Enolase expression

Sousa, L. R, B. M. Silva, B. S. Brasil et al. Plasminogen/plasmin regulates alpha-enolase expression through the MEK/ERK pathway. Biochem Bionhvx Rex Commun 337(4), 2005 1065-71. 

Another 3-D cornea model, comprising rabbit primary cultures of epithelial and stromal cells as well as mouse immortalized endothelial cells, was described in 1994 by Zieske and coworkers [70], They showed the influence of endothelial cells on the formation of a tightly packed, multilayered epithelium as well as the expression of laminin, type VII collagen, a6 integrin, keratin K3, and a-enolase. Furthermore, their findings suggested that the formation of an in vivo-like epithelium requires the cultivation of the 3-D corneal construct under AIC conditions. By contrast, LCC methods of cultivating corneal equivalents in the absence of endothelial cells failed to promote the expression of differentiation markers and basement membrane components. 

Pahiman, S., Esscher, T., and Nilsson, K. (1986) Expression of gamma-subunit of enolase, neuron-specific enolase, in hnman non-neuroendocrine tumors and derived cell lines. Lab. Invest. 54, 554-560. 

The differential expression of paired cancerous and non-cancerous tissues was visually compared, and 11 spots were up-regulated in cancerous tissues alpha-enolase, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) 2 (spots), triosephosphate isomerase, transgelin, calmodulin, MnSOD, PDI A3, cyclophilinA, GST-P, and apolipoprotein A-I precursor (23). 

Table 3 shows the proteins up-regulated or down-regulated in panereatie eaneer tissues. Shen et al. reported that, in panereatie eaneer tissues, expressions of Mn-SOD, S100A8, annexin A4, eathepsin D, 14-3-3 zeta, tropomyosin 2, aetin, ferritin light chain, alpha-enolase, galectin-1, and cyclophilin A increased, and that those of peroxiredoxin... 

In brain tissues, specific isoforms of glycolytic enzymes are also expressed there are specific brain isoforms for PFK (PFK-C), fructose-1,6-bisphosphate aldolase (aldolase C), enolase (enolase y), but not for GAPDH. The isoforms bear the same catalytic functions however, they could be specialized to form different ultrastructural entities. For example, muscle PFK (a dissociable tetrameric form) binds to microtubules and bundle them [94, 95], however, the brain isoenzyme (stable tetramer) does not [96]. 

Jiang, B. H., Agani, F., Passaniti, A., and Semenza, G. L. (1997). V-SRC induces expression of hypoxia-inducible factor 1 (HIF-1) and transcription of genes encoding vascular endothelial growth factor and enolase 1 involvement of HIF-1 in tumor progression. Cancer Res. 57, 5328-5335. 

The coding region of A. altemata enolase cDNA was also cloned into pMW 172 and transformed in E. coli. Purification of expressed Alt a 5 was done by inclusion body preparation followed by isopropanol and ammonium sulfate precipitations. Finally Sephacryl chromatography was performed ending up with a material which appeared as a single band with essentially no contamination on reducing SDS-PAGE. 

Wagner S, Breiteneder H, Simon-Nobbe B, Susani M, Krebitz M, Niggemann B, Brehler R, Scheiner O, Hoffmann-Sommergruber K Hev b 9, an enolase and a new cross-reactive allergen from Hevea latex and molds. Purification, characterization, cloning and expression. Eur J Biochem... 

The enolase from lobster has been expressed and the crystal structures of the apoenzyme and a ternary complex with Mn(II) and the inhibitor phosphoglycolate determined. The Mn(n) ion is bound to three carboxylate side chains and three water molecules as found in the crystal structure of yeast enolase. As opposed to the yeast enzyme shown in Figure 13C, the phosphoglycolate inhibitor does not bind to the metal, but is H-bonded to a coordinated water, and is next to Hisl57, possibly the base that abstracts the C2-H proton, which is followed by removal of the C2-OH hydroxyl group by the metal to form the PEP product (Figure 13F). This suggested mechanism is different from that proposed on the basis of the crystal structure of the yeast enzyme, but consistent with earlier biochemical and spectroscopic data. 

Andersen JK, Garber DA, Meaney CA, Breakefield XO (1992) Gene transfer into mammalian central nervous system using herpes virus vectors Extended expression of bacterial lacZ in neurons using the neuron-specific enolase promoter. Hum Gene Ther 3 487-499. 

Meisler We expect that all of the cells are expressing this construct. It is the NSE promoter for the neural-specific enolase gene. However, we haven t done histology to demonstrate pan-neuronal expression, because the level of expression is so low it is hard to detect. 

From a cell biological perspective, PrPc expressed from a neuron-specific enolase promoter could rescue granule cell degeneration but not a Dpl-specified leukoencephalopathy. In a reverse fashion, PrP expressed in trans from a myelin basic protein promoter could rescue leukoencephalopathy but not granule cell death [127]. 

Kayser K, Schmid W, Ebert W, Wiedenmann B. Expression of neuroendocrine markers (neuronspecific enolase, synaptophysin and bombesin) in carcinoma of the lung. Pathol Res Pract. 1988 183 412-417. 

The tumors are positive for synaptophysin, chromogranin, and neuron-specific enolase and may express a variety of hormones (growth hormone, prolactin, TSH, ACTH, and FSH). A few are hormone negative and are designated as null-cell adenomas. Almost all are positive for CAM 5.2, either focally or diffusely, and about half are positive for AE 1/3. They are negative for cytokeratin 7, 19, and 20, as well as S-100 protein. Pituitary transcription factor-1 is selectively expressed in tumors that express growth hormone, prolactin, and TSH. No diagnostic molecular markers are currently in use for sporadic pituitary lesions. ... 

ES/PNETs are positive for glycogen (PAS stain), vimentin, and CD 99 (Pig. 9.15). Some may also express synaptophysin, chromogranin, neuron-specific enolase, Eeu-7, PGP 9.5, and NB-84. Up to 20% may also be positive, either locally or diffusely, for cytokeratin AE 1/3 and/or CAM 5.2. " Rarely, desmin may be locally positive. 

These three neuroendocrine tumors of the larynx all display positivity for typical neuroendocrine markers such as chromogranin, synaptophysin, and neuron-specific enolase. They may also be positive for carcinoembryonic antigen (CEA) or epithelial membrane antigen (EMA). Atypical carcinoid and SCNEC can also express other neuroendocrine markers such as serotonin, calcitonin, and somatostatin. TTE-1 is probably not a useful marker to distinguish metastatic pulmonary small cell carcinoma from primary tumors in the head and neck because up to 50% of extrapulmonary small cell carcinomas are positive for TTR-l.i 8... 

A. Zero of 10 squamous carcinomas, 4 of 26 adenocarcinomas, and 0 of 11 large cell undifferentiated carcinomas showed immunostaining for Leu7. Six of 10 squamous carcinomas, 15 of 26 adenocarcinomas, and 7 of 11 large cell undifferentiated carcinomas showed immunostaining for neuron-specific enolase. Six of 10 squamous carcinomas, 16 of 26 adenocarcinomas, and 7 of 11 large cell undifferentiated carcinomas showed immunostaining for synaptophysin. Overall, 34 of 47 (79%) carcinomas without neuroendocrine features expressed at least one neuroendocrine immunohistochemical marker. Nineteen of 19 (100%) of neuroendocrine carcinomas expressed at least one neuroendocrine marker. 

The bottom line for pathologists is that lung neoplasms that are not classified by histologic criteria as being a neuroendocrine neoplasm may express neuroendocrine markers by immunohistochemistry. A summary of these studies showing the frequency of expression of chromogranin A, synaptophysin, neuron-specific enolase, and Leu7 is shown in Fig. 12.41. 

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