Increased expression of alternatively spliced variants of the CD44 family of cell adhesion molecules has been associated with tumour metastasis.
Differentiated myofibroblasts can be distinguished from fibroblasts by de novo synthesis of α-smooth muscle actin (α-SMA), increased expression of alternatively spliced fibronectin (EDA) and assembly of stress fibers [ 4].
Alternatively, increased expression of such transcripts in liver may reflect an influx of monocytes, macrophages, T-cells and other white blood cells [17], [18], which express at high levels genes encoding antigens and proteins central to immune processes.
Alternatively, increased expression of αS as occurs in Parkinson's disease may generate excess Fe(II) a metal that can catalyse the Fenton reaction and generate excess reactive oxygen species which may result in apoptosis.
Alternatively, increased expression of these genes may be a result of elevated ethylene levels.
Alternatively, increased expression of CEACAM1 on neutrophils is associated with delayed apoptosis, which may be related to the observed persistence of inflammation in KD patients failing to respond to IVIG [ 8, 13].
Alternatively, increased expression of molecules such as Txnrd1 and Hmox-1, both of which are up-regulated in response to MTS in our model (Table- 1, Figure 3) may counteract inflammatory signals.
Alternatively, increased expression of Nck2 could passively destroy proper stoichiometry of molecular complexes and in this manner, indirectly contributes to cancer progression by altering signaling pathways regulating the actin cytoskeleton network supporting cell migration.
Alternatively, increased expression of glycogen synthesis genes may simply represent abnormal transcriptional patterns that could result from direct damage to DNA and/or polypeptides (Wei and Lee 2002) rather than a compensatory or defensive response to stress induced damage or impaired cellular function.
Alternatively, it is also possible that increased expression of proangiogenic VEGF isoforms caused the observed increase in intraplacental arterial diameters but that the adjacent capillaries failed to respond due to reduced angiogenic sensitivity.
Alternatively, if the Wnt pathway target gene is not strongly expressed at the L2/L3 molt, we expect increased expression with exposure to ΔNTBAR-1 but little change in expression in response to ΔNTPOP-1 (termed "class 2" targets).
