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FEZ1


Official Full Name
fasciculation and elongation protein zeta 1
Organism
Homo sapiens
Gene ID
9638
Background
This gene is an ortholog of the C. elegans unc-76 gene, which is necessary for normal axonal bundling and elongation within axon bundles. Expression of this gene in C. elegans unc-76 mutants can restore to the mutants partial locomotion and axonal fasciculation, suggesting that it also functions in axonal outgrowth. The N-terminal half of the gene product is highly acidic. Alternatively spliced transcript variants encoding different isoforms of this protein have been described. [provided by RefSeq, Jul 2008]
Synonyms
UNC-76

Cat.No. Product Name Price
SHH055973 shRNA set against Rat Fez1(NM_031066.1) Inquiry
SHH169481 shRNA set against Rat Lzts1(NM_153470.1) Inquiry
SHH294182 shRNA set against Human FEZ1 (NM_005103.4) Inquiry
SHH294185 shRNA set against Mouse FEZ1 (NM_183171.4) Inquiry
SHH294189 shRNA set against Rat FEZ1 (NM_031066.1) Inquiry
SHH336351 shRNA set against Human LZTS1 (NM_021020.2) Inquiry
SHH336355 shRNA set against Mouse LZTS1 (NM_199364.2) Inquiry
SHH336359 shRNA set against Rat LZTS1 (NM_153470.1) Inquiry
SHW018457 shRNA set against Danio rerio FEZ1 (NM_213396) Inquiry
Cat.No. Product Name Price
MiUTR4H-TG05256 LZTS1 miRNA 3'UTR clone Inquiry
MiUTR3H-07126 FEZ1 miRNA 3'UTR clone Inquiry
MiUTR1R-03637 LZTS1 miRNA 3'UTR clone Inquiry
CDCB194552 Rabbit LZTS1 ORF clone (XM_008267266.1) Inquiry
MiUTR1R-01871 FEZ1 miRNA 3'UTR clone Inquiry
CDFR014604 Rat Lzts1 cDNA Clone(NM_153470.1) Inquiry
CDFR012541 Rat Fez1 cDNA Clone(NM_031066.1) Inquiry
CDFL007262 Mouse Lzts1 cDNA Clone(NM_199364.2) Inquiry
MiUTR3H-07127 FEZ1 miRNA 3'UTR clone Inquiry
CDCS412099 Human FEZ1 ORF Clone (BC009545) Inquiry
CDCR379563 Rat Fez1 ORF Clone(NM_031066.1) Inquiry
CDCR276883 Mouse Lzts1 ORF Clone(NM_199364.2) Inquiry
CDCB196443 Rabbit LOC103349268 ORF clone (XM_008260957.1) Inquiry
CDCB185323 Rabbit FEZ1 ORF clone (XM_002708685.2) Inquiry
CDCB179932 Danio rerio FEZ1 ORF Clone (NM_213396) Inquiry
CDCR381691 Rat Lzts1 ORF Clone(NM_153470.1) Inquiry
CDCB158049 Human FEZ1 ORF clone (BC009545) Inquiry

Detailed Information

The FEZ1 gene is located on chromosome 8p22, and it encodes a leucine zipper protein with a relative molecular mass of 67 × 103, which has a growth regulation effect. FEZ1 gene plays a very important role in the occurrence and development of many human malignant tumors, including prostate cancer, gastric cancer, head and neck cancer, bladder cancer, hepatocellular carcinoma, cholangiocarcinoma, and hematological malignancies.

FEZ proteins cytoplasmic function as transport bivalent adaptors.Figure 1. FEZ proteins cytoplasmic function as transport bivalent adaptors. (Teixeira, M., et al. 2019)

FEZ1 Expression in the Organization

In lung cancer, the researchers used immunohistochemical methods to analyze 103 cases of primary lung cancer (including 98 cases of non-small cell lung cancer, 57 cases of adenocarcinoma, 32 cases of squamous cell carcinoma, 7 cases of large cell carcinoma, and 2 cases). The expression of FEZ1 gene in 5 cases of other tissue types) and 5 cases of small cell carcinoma. The results showed that 27 cases had FEZ1 gene deletion, and 43 cases had significantly reduced expression. In addition, the results showed that the FEZ1 gene was positively correlated with tumor grade. Therefore, it is believed that FEZ1 gene plays an important role in lung cancer, and it is speculated that it may be used as a new prognostic indicator of lung cancer.

In bladder cancer, researchers used Western blot and immunohistochemistry methods to study the expression of FEZ1 protein in bladder transitional cell carcinoma-derived cell lines and primary bladder cancer. Among the bladder transitional cell carcinoma-derived cell lines, FEZ1 protein was missing or down-regulated in 4/5 cell lines, and FEZ1 protein was missing or down-regulated in 37 of 60 primary cancers. Another 37% of primary transitional cell carcinoma of the bladder and 70% of bladder transitional cell carcinoma-derived cell lines showed a significant decrease in FEZ1 protein expression. At the same time, statistical analysis showed that the down-regulation and lack of FEZ1 expression are significantly correlated with the grade of bladder cancer. In addition, studies have shown that the mRNA level and transcription products of FEZ1 gene are significantly reduced in most bladder transitional cell carcinoma-derived cell lines and primary bladder cancer, and it is believed that the mechanism of FEZ1 gene inactivation may be the promoter hypermethylation.

FEZ1 Inhibits Tumor Cell Growth

Using gastric cancer carcinogen NMBA to induce tumors in mice lacking endogenous FEZ1 gene to study the role of FEZ1 in living tumors. The results of the study showed that after 6 weeks of administration, FEZ1 (-/-) mice (20/20) and FEZ1 (+/-) mice had complex tumor growth in the cardiac sinus, while only (5/19) Wild-type mice have the potential to develop tumors. In addition, only the first two types of mice have invasive growth tumors, and wild-type mice show a series of injuries including hyperplasia and papilloma.

It was observed that untreated mice lacking the FEZ1 gene had spontaneous tumors after 2 years. 5 FEZ1 (-/-) and FEZ1 (+/-) mice had new tumor growth, while 3 wild-type mice No new tumors were found in the mice. Observing spontaneous tumors and induced tumors in mice with inactivated FEZ1 alleles, researchers infer that FEZ1 can inhibit the growth of tumor cells. In addition, when researchers studied bladder cancer cell lines lacking the endogenous FEZ1 gene, they were transduced to restore expression in vitro, and they also observed the inhibitory effect of FEZ1 on tumor cell growth. This effect is related to FEZ1's ability to regulate cell mitosis.

References:

  1. Teixeira, M., Alborghetti, M. R., & Kobarg, J. (2019). Fasciculation and elongation zeta proteins 1 and 2: From structural flexibility to functional diversity. World Journal of Biological Chemistry, 10(2), 28-43.
  2. Huang, P., Summers, B. J., Xu, C., Perilla, J. R., Malikov, V., Naghavi, M. H., & Xiong, Y. (2019). FEZ1 Is Recruited to a Conserved Cofactor Site on Capsid to Promote HIV-1 Trafficking. Cell Reports, 28(9).
  3. Chen, X., Ku, L., Mei, R., Liu, G., Xu, C., Wen, Z., Zhao, X., Wang, F., Xiao, L., & Feng, Y. (2017). Novel schizophrenia risk factor pathways regulate FEZ1 to advance oligodendroglia development. Translational psychiatry, 7(12), 1293.
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