liminfoCell Biology Reference
Free reference guide: Cell Biology Reference
About Cell Biology Reference
The Cell Biology Reference is a searchable guide covering essential cell biology topics organized into three major categories. The Organelles section covers the nucleus (nuclear pore complex, importin/exportin transport), mitochondria (oxidative phosphorylation, mtDNA, apoptotic cytochrome c release), endoplasmic reticulum (rough ER protein folding with BiP/PDI, smooth ER lipid synthesis), Golgi apparatus (COPI/COPII vesicle transport, mannose-6-phosphate tagging), lysosomes, cytoskeleton (microtubules, actin filaments, intermediate filaments), cell junctions (tight, gap), endocytosis, and autophagy.
The Cell Cycle section details each phase: G1 (Cyclin D/CDK4,6, Rb phosphorylation, restriction point), S phase (DNA replication origins, histone synthesis), G2 (checkpoint and Cyclin B/CDK1 accumulation), and M phase (prophase through cytokinesis with MPF regulation). It also covers stem cell potency levels (totipotent through unipotent, Yamanaka factors) and telomere biology (TTAGGG repeats, telomerase, Hayflick limit).
The Signaling section covers major pathways including p53 tumor suppressor (ATM/ATR activation, p21-mediated G1 arrest), Ras/MAPK (RTK to ERK cascade, KRAS mutations in cancer), PI3K/Akt/mTOR (PTEN regulation, rapamycin inhibition), Wnt/beta-catenin (APC mutations in colorectal cancer), apoptosis (intrinsic and extrinsic caspase cascades), NF-kB inflammatory signaling, JAK-STAT cytokine signaling, and GPCR second messenger systems.
Key Features
- Organelle reference covering nucleus, mitochondria, ER, Golgi, lysosomes, and cytoskeleton with molecular details
- Cell cycle phases (G1, S, G2, M) with cyclin-CDK regulatory complexes and checkpoint mechanisms
- Major signaling pathways: Ras/MAPK, PI3K/Akt/mTOR, Wnt/beta-catenin, NF-kB, and JAK-STAT
- Apoptosis pathways with intrinsic (mitochondrial) and extrinsic (death receptor) caspase cascades
- GPCR second messenger systems including Gas/cAMP/PKA and Gaq/PLC/IP3/DAG pathways
- Stem cell potency hierarchy from totipotent to unipotent with Yamanaka reprogramming factors
- Telomere biology covering telomerase, Hayflick limit, and cancer cell ALT mechanisms
- Cell junction types (tight, gap) and membrane trafficking (clathrin-mediated endocytosis, autophagy)
Frequently Asked Questions
What are the main phases of the cell cycle and their regulators?
G1 phase uses Cyclin D/CDK4,6 to phosphorylate Rb and pass the restriction point. S phase uses Cyclin A/CDK2 for DNA replication across 30,000-50,000 origins. G2 phase accumulates Cyclin B/CDK1 while checking DNA replication completion. M phase is driven by MPF (Cyclin B/CDK1) activation for chromosome condensation, alignment, separation, and cytokinesis.
How does the Ras/MAPK signaling pathway work?
Growth factor binds RTK, activating Grb2/SOS which loads GTP onto Ras. Active Ras-GTP recruits Raf, which phosphorylates MEK, which phosphorylates ERK. ERK activates transcription factors (Myc, Fos) driving cell proliferation. KRAS mutations occur in approximately 30% of cancers, and RAF inhibitors like Vemurafenib target melanoma.
What is the difference between intrinsic and extrinsic apoptosis?
Intrinsic (mitochondrial) pathway: BCL-2 family proteins regulate mitochondrial membrane permeability, releasing cytochrome c which forms the apoptosome with Apaf-1, activating Caspase-9 then Caspase-3. Extrinsic (death receptor) pathway: FasL or TNF binds death receptors forming DISC, activating Caspase-8 then Caspase-3.
How does p53 function as a tumor suppressor?
DNA damage activates ATM/ATR kinases which stabilize p53 protein. p53 then induces p21 expression to inhibit CDKs and arrest the cell cycle at G1. If damage is severe, p53 activates BAX to trigger apoptosis. p53 also promotes DNA repair pathways. Mutations in p53 occur in approximately 50% of all human cancers.
What are the differences between rough and smooth endoplasmic reticulum?
Rough ER (RER) has ribosomes attached and synthesizes secretory and membrane proteins, performs N-glycosylation, and folds proteins using chaperones like BiP and PDI. Smooth ER (SER) lacks ribosomes and specializes in lipid synthesis, calcium storage, and detoxification through cytochrome P450 enzymes.
How does the Wnt/beta-catenin pathway relate to cancer?
Without Wnt signal, the APC/Axin/GSK3 destruction complex phosphorylates beta-catenin for degradation. When Wnt binds Frizzled receptor, Dishevelled inhibits GSK3, allowing beta-catenin to accumulate and enter the nucleus to activate TCF/LEF target genes (c-Myc, Cyclin D1). APC mutations cause familial adenomatous polyposis (FAP) and most colorectal cancers.
What determines stem cell potency from totipotent to unipotent?
Totipotent cells (zygote to 8-cell stage) can form all cell types including placenta. Pluripotent cells (ES cells, iPSCs) form all body cell types. Multipotent cells (e.g., hematopoietic stem cells) differentiate into related lineages. Oligopotent and unipotent cells are progressively more restricted. Yamanaka factors (Oct4, Sox2, Klf4, c-Myc) can reprogram somatic cells to pluripotency.
How do telomeres and telomerase affect cellular aging and cancer?
Telomeres are TTAGGG repeats (5-15 kb) at chromosome ends. Normal cells lose 50-200 bp per division, reaching the Hayflick limit (50-70 divisions) and triggering senescence. Cancer cells bypass this by reactivating telomerase (hTERT + TERC) in 85-90% of cases, or by using the Alternative Lengthening of Telomeres (ALT) mechanism.