FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2008741758> ?p ?o ?g. }

• W2008741758 endingPage "319" @default.
• W2008741758 startingPage "287" @default.
• W2008741758 abstract "Programmed cell death or apoptosis occurs under physiological conditions as a result of physiological effectors. It is a relatively slower process and requires active participation of the cell in the suicidal mechanism. Apoptosis is controlled by precise intrinsic genetic programme and may be induced by almost all those stimuli causing necrosis. The role played by the intensity in determining the death process and the underlying mechanism is imperfectly understood. Morphologically apoptotic cells appear as small condensed body. The chromatin is dense and fragmented, packed into compact membrane-bound bodies together with randomly distributed cell organelles. The plasma membrane loses its characteristic architecture and shows extensive blebbing. It buds off projections so that the whole cell may split into several membrane-bound apoptotic bodies. Significant chemical changes take place in the plasma membrane. This helps in recognition of the apoptotic bodies by phagocytes. At this moment it is unclear if all cells can undergo apoptosis or it is a characteristic of only some tissues which are predisposed to apoptotic death being directly under the control of hormones or growth factors. Experimental studies aimed at comparison of induction of apoptosis in cells of different origin are warranted to elucidate this point. Biochemically a pre-commitment step for induction of death programmation through macromolecular synthesis is essential for most systems. The double-stranded linker DNA between nucleosomes is cleaved at regular inter-nucleosomal sites through the action of a Ca2+, Mg(2+)-sensitive neutral endonuclease. Zinc is a potent inhibitor of the enzyme. Calcium probably plays a key controlling role in activation of the enzyme since prevention of Ca2+ increase prevents endonuclease activation. It is becoming evident that signal transduction through appropriate receptors control the Ca2+ flux in the cells. Most apoptotic cells require synthesis of RNA and proteins. Delay or abrogation of apoptosis by inhibition of macromolecular synthesis is well known. The dying cells show high mRNA levels for several enzymes. Several degradative enzymes become active. Regulatory proteins maintain control over the apoptotic cascade. At the molecular level, search has been initiated for the mammalian equivalents of the cell death (ced) gene. Activation of several specific genes is indicated. Specific expression of cell death-associated gene products (e.g. TRPM-2/SGP-2) has been reported in several unrelated apoptotic cell systems. Sequential induction of c-fos, c-myc and 70 kDa heat shock protein is reported. Studies demonstrate that certain genes must remain in a transcriptionally active demethylated state during programmed cell death. Recent evidences clearly indicate that apoptosis may be positively or negatively modulated by certain genes.(ABSTRACT TRUNCATED AT 400 WORDS)" @default.
• W2008741758 created "2016-06-24" @default.
• W2008741758 creator A5081258279 @default.
• W2008741758 date "1992-08-01" @default.
• W2008741758 modified "2023-09-23" @default.
• W2008741758 title "PROGRAMMED CELL DEATH: CONCEPT, MECHANISM AND CONTROL" @default.
• W2008741758 cites W1213026117 @default.
• W2008741758 cites W128219340 @default.
• W2008741758 cites W138285015 @default.
• W2008741758 cites W144208816 @default.
• W2008741758 cites W1514575046 @default.
• W2008741758 cites W1522189944 @default.
• W2008741758 cites W1524553190 @default.
• W2008741758 cites W1527910889 @default.
• W2008741758 cites W1545130210 @default.
• W2008741758 cites W1550978696 @default.
• W2008741758 cites W1551716997 @default.
• W2008741758 cites W1552857477 @default.
• W2008741758 cites W1555800917 @default.
• W2008741758 cites W1589415602 @default.
• W2008741758 cites W1605973129 @default.
• W2008741758 cites W169577875 @default.
• W2008741758 cites W1816032677 @default.
• W2008741758 cites W1893944723 @default.
• W2008741758 cites W1909751364 @default.
• W2008741758 cites W194853175 @default.
• W2008741758 cites W1967183934 @default.
• W2008741758 cites W1967884605 @default.
• W2008741758 cites W1968210150 @default.
• W2008741758 cites W1968442371 @default.
• W2008741758 cites W1969259365 @default.
• W2008741758 cites W1969331809 @default.
• W2008741758 cites W1969502142 @default.
• W2008741758 cites W1969542766 @default.
• W2008741758 cites W1970671971 @default.
• W2008741758 cites W1971776926 @default.
• W2008741758 cites W1971908328 @default.
• W2008741758 cites W1971927260 @default.
• W2008741758 cites W1972364920 @default.
• W2008741758 cites W1973196306 @default.
• W2008741758 cites W1973792489 @default.
• W2008741758 cites W1974391793 @default.
• W2008741758 cites W1974549897 @default.
• W2008741758 cites W1976062079 @default.
• W2008741758 cites W1976133790 @default.
• W2008741758 cites W1976217600 @default.
• W2008741758 cites W1976692354 @default.
• W2008741758 cites W1978240885 @default.
• W2008741758 cites W1978469465 @default.
• W2008741758 cites W1978594436 @default.
• W2008741758 cites W1978880186 @default.
• W2008741758 cites W1980045425 @default.
• W2008741758 cites W1980897761 @default.
• W2008741758 cites W1982061874 @default.
• W2008741758 cites W1982525385 @default.
• W2008741758 cites W1983950526 @default.
• W2008741758 cites W1985832983 @default.
• W2008741758 cites W1987272121 @default.
• W2008741758 cites W1987352212 @default.
• W2008741758 cites W1988335634 @default.
• W2008741758 cites W1988951544 @default.
• W2008741758 cites W1989508434 @default.
• W2008741758 cites W1989776585 @default.
• W2008741758 cites W1991605327 @default.
• W2008741758 cites W1992605331 @default.
• W2008741758 cites W1993276674 @default.
• W2008741758 cites W1994087362 @default.
• W2008741758 cites W1995142571 @default.
• W2008741758 cites W1996100805 @default.
• W2008741758 cites W1996729484 @default.
• W2008741758 cites W1998439050 @default.
• W2008741758 cites W2001857415 @default.
• W2008741758 cites W2002772701 @default.
• W2008741758 cites W2003501749 @default.
• W2008741758 cites W2004008931 @default.
• W2008741758 cites W2005182680 @default.
• W2008741758 cites W2005409372 @default.
• W2008741758 cites W2005655875 @default.
• W2008741758 cites W2006493954 @default.
• W2008741758 cites W2006910485 @default.
• W2008741758 cites W2007579029 @default.
• W2008741758 cites W2007861801 @default.
• W2008741758 cites W2008898220 @default.
• W2008741758 cites W2009183764 @default.
• W2008741758 cites W2009389356 @default.
• W2008741758 cites W2009946316 @default.
• W2008741758 cites W2012872697 @default.
• W2008741758 cites W2013317272 @default.
• W2008741758 cites W2013711614 @default.
• W2008741758 cites W2014636825 @default.
• W2008741758 cites W2014835562 @default.
• W2008741758 cites W2016168521 @default.
• W2008741758 cites W2017412059 @default.
• W2008741758 cites W2017715943 @default.
• W2008741758 cites W2019240309 @default.
• W2008741758 cites W2020233983 @default.
• W2008741758 cites W2020524468 @default.
• W2008741758 cites W2021632599 @default.

• next