.1 was ectopically induced anteriorly in neurectoderm in response to RA on day 8. Hox-2.1 remained responsive on day 9, whereas Hox-2.6 was no longer responsive at this stage. The expression of the 5′ gene Hox-2.5 was not detectably altered at any of these stages by RA treatments. We also examined the response of other genes whose expression is spatially regulated in early embryos. The expression of En-2 and Wnt-7b was not detectably altered by RA, whereas RAR beta expression was induced anteriorly by RA on day 7 and 8. Krox-20 expression was reduced in a stage- and region-specific manner by RA. The ectopic anterior expression of Hox-2.8 and Hox-2.9 induced by RA on day 7 was persistent to day 8, as was the altered expression of Krox-20. The altered pattern of expression of these genes in response to RA treatment on day 7 may be indicative of a transformation of anterior hindbrain to posterior hindbrain, specifically, a transformation of rhombomeres 1 to 3 towards rhombomere 4 identity with an anterior expansion of rhombomere 5. The ectopic expression of the 3′ Hox-2 genes in response to RA is consistent with a role for these genes in mediating the teratogenic effects of RA; the rapid response of the Hox-C genes to RA is consistent with a role for endogenous RA in refining 3′ Hox-C gene expression boundaries early in development.

APA, Harvard, Vancouver, ISO, and other styles

39

Osmond, Brian, Caroline O. Facey, Lynn M. Opdenaker, Chi Zhang, and Bruce M. Boman. "Abstract 2446: An investigation of HOX-regulatory mechanisms and their role in the SC origin of human CRC." Cancer Research 83, no. 7_Supplement (April 4, 2023): 2446. http://dx.doi.org/10.1158/1538-7445.am2023-2446.

Full text

Abstract:

Abstract HOX genes are a highly conserved subset of genes that encode for transcription factors critical for stem cell (SC) function and embryonic development. Several HOX genes have also been implicated in a myriad of cancers, including colorectal cancer (CRC). However, the mechanisms by which HOX genes contribute to cancer development are still not fully understood. Specifically, the mechanisms by which HOX genes regulate SC populations and how SC dysregulation leads to tumorigenesis needs to be clarified. Current research indicates that HOX genes are regulated by WNT and retinoic acid (RA) signaling. Goal: To ascertain how HOX-regulatory mechanisms play a role in the SC origin of human CRC. Hypotheses: (1) HOX genes regulated by RA and WNT signaling control SC differentiation along various lineages in normal human colonic epithelium. (2) Aberrant expression of HOX genes leads to decreased differentiation and CSC overpopulation in CRC. Preliminary data shows that RA signaling occurs in ALDH+ SCs and HOXA4, HOXA9 & HOXD10 are selectively expressed in ALDH+ SCs. Moreover, treatment of CRC cells with all-trans retinoic acid (ATRA) modulates expression of HOXA4, HOXA9, HOXC8, HOXC9, & HOXD10 while also reducing cell count. Nanostring profiling also shows that expression of select HOX genes (HOXA3, HOXA4, HOXA5, HOXA10, HOXB6, HOXB8, HOXB9, & HOXD9) significantly changes in response to ATRA. Bioinformatics analysis has identified RA response elements (RAREs) within the promoters of all mentioned HOX genes. Understanding how HOX genes control normal colonic SCs, and, how they become dysregulated in CSCs will identify mechanisms that help explain how HOX genes contribute to SC overpopulation that drives colorectal cancer (CRC) growth. Citation Format: Brian Osmond, Caroline O. Facey, Lynn M. Opdenaker, Chi Zhang, Bruce M. Boman. An investigation of HOX-regulatory mechanisms and their role in the SC origin of human CRC [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2023; Part 1 (Regular and Invited Abstracts); 2023 Apr 14-19; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2023;83(7_Suppl):Abstract nr 2446.

APA, Harvard, Vancouver, ISO, and other styles

40

Kramarzova, Karolina, Harry Drabkin, Jan Zuna, Zuzana Zemanova, Jan Stary, Jan Trka, and Julia Starkova. "Transcription Regulation of HOX Genes in Normal Hematopoiesis and Leukemogenesis in Children." Blood 120, no. 21 (November 16, 2012): 4614. http://dx.doi.org/10.1182/blood.v120.21.4614.4614.

Full text

Abstract:

Abstract Abstract 4614 Introduction: The homeodomain genes (HOX genes) encode a family of highly conserved transcription factors that play fundamental roles during embryogenesis. HOX genes are also important regulators in hematopoiesis. In leukemogenesis, dysregulated expression of HOX genes has been found. Despite many correlative studies, the mechanism of establishment of leukemia specific HOX gene expression patterns in hematopoietic cells remains to be elucidated. Histone methylases and demethylases (Trithorax (TrxG), JMJD3 and Polycomb-group (PcG) genes) are chromatin modifiers regulating global gene expression through chromatin remodeling in many biological processes. PcG genes can also interact with DNA methyltransferases and alter their activity. Our previously published data showed that HOX gene expression correlated with the level of DNA methylation. These data together with the stabilizing function of PcG genes on HOX expression in embryogenesis suggest the involvement of histone modifiers in the regulation of hematopoietic HOX gene expression. Methods: To investigate the regulation of HOX expression in leukemogenesis, we determined mRNA levels of the representative groups of HOX genes (HOXA, HOXB, CDX1/2), PcG genes (EZH2, BMI1), MLL and demethylases (JMJD3, UTX) in samples of childhood AML (N=41) and healthy controls (N=5). We also studied the dynamics of HOX genes and chromatin modifiers in preleukemic and diagnostic samples of a patient who underwent secondary leukemia. Quantification of gene expression was performed using qPCR assays as previously described. Results: Expression patterns for the majority of HOX genes differed significantly among morphologically defined subgroups of AML with AML M3 having the lowest expression of all HOX genes. Children with AML M5 expressed HOXA cluster at the highest level, while HOXB genes were highly expressed in M5 and M4 subtype. Subgroups defined according to molecular genetics showed similar results. The presence of PML/RARa fusion gene was associated with very low expression of all HOX genes whereas MLL+ and CBFb/MYH11+ patients expressed higher levels of HOXA genes. We also assessed the prognostic significance of particular HOX genes and found that the HOXA cluster was expressed at very low levels in standard risk cases compared to the high risk group (P<0.0001 for most HOXA genes), which is in concordance with previously published results in adult AML (Andreeff et al. 2008). Determination of mRNA levels of histone modifiers showed an overall level of high expression across various AML subgroups. Nevertheless, some were uniformly expressed in AML patients (EZH2, MLL), while others were differentially expressed with the lowest level in the M3 subtype (BMI1, JMJD3). Interestingly, we found a correlation between HOX gene expression and levels of JMJD3, which was mainly evident in CBFb-MYH11+, PML-RARa+ and AML1-ETO+ patients. JMJD3 levels were also correlated with another demethylase, UTX. A positive trend between HOX gene expression and JMJD3 was identified in healthy controls as well. Analysis of the sample from preleukemic period of the patient with secondary leukemia (secALL with MLL translocation) allowed us to study the dynamics of HOX gene expression during leukemogenesis. The diagnostic secALL sample showed an expression pattern of HOX genes typical for MLL+ leukemia. However, the profile of HOX genes in preleukemic sample (16 months before secALL) resembled the pattern found in healthy controls. Nonetheless, 90% of these seemingly normal hematopoietic cells were confirmed by FISH analysis to carry MLL/FOXO3A. Thus, even though MLL is a well known regulator of HOX genes, there must be an additional mechanism, that establishes the expression pattern of HOX genes typical in MLL+ patients. Conclusion: In summary, we identified different expression patterns of HOX genes in particular subtypes of childhood AML that significantly correlated with prognosis. Our results indicate that histone modifiers JMJD3 and UTX might be involved in the regulation of HOX gene expression. Moreover, these data also suggest that histone demethylases could cooperate with specific genetic aberrations implicated in chromatin remodeling on regulation of HOX genes. The analysis of secondary leukemia suggests that additional alterations are required to deregulate HOX expression in at least some MLL+ patients. Disclosures: No relevant conflicts of interest to declare.

APA, Harvard, Vancouver, ISO, and other styles

41

Osmond, Brian T., Caroline O. Facey, Lynn O. Opdenaker, Chi Zhang, and Bruce M. Boman. "Abstract 5599: Role of HOX gene expression in differentiation of colon cancer stem cells." Cancer Research 84, no. 6_Supplement (March 22, 2024): 5599. http://dx.doi.org/10.1158/1538-7445.am2024-5599.

Full text

Abstract:

Abstract HOX genes encode a highly conserved set of transcription factors critical for stem cell (SC) function and embryonic development. Several HOX genes have also been implicated in a myriad of cancers, including colorectal cancer (CRC). However, how HOX genes play a role in SC regulation and contributes to cancer development is unclear. HOX expression is regulated by WNT, FGF, and retinoic acid (RA) signaling - pathways which also become dysregulated in cancer. Goal: To determine how regulation of HOX genes specifies differentiation of colonic SCs into specialized cell lineages and how dysregulation of HOX genes contributes to CRC development. Hypotheses: i) Each of the different cell types within human colonic epithelium has a distinct HOX gene expression signature; ii) All-trans retinoic acid (ATRA) induced differentiation of CRC cells changes HOX expression that correlates with specific HOX expression signatures in normal colon and CRC cells. Results: Immunostaining shows that specific HOX proteins (e.g., HOXA9 & HOXC9) are selectively expressed in ALDH-positive SCs and expression of these HOX genes is increased in CRC tissues compared to normal epithelium. Bioinformatics analysis predicted that these HOX genes (plus HOXA4, HOXA10, HOXC8) are regulated by RA signaling. Accordingly, we studied how ATRA influences HOX expression in CRC cells (HT29 & SW480). We found ATRA treatment: 1) Decreases proliferation and increases neuroendocrine cell (NEC) differentiation; and 2). Leads to specific changes in HOX gene expression patterns. Using NanoString profiling, we also discovered that LGR5+ SCs, ALDH+ SCs and GLP2R+ NECs have unique HOX signatures. By defining how these HOX gene expression changes in response to ATRA treatment in comparison to the HOX gene signatures of different colonic cell lineages will help us understand the role that HOX genes play in SC differentiation and how dysregulation of HOX gene expression contributes to CRC development. Citation Format: Brian T. Osmond, Caroline O. Facey, Lynn O. Opdenaker, Chi Zhang, Bruce M. Boman. Role of HOX gene expression in differentiation of colon cancer stem cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2024; Part 1 (Regular Abstracts); 2024 Apr 5-10; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2024;84(6_Suppl):Abstract nr 5599.

APA, Harvard, Vancouver, ISO, and other styles

42

Mathews, CH, K. Detmer, E. Boncinelli, HJ Lawrence, and C. Largman. "Erythroid-restricted expression of homeobox genes of the human HOX 2 locus." Blood 78, no. 9 (November 1, 1991): 2248–52. http://dx.doi.org/10.1182/blood.v78.9.2248.2248.

Full text

Abstract:

Abstract We have previously reported that certain members of the HOX 1 and HOX 2 clusters of class 1 homeobox-containing genes showed lineage-restricted patterns of expression in a small series of human hematopoietic cell lines. We now report on the expression patterns of the entire HOX 2 cluster, consisting of nine homeobox genes, in a broad survey of leukemic cell lines of different phenotypes. The most striking observation is that all but one of the HOX 2 genes are consistently expressed in cells with erythroid character and/or potential, but, with rare exception, not in cells with myelomonocytic or T- or B-lymphoid phenotype. By contrast, several genes of the HOX 1 and 3 loci are not expressed in erythroid lines. Within erythroid cell lines, many of the HOX 2 genes are expressed as multiple transcripts. Expression of some HOX 2 genes is detectable in normal human marrow. These data show that in human hematopoietic cell lines HOX 2 homeobox gene expression is largely restricted to cells of erythroid phenotype and suggest that these genes play a role in erythropoiesis.

APA, Harvard, Vancouver, ISO, and other styles

43

Mathews, CH, K. Detmer, E. Boncinelli, HJ Lawrence, and C. Largman. "Erythroid-restricted expression of homeobox genes of the human HOX 2 locus." Blood 78, no. 9 (November 1, 1991): 2248–52. http://dx.doi.org/10.1182/blood.v78.9.2248.bloodjournal7892248.

Full text

Abstract:

We have previously reported that certain members of the HOX 1 and HOX 2 clusters of class 1 homeobox-containing genes showed lineage-restricted patterns of expression in a small series of human hematopoietic cell lines. We now report on the expression patterns of the entire HOX 2 cluster, consisting of nine homeobox genes, in a broad survey of leukemic cell lines of different phenotypes. The most striking observation is that all but one of the HOX 2 genes are consistently expressed in cells with erythroid character and/or potential, but, with rare exception, not in cells with myelomonocytic or T- or B-lymphoid phenotype. By contrast, several genes of the HOX 1 and 3 loci are not expressed in erythroid lines. Within erythroid cell lines, many of the HOX 2 genes are expressed as multiple transcripts. Expression of some HOX 2 genes is detectable in normal human marrow. These data show that in human hematopoietic cell lines HOX 2 homeobox gene expression is largely restricted to cells of erythroid phenotype and suggest that these genes play a role in erythropoiesis.

APA, Harvard, Vancouver, ISO, and other styles

44

Buffry, Alexandra D., and Alistair P. McGregor. "Micromanagement of Drosophila Post-Embryonic Development by Hox Genes." Journal of Developmental Biology 10, no. 1 (February 18, 2022): 13. http://dx.doi.org/10.3390/jdb10010013.

Full text

Abstract:

Hox genes function early in development to determine regional identity in animals. Consequently, the loss or gain of Hox gene expression can change this identity and cause homeotic transformations. Over 20 years ago, it was observed that the role of Hox genes in patterning animal body plans involves the fine-scale regulation of cell fate and identity during development, playing the role of ‘micromanagers’ as proposed by Michael Akam in key perspective papers. Therefore, as well as specifying where structures develop on animal bodies, Hox genes can help to precisely sculpt their morphology. Here, we review work that has provided important insights about the roles of Hox genes in influencing cell fate during post-embryonic development in Drosophila to regulate fine-scale patterning and morphology. We also explore how this is achieved through the regulation of Hox genes, specific co-factors and their complex regulation of hundreds of target genes. We argue that further investigating the regulation and roles of Hox genes in Drosophila post-embryonic development has great potential for understanding gene regulation, cell fate and phenotypic differentiation more generally.

APA, Harvard, Vancouver, ISO, and other styles

45

Pineault, Nicolas, Carolina Abramovich, Hideaki Ohta, and R. Keith Humphries. "Differential and Common Leukemogenic Potentials of Multiple NUP98-Hox Fusion Proteins Alone or with Meis1." Molecular and Cellular Biology 24, no. 5 (March 1, 2004): 1907–17. http://dx.doi.org/10.1128/mcb.24.5.1907-1917.2004.

Full text

Abstract:

ABSTRACT NUP98-Hox fusion genes are newly identified oncogenes isolated in myeloid leukemias. Intriguingly, only Abd-B Hox genes have been reported as fusion partners, indicating that they may have unique overlapping leukemogenic properties. To address this hypothesis, we engineered novel NUP98 fusions with Hox genes not previously identified as fusion partners: the Abd-B-like gene HOXA10 and two Antennepedia-like genes, HOXB3 and HOXB4. Notably, NUP98-HOXA10 and NUP98-HOXB3 but not NUP98-HOXB4 induced leukemia in a murine transplant model, which is consistent with the reported leukemogenic potential ability of HOXA10 and HOXB3 but not HOXB4. Thus, the ability of Hox genes to induce leukemia as NUP98 fusion partners, although apparently redundant for Abd-B-like activity, is not restricted to this group, but rather is determined by the intrinsic leukemogenic potential of the Hox partner. We also show that the potent leukemogenic activity of Abd-B-like Hox genes is correlated with their strong ability to block hematopoietic differentiation. Conversely, coexpression of the Hox cofactor Meis1 alleviated the requirement of a strong intrinsic Hox-transforming potential to induce leukemia. Our results support a model in which many if not all Hox genes can be leukemogenic and point to striking functional overlap not previously appreciated, presumably reflecting common regulated pathways.

APA, Harvard, Vancouver, ISO, and other styles

46

Gentile, Claudia, and Marie Kmita. "The remote transcriptional control of Hox genes." International Journal of Developmental Biology 62, no. 11-12 (2018): 685–92. http://dx.doi.org/10.1387/ijdb.180198mk.

Full text

Abstract:

Since the discovery by Ed Lewis that the order of Hox genes on the chromosome reflects the partitioning of their patterning function along the anterior-posterior axis of the developing fruit fly embryo, extensive efforts have been dedicated to uncovering the regulatory events underlying the collinear expression of Hox genes. These studies have revealed various aspects of Hox regulation, including short-range and long-range transcriptional enhancers, insulator elements and non-coding RNAs. With the development of technologies allowing for high resolution probing of chromatin architecture, notably Chromosome Conformation Capture (3C)-based techniques, a clear relationship is emerging between long-range regulation of Hox genes and the three-dimensional organization of the genome. Here, we provide an overview of these studies and in particular we discuss the functional relevance of genome compartmentalization, CTCF- mediated insulation and the Polycomb Repressive Complexes in the remote control of Hox genes.

APA, Harvard, Vancouver, ISO, and other styles

47

Janssen, Ralf, Bo Eriksson, Noel N. Tait, and Graham E. Budd. "Onychophoran Hox genes and the evolution of arthropod Hox gene expression." Frontiers in Zoology 11, no. 1 (2014): 22. http://dx.doi.org/10.1186/1742-9994-11-22.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

Dolomatov, Sergey, Vera Kazakova, and Walery Zukow. "Hox genes in the coordination of embryonic development. Model of hourglass in the description of vertebrate ontogenesis." Journal of Education, Health and Sport 11, no. 12 (December 4, 2021): 24–37. http://dx.doi.org/10.12775/jehs.2021.11.12.002.

Full text

Abstract:

The paper analyzes the role of HOX genes in the processes of embryonic development of vertebrates. Based on the analysis, it is concluded that HOX genes are the most important regulators of embryonic development. The HOX genes predominantly realize their influence through specific HOX proteins that have the ability to regulate the expression of target genes. The order of expression of the HOX genes, as a rule, obeys the rule of temporal and spatial colinearity. This mechanism determines the temporal and spatial course of tissue morphogenesis during embryonic development and tissue regeneration in organisms that have reached the stage of maturity. The process of embryo morphogenesis, determined by highly conserved HOX genes, explains the appearance of the phylotypic period - the stage of embryonic development of vertebrates, at which embryos of different classes of vertebrates have distinct morphological similarities.

APA, Harvard, Vancouver, ISO, and other styles

49

Chen, Hexin, and Saraswati Sukumar. "HOX Genes — Emerging Stars in Cancer." Cancer Biology & Therapy 2, no. 5 (May 4, 2003): 524–25. http://dx.doi.org/10.4161/cbt.2.5.525.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Powers, Thomas, and Chris Amemiya. "Evolutionary Plasticity of Vertebrate Hox Genes." Current Genomics 5, no. 6 (August 1, 2004): 459–72. http://dx.doi.org/10.2174/1389202043349048.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!