£46.96

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£47 today · cheaper than every other day in the last 3 months

Springer Fas Signaling - Death Receptor Biology & Apoptosis Research

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Price History & Forecast

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Last 49 days · 49 data points (no recent data)

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£61.68 £45.49 £49.02 £52.55 £56.09 £59.62 £63.15 26 July 2026 07 August 2026 19 August 2026 31 August 2026 12 September 2026
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Price Distribution

Price distribution over 49 days • 2 price levels

Days at Price
Current Price
19 days · current 30 days 0 8 15 23 30 £47 £62 Days at Price

Price Analysis

Most common price: £62 (30 days, 61.2%)

Price range: £47 - £62

Price levels: 2 different prices over 49 days

Description

Fas Signaling by Springer provides a comprehensive examination of Fas (CD95/APO-1) death receptor mechanisms and cellular biology. This Medical Intelligence Unit volume explores both established apoptosis pathways and emerging roles of Fas as a proinflammatory cytokine and alternative cell death inducer. The book delivers current research findings across multiple aspects of Fas biology, addressing open questions in the field through detailed chapter coverage. Designed for Ph.D. and post-doctoral students entering immunology research, this reference also serves experienced practitioners seeking updated knowledge on death receptor signaling, cellular apoptosis mechanisms, and inflammatory cytokine function in modern immunological science.

Key Features

Fas Signaling covers comprehensive death receptor mechanisms including CD95 and APO-1 signalling pathways and their cellular effects.

The Medical Intelligence Unit volume addresses both classical apoptosis functions and emerging roles of Fas as a proinflammatory cytokine.

Springer's text explores alternative forms of cell death induced by Fas signaling beyond traditional apoptotic mechanisms.

Designed for Ph.D. and post-doctoral researchers beginning work in immunology and cell death biology, with accessible coverage of complex topics.

The book systematically addresses open research questions in Fas biology, providing current perspectives on death receptor function.

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