\begin{table}[]
\begin{tabular}{|l|ll|l|l|l|l|l|}
\hline
\textbf{Target} & \multicolumn{1}{l|}{\textbf{Source}} & \textbf{Deduced Activation Time} & \textbf{Duration + Action} & \textbf{Boolean functin} & \textbf{biological function} & \textbf{Temporal References} & \textbf{Functional Reference} \\ \hline
Receptor & \multicolumn{1}{l|}{Mitogen} & \multirow{2}{*}{0-4,5 hours} & Nanoseconds-4 hours & Receptor=Mitogen & physical binding of receptor, stay activated till late G1 phase. Once cell become independent of extracellular signal, either the ligand or the reeptor are degraded and sequestered via endocytic vehisicle OR through arrestin process Or by PTP process. & \multirow{109}{*}{} & \multirow{109}{*}{} \\ \cline{1-2} \cline{4-6}
Lipid & \multicolumn{1}{l|}{Receptor} & & 0-4 hours- Remains Active throiughout the cell cycle & Lipid=Receptor & membrane dynamics help control cell cycle events and orgenll regulations. & & \\ \cline{1-6}
PLC & \multicolumn{1}{l|}{Lipid/Receptor} & 2 & 0 minutes- closed in 30 mins after playing role in channel activation and calcium est., & PLC=Lipid & Activity is dependant on receptor signal. One possible deactivation is the internal negative environment which repels the XY linkers in the PLC domain for autoinhibition. Involved in K, Ca+ TRPVs channel opening & & \\ \cline{1-6}
PIP2 & \multicolumn{1}{l|}{PLC} & 2 & Formation 200- 500 sec Hydrolysis 5-10 sec- 2 minutes- duration is 10-30 mins unstable half life, bit shorter than IP3. PLC cleaves PI into PIP2 and DAG & PIP2=PLC & PLC hydrolyse PIP2 to make IP3. Involved in activation of Potasium and NHE channels along with its intense role in Actin regulation via Ezrin and direct binding. Half life of PIP2 is 10mins & & \\ \cline{1-6}
\multirow{2}{*}{PKC} & \multicolumn{1}{l|}{Ca1} & 10 & \multirow{2}{*}{2 min onward- Sustained activation for clswell or remian on because it is responsible for MLC phospho} & \multirow{2}{*}{PKC=Ca1||to Ca8||PIP2} & \multirow{2}{*}{PKC also acts to activate RhoA by activating ROCK. Also, the activation of channels Therefore, its activity is required} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{PIP2} & 3 & & & & & \\ \cline{1-6}
\multirow{2}{*}{IP3} & \multicolumn{1}{l|}{PLC} & \multirow{2}{*}{2} & \multirow{2}{*}{5 mins onward- Untill depolimerization} & \multirow{2}{*}{IP3= PKC||PLC\&PIP2} & \multirow{2}{*}{PLC hydrolyse PIP2 to make IP3. IP3 acts synyergistically in presence of PKC. duration is 40 mins and depends on Calcium production} & & \\ \cline{2-2}
& \multicolumn{1}{l|}{PIP2} & & & & & & \\ \cline{1-6}
\multirow{2}{*}{IEG} & \multicolumn{1}{l|}{RAS} & 5 & \multirow{2}{*}{15-10min- duration is 2 hours} & \multirow{2}{*}{IEG=RAS\&MAPK} & \multirow{2}{*}{no direct interaction is found. However, it activates IEG through downstream signaling processes. MAPK trnaslocates into the nucleus which is why there's no signalling. This translocation causes transcription of IEG which stops after 2hrs} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{MAPK} & 3 & & & & & \\ \cline{1-6}
RAS & \multicolumn{1}{l|}{PIP2} & 1 & 5-10 min- closed in 4th hour once mapk is transported to nucleaus & RAS=PIP2 & PIP2 activates RAS when its cleaved into DAG. DAG activates RAS when only when its C1 responsive domain is active. Ras activation slows down and eventually stops during mid G1 when MAPK activity is highest & & \\ \cline{1-6}
\multirow{5}{*}{MP1} & \multicolumn{1}{l|}{PKC+MLC} & 10 & \multirow{5}{*}{ATP consumption causes Katp to shutdown- between depol.} & \multirow{5}{*}{MP1=PKC\&Lipids||PIP2\&Ca3\&!Depol} & \multirow{5}{*}{Ion channels open a transient and quick opening, depending on the environment and signal received.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Lipid} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{PIP2} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca3} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Depolimerization} & 1 & & & & & \\ \cline{1-6}
\multirow{2}{*}{MAPK} & \multicolumn{1}{l|}{RAS} & 1 & \multirow{2}{*}{10 min onwards- full time} & \multirow{2}{*}{MPAK=RAS\&Ca1} & \multirow{2}{*}{Active at basal level throughout G1 phase. Around mid the signal is tranlocated to the Nucleas.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca1} & 1 & & & & & \\ \cline{1-6}
\multirow{5}{*}{MP2} & \multicolumn{1}{l|}{PKC} & 8 & \multirow{5}{*}{10-40 minutes-} & \multirow{5}{*}{MP2=PKC\&Ca1,2,3,4} & \multirow{5}{*}{on channels open a transient and quick opening, depending on the environment and signal received. Most channels in MP2 are involved in bringing in the exogenous calcium inside for calcium establishment and help in maintaining the depolymerization.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca1} & 5 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca2} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca3} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca4} & 1 & & & & & \\ \cline{1-6}
mTorC2 & \multicolumn{1}{l|}{PIP2} & 3 & 5-10 minutesto 4-5 hours, closed by AKT & MTorC2=PIP2\&!AKT & it gets active in 2-3 steps after activation of PIP2 and is inhibited by Akt in its abundance. & & \\ \cline{1-6}
\multirow{2}{*}{AKT} & \multicolumn{1}{l|}{mTorC2} & 3 & \multirow{2}{*}{5 minutes duraiton is 2 hours or arround mid.} & \multirow{2}{*}{AKT=mTorC2\&IP3} & \multirow{2}{*}{Phosphorylation leads to activation of Akt around 5th hour. PIP2-PIP3 conversion leads to activaiton of PDK1 which then activates AKT. The Adaptor protein in Mtorc2 complex phosph. AKT to turn it on.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{IP3} & 5 & & & & & \\ \cline{1-6}
\multirow{9}{*}{ER} & \multicolumn{1}{l|}{Ca1} & 1 & \multirow{18}{*}{10-40 mins- before depolimerization} & \multirow{9}{*}{ER=All Calicum \&IP3} & \multirow{18}{*}{Major role of ER is to help in calcium release and calium establishments and also in sequestration of calicum after depolymerization.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca2} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca3} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca4} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca5} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca6} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca7} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca8} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{IP3} & 1 & & & & & \\ \cline{1-3} \cline{5-5}
Ca1 & \multicolumn{1}{l|}{ER} & 1 & & Ca1=ER & & & \\ \cline{1-3} \cline{5-5}
\multirow{2}{*}{Ca2} & \multicolumn{1}{l|}{ER} & 1 & & \multirow{2}{*}{Ca2=ER\&MP2} & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{MP2} & 6 & & & & & \\ \cline{1-3} \cline{5-5}
Ca3 & \multicolumn{1}{l|}{\multirow{6}{*}{ER}} & 1 & & \multirow{6}{*}{Ca3,4,5,6,7||8=ER} & & & \\ \cline{1-1} \cline{3-3}
Ca4 & \multicolumn{1}{l|}{} & 1 & & & & & \\ \cline{1-1} \cline{3-3}
Ca5 & \multicolumn{1}{l|}{} & 1 & & & & & \\ \cline{1-1} \cline{3-3}
Ca6 & \multicolumn{1}{l|}{} & 0 & & & & & \\ \cline{1-1} \cline{3-3}
Ca7 & \multicolumn{1}{l|}{} & 0 & & & & & \\ \cline{1-1} \cline{3-3}
Ca8 & \multicolumn{1}{l|}{} & 0 & & & & & \\ \cline{1-6}
\multirow{2}{*}{CaM} & \multicolumn{1}{l|}{Ca3} & \multirow{2}{*}{20} & \multirow{2}{*}{untill end} & \multirow{2}{*}{CaM=Ca3-8\&!P21} & \multirow{2}{*}{CaM has been shown to be essential for CDK4 activation and nuclear cyclin D1–CDK4 complex accumulation during the G1 phase. Also assist in complex nuclear localization.} & & \\ \cline{2-2}
& \multicolumn{1}{l|}{P21} & & & & & & \\ \cline{1-6}
\multirow{12}{*}{Depolymerization} & \multicolumn{1}{l|}{MP1 and 2} & 5 & \multirow{12}{*}{5 mins onward- Untill depolimerization} & \multirow{12}{*}{Depol=Ca1-8||MP1||MP2\&PIP2\&Rho} & Katp majorly from the MP1 and Exogenous Calcium and TRPVs from MP2 & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{PIP2} & 2 & & & PIP2 regulate cofilin activity by sequestration & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Ca1} & 1 & & & \multirow{8}{*}{Calcium acts on cofilin and gelsolin proteins for destablising the cytoskeleton. Further, it directly helps in dissociation of polymers with phisical binding with the help of ATP.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca2} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca3} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca4} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca5} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca6} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca7} & 1 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{Ca8} & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MLC} & 1 & & & MLC phosphatase upon receing signal from rho gtpase causes stress in cytoskeleton which further is depolymerised via cofilin severing the polymers & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{RhoA} & 2 & & & Rho activation through & & \\ \cline{1-6}
\multirow{3}{*}{MP3a} & \multicolumn{1}{l|}{RhoA} & & \multirow{3}{*}{} & \multirow{3}{*}{MP3a=Ca3\&PKC\&Rho} & Rho GTPase pathways are Needed for Chloride channel functional but not activaiton. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Ca3} & 1 & & & Exogenouse calcium is needed for Chloride channel activation & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{PKC} & 31 & & & ref from latex & & \\ \cline{1-6}
\multirow{5}{*}{Shrinkage} & \multicolumn{1}{l|}{mTorC2} & 1 & \multirow{5}{*}{5-40 minutes} & \multirow{5}{*}{Shrinkage=mTorC2\&Ca2||Ca3\&MP3a\&MP3b} & MtorC2 role in shrinkage is advised via depolymerization and MLC & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Ca2} & 1 & & & Exogenouse calcium along with Cytosolic Ca help help in Chloride channel activation which ultimately leads to Osmolyte release after depolymerization. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Ca3} & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MP3a} & 1 & & & MLC is connected with the channel through actin cytoskeletal rearrangments & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MP3b} & 10 & & & & & \\ \cline{1-6}
\multirow{2}{*}{MP3b} & \multicolumn{1}{l|}{MP3a} & \multirow{2}{*}{10} & \multirow{2}{*}{As previous} & \multirow{2}{*}{MP3b=MP3a\&PKC} & \multirow{2}{*}{Shrinkage and hyperppolarization induced KCC and Cl channel leads to release of Osmolyte and taurine.} & & \\ \cline{2-2}
& \multicolumn{1}{l|}{PKC} & & & & & & \\ \cline{1-6}
\multirow{3}{*}{MP4} & \multicolumn{1}{l|}{Depolimerization} & \multirow{3}{*}{} & \multirow{3}{*}{MP4 is switched off because of hypotonic environment} & \multirow{3}{*}{MP4=MLC\&PKC\&PIP2} & When Depolimerization ends. It should turn ON till end to produce hypotonic environment to shutdown mp4 (because mp4 is deactivated by hypotonic environment) and during it’s activation when a.a are being influxed in cell along with volume and other ions. The mtorc1 senses a.a… only a.a channels in mp5 turn off and AQ channels remains open & & \\ \cline{2-2} \cline{6-6}
& \multicolumn{1}{l|}{MLC} & & & & Depolymerization is needed to activate NKCC in MP4 & & \\ \cline{2-2} \cline{6-6}
& \multicolumn{1}{l|}{PKC} & & & & Ref from Latex & & \\ \cline{1-6}
\multirow{4}{*}{Swelling} & \multicolumn{1}{l|}{MP4} & 5 & \multirow{4}{*}{after 10 mins of mtorc1 ending} & \multirow{4}{*}{Swelling= MP4\&MP5\&Clswell\&Repolimerization} & It is suggested that with the osmolyte influx there is a net influx of water for cell swelling and migration purposes. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MP5} & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{CSwell} & 30 & & & & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Repolimerization} & 240 & & & should be till end, because its dependant on MP5 and MP4. & & \\ \cline{1-6}
\multirow{3}{*}{RhoA} & \multicolumn{1}{l|}{mTorC2} & 25 & \multirow{3}{*}{15 mins to 3 hours- Through phospho around 10 mins prior to MLC} & \multirow{3}{*}{RhoA=mTorC2||CycD1\&!P21} & RhoA is activated through phosphorylation mediated by mTORC2. Activated rhoA directly recruits chloride intracellular channels to the membrane. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{CycD1} & 2 & & & Rho signaling is both sufficient to induce cyclin D1 transcriptional activity, and is required for EGF to induce cyclin D1 promoter activity. Also Rho helps in the translocation of CycD complex into nucleas & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{P21} & 5 & & & P21 is reponsible to RhoA inhibition to cease the downregulation effects of RhoA on cell's cytoskeleton. & & \\ \cline{1-6}
\multirow{3}{*}{MLC} & \multicolumn{1}{l|}{PKC} & 35 & \multirow{3}{*}{takes 30 mins to phosphorylate and activates via Rho and Cam- Untill repolimerization} & \multirow{3}{*}{MLC=PKC||CaM\&RhoA} & increases the phosphorylation of MLC to activate it and it remains activated until repolimerization is done & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{CaM} & 3 & & & CaM binds and activates MLCK which phosphorylates MLC for its activation & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{RhoA} & 30 & & & RhoA GTPase phosphorylates the MLCKs for cytoskeleton contraction which ultimately leads to deolymerization. & & \\ \cline{1-6}
\multirow{3}{*}{Repolimerization} & \multicolumn{1}{l|}{PIP2} & 35 & \multirow{3}{*}{After MLC phospho- should be closed where swelling is stopped} & \multirow{3}{*}{Repol=PIP2\&MLC\&!Ca1-8} & PIP2 interacts with cytoskeletal proteins and help in repolimerization & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{RhoA} & & & & Through the activaiton of MLC and deactivaiton of Cofilin protein. It helps in repolymerization & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MLC} & 1 & & & increases the phosphorylation of MLC to activate it and it remains activated until repolimerization is done & & \\ \cline{1-6}
\multirow{3}{*}{Clbicarb} & \multicolumn{1}{l|}{IP3 and PKC} & & \multirow{3}{*}{} & \multirow{3}{*}{ClSwell=RhoA\&MP4} & \multirow{3}{*}{IP3 and PKC are the regulator of Cl-/HCO3- channel when there is excessive protonation in the cell to normalise the pH of the cell. This exchange is countered via Chloride for hyperpolarization.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{RhoA} & 10 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{MP4} & 240 & & & & & \\ \cline{1-6}
\multirow{2}{*}{CycD1} & \multicolumn{1}{l|}{CaM} & 1 & \multirow{2}{*}{Basal- full time} & \multirow{2}{*}{CycDComplex=CaM\&P21} & \multirow{2}{*}{Basal Cyclin D presence is regulated via Calcium/calmadulin and P21 proteins for activity and stability.} & & \\ \cline{2-3}
& \multicolumn{1}{l|}{P21} & 1 & & & & & \\ \cline{1-6}
\multirow{3}{*}{CycD2} & \multicolumn{1}{l|}{CaM} & 200 & \multirow{3}{*}{1 hour to 4 and then starts in the middle of S till M- full time from activation} & \multirow{3}{*}{CycDProduction=CaM\&IEG||MAPK} & Once, the IEG is activated via MAPK pathway kinases the production starts and CycD/CDK4 complex is formed for further regulation of pRb. & & \\ \cline{2-3}
& \multicolumn{1}{l|}{IEG} & 230 & & & & & \\ \cline{2-3}
& \multicolumn{1}{l|}{P21} & 1 & & & & & \\ \cline{1-6}
\multirow{2}{*}{E2F} & \multicolumn{1}{l|}{CycD2} & 15 & \multirow{2}{*}{4th hours till end from activation} & \multirow{2}{*}{E2F=CycD1||CycD\&PrB} & Produced cyclin D along with basal help in partial phosphorylation of pRb. Cyclin E after helps in complete phosphorylation of the Prb. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{CycE1} & 10 & & & & & \\ \cline{1-6}
\multirow{4}{*}{MP5} & \multicolumn{1}{l|}{PLC} & 50 & \multirow{4}{*}{after 10 mins of mtorc1 ending} & \multirow{4}{*}{MP5=PLC\&MLC||ClSwell} & Phospho lipid contects (PLA) play a role in the activation of Osmolyte channels via mechanosensitvity & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MLC+PKC} & 50 & & & MLC through Phosphorylation and lnks via cytoskeleton. While, PKC has integral role in the Taurine channel activation & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Swelling} & 210 & & & Swelling and Chloride Bi carbonate exchanger help in maintaining the charge balance of Osmolytic protein entrance. Also, with osmolyte influx there is a net influx of water for cell swelling and migration purposes. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Clbicarb} & 0 & & & & & \\ \cline{1-6}
RHEB & \multicolumn{1}{l|}{AKT} & 300 & around 300 mins to turn on mtorc1 & Rheb=AKT & AKT acts at TCS2 to activate it which further releases the Rheb Protein. & & \\ \cline{1-6}
\multirow{3}{*}{mTorC1} & \multicolumn{1}{l|}{MAPK} & 140 & \multirow{3}{*}{after enriching with a.a it takes almost 20 mins to one hours for activation of mtorc1- As previous} & \multirow{3}{*}{MtorC1=MAPK\&Rheb\&MP5} & Proteins of MAPK pathway downregulates mTORC1 activity by downregulating cytoplasmic amino acid content & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{Rheb} & 20 & & & Rheb Activation helps mToRc1 in sensing the A.A sufficiency which then leads to the termination of the osmolytic intake along with water content. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{MP5} & 200 & & & Through MP5 the osmolytic intake produce a causal effect on A.A sensing. & & \\ \cline{1-6}
CycE1 & \multicolumn{1}{l|}{mTorC1} & 1 & & CycE(Basal)=mTorC1 & Once, mTorC1 is activated to sense A.A. It further releases P21 from basal Cyclin E. This Free/Active CycE helps in complete phosphorylation of pRb. & & \\ \cline{1-6}
\multirow{2}{*}{CycE2} & \multicolumn{1}{l|}{P21} & 5 & \multirow{2}{*}{2 hours prior to S} & \multirow{2}{*}{CycE2(Prod)=pRb\&E2F\&p21} & PIP2 interacts with cytoskeletal proteins and help in depolimerization & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{E2F} & 180 & & & the Active T.F (E2F) is responsible for Cyclin E production in bulk. & & \\ \cline{1-6}
CycE3 & \multicolumn{1}{l|}{P21} & 460 & At G1/S Boundry & CycE3(Bound)=!p21\&RhoA & The Produced Cyclin bounds with p21 to stay nuetral unless it recives a signal. & & \\ \cline{1-6}
\multirow{3}{*}{P21} & \multicolumn{1}{l|}{MAPK} & 32 & \multirow{3}{*}{Degrading from start and finishes at around end to free E2} & \multirow{3}{*}{P21=MAPK\&CycD1,2\&!RhoA} & MAPK pathways help the transcription of P21 and along with basal amounts this p21 helps in the sequestration of CycD into the nucleus. & & \\ \cline{2-3} \cline{6-6}
& \multicolumn{1}{l|}{CycD1} & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& Rho & 420 & & & RhoA has a sugnificant role in P21 degradation along with ubiquitin ligase proteins to help activate the Cyclin E for G1/S transfer. & & \\ \hline
\end{tabular}
\end{table}```
答案1
据我所知，所有 102 个 [!!] 实例\multirow都是错误的，应该删除。以下解决方案就是这样，允许在所有列中换行，使用横向模式和longtable环境，最终得到一个长达 18 [!] 页的表格。
以下屏幕截图显示了 18 页表格的第一页的前几行。表格仍需要大量调整才能看起来很棒。我只是希望下面的代码能让你走得更远。
\documentclass{article} % or some other suitable class
\usepackage[T1]{fontenc} % omit if compiling with LuaLaTeX or XeLaTeX
\usepackage{array,ragged2e,pdflscape,longtable}
\newcolumntype{L}[1]{>{\RaggedRight\hspace{0pt}}p{#1}}
\hyphenation{de-poly-mer-i-za-tion de-poli-mer-i-za-tion re-poli-mer-i-za-tion CycD-Complex}
\begin{document}
\begin{landscape}
\setlength\tabcolsep{4pt} % default: 6pt
\begin{longtable}{|L{1.75cm}|L{1.8cm}L{1.95cm}|L{2.5cm}|L{2.1cm}|L{4cm}|L{1.9cm}|L{1.9cm}|}
\hline
\textbf{Target} &
\textbf{Source} &
\textbf{Deduced Activation Time} &
\textbf{Duration + Action} &
\textbf{Boolean function} &
\textbf{Biological function} &
\textbf{Temporal References} &
\textbf{Functional Reference} \\
\hline
\endhead
\hline
\endfoot
Receptor & Mitogen & 0--4,5 hours & Nanoseconds--4 hours & Receptor = Mitogen & physical binding of receptor, stay activated till late G1 phase. Once cell become independent of extracellular signal, either the ligand or the reeptor are degraded and sequestered via endocytic vehisicle OR through arrestin process Or by PTP process. & & \\ \cline{1-2} \cline{4-6}
Lipid & Receptor & & 0--4 hours- Remains Active throiughout the cell cycle & Lipid = Receptor & membrane dynamics help control cell cycle events and orgenll regulations. & & \\ \cline{1-6}
PLC & Lipid\slash Receptor & 2 & 0 minutes- closed in 30 mins after playing role in channel activation and calcium est., & PLC = Lipid & Activity is dependant on receptor signal. One possible deactivation is the internal negative environment which repels the XY linkers in the PLC domain for autoinhibition. Involved in K, Ca+ TRPVs channel opening & & \\ \cline{1-6}
PIP2 & PLC & 2 & Formation 200--500 sec Hydrolysis 5--10 sec--2 minutes- duration is 10--30 mins unstable half life, bit shorter than IP3. PLC cleaves PI into PIP2 and DAG & PIP2 = PLC & PLC hydrolyse PIP2 to make IP3. Involved in activation of Potasium and NHE channels along with its intense role in Actin regulation via Ezrin and direct binding. Half life of PIP2 is 10mins & & \\ \cline{1-6}
PKC & Ca1 & 10 & 2 min onward- Sustained activation for clswell or remian on because it is responsible for MLC phospho & PKC = Ca1||to Ca8||PIP2 & PKC also acts to activate RhoA by activating ROCK. Also, the activation of channels Therefore, its activity is required & & \\ \cline{2-3}
& PIP2 & 3 & & & & & \\ \cline{1-6}
IP3 & PLC & 2 & 5 mins onward- until depolimerization & IP3 = PKC||PLC\& PIP2 & PLC hydrolyse PIP2 to make IP3. IP3 acts synyergistically in presence of PKC. duration is 40 mins and depends on Calcium production & & \\ \cline{2-2}
& PIP2 & & & & & & \\ \cline{1-6}
IEG & RAS & 5 & 15--10min- duration is 2 hours & IEG = RAS\&MAPK & no direct interaction is found. However, it activates IEG through downstream signaling processes. MAPK trnaslocates into the nucleus which is why there's no signalling. This translocation causes transcription of IEG which stops after 2hrs & & \\ \cline{2-3}
& MAPK & 3 & & & & & \\ \cline{1-6}
RAS & PIP2 & 1 & 5--10 min- closed in 4th hour once mapk is transported to nucleaus & RAS = PIP2 & PIP2 activates RAS when its cleaved into DAG. DAG activates RAS when only when its C1 responsive domain is active. Ras activation slows down and eventually stops during mid G1 when MAPK activity is highest & & \\ \cline{1-6}
MP1 & PKC+MLC & 10 & ATP consumption causes Katp to shutdown- between depol. & MP1 = PKC\& Lipids|| PIP2\&Ca3\&! Depol & Ion channels open a transient and quick opening, depending on the environment and signal received. & & \\ \cline{2-3}
& Lipid & 1 & & & & & \\ \cline{2-3}
& PIP2 & 1 & & & & & \\ \cline{2-3}
& Ca3 & 1 & & & & & \\ \cline{2-3}
& Depolimerization & 1 & & & & & \\ \cline{1-6}
MAPK & RAS & 1 & 10 min onwards- full time & MPAK = RAS\&Ca1 & Active at basal level throughout G1 phase. Around mid the signal is tranlocated to the Nucleas. & & \\ \cline{2-3}
& Ca1 & 1 & & & & & \\ \cline{1-6}
MP2 & PKC & 8 & 10-40 minutes- & MP2 = PKC\& Ca1,2,3,4 & on channels open a transient and quick opening, depending on the environment and signal received. Most channels in MP2 are involved in bringing in the exogenous calcium inside for calcium establishment and help in maintaining the depolymerization. & & \\ \cline{2-3}
& Ca1 & 5 & & & & & \\ \cline{2-3}
& Ca2 & 1 & & & & & \\ \cline{2-3}
& Ca3 & 1 & & & & & \\ \cline{2-3}
& Ca4 & 1 & & & & & \\ \cline{1-6}
mTorC2 & PIP2 & 3 & 5--10 minutes to 4--5 hours, closed by AKT & MTorC2 = PIP2\&!AKT & it gets active in 2--3 steps after activation of PIP2 and is inhibited by Akt in its abundance. & & \\ \cline{1-6}
AKT & mTorC2 & 3 & 5 minutes duration is 2 hours or around mid. & AKT = mTorC2\&IP3 & Phosphorylation leads to activation of Akt around 5th hour. PIP2-PIP3 conversion leads to activaiton of PDK1 which then activates AKT. The Adaptor protein in Mtorc2 complex phosph. AKT to turn it on. & & \\ \cline{2-3}
& IP3 & 5 & & & & & \\ \cline{1-6}
ER & Ca1 & 1 & 10--40 mins- before depolimerization & ER = All Calicum \&IP3 & Major role of ER is to help in calcium release and calium establishments and also in sequestration of calicum after depolymerization. & & \\ \cline{2-3}
& Ca2 & 1 & & & & & \\ \cline{2-3}
& Ca3 & 1 & & & & & \\ \cline{2-3}
& Ca4 & 1 & & & & & \\ \cline{2-3}
& Ca5 & 1 & & & & & \\ \cline{2-3}
& Ca6 & 1 & & & & & \\ \cline{2-3}
& Ca7 & 1 & & & & & \\ \cline{2-3}
& Ca8 & 1 & & & & & \\ \cline{2-3}
& IP3 & 1 & & & & & \\ \cline{1-3} \cline{5-5}
Ca1 & ER & 1 & & Ca1 = ER & & & \\ \cline{1-3} \cline{5-5}
Ca2 & ER & 1 & & Ca2 = ER\&MP2 & & & \\ \cline{2-3}
& MP2 & 6 & & & & & \\ \cline{1-3} \cline{5-5}
Ca3 & ER & 1 & & Ca3,4,5,6,7||8 = ER & & & \\ \cline{1-1} \cline{3-3}
Ca4 & & 1 & & & & & \\ \cline{1-1} \cline{3-3}
Ca5 & & 1 & & & & & \\ \cline{1-1} \cline{3-3}
Ca6 & & 0 & & & & & \\ \cline{1-1} \cline{3-3}
Ca7 & & 0 & & & & & \\ \cline{1-1} \cline{3-3}
Ca8 & & 0 & & & & & \\ \cline{1-6}
CaM & Ca3 & 20 & until end & CaM = \mbox{Ca3-8}\&!P21 & CaM has been shown to be essential for CDK4 activation and nuclear cyclin D1–CDK4 complex accumulation during the G1 phase. Also assist in complex nuclear localization. & & \\ \cline{2-2}
& P21 & & & & & & \\ \cline{1-6}
Depolymerization & MP1 and 2 & 5 & 5 mins onward- until depolimerization & Depol = \mbox{\mbox{Ca1-8}}|| MP1||MP2\& PIP2\&Rho & Katp majorly from the MP1 and Exogenous Calcium and TRPVs from MP2 & & \\ \cline{2-3} \cline{6-6}
& PIP2 & 2 & & & PIP2 regulate cofilin activity by sequestration & & \\ \cline{2-3} \cline{6-6}
& Ca1 & 1 & & & Calcium acts on cofilin and gelsolin proteins for destablising the cytoskeleton. Further, it directly helps in dissociation of polymers with physical binding with the help of ATP. & & \\ \cline{2-3}
& Ca2 & 1 & & & & & \\ \cline{2-3}
& Ca3 & 1 & & & & & \\ \cline{2-3}
& Ca4 & 1 & & & & & \\ \cline{2-3}
& Ca5 & 1 & & & & & \\ \cline{2-3}
& Ca6 & 1 & & & & & \\ \cline{2-3}
& Ca7 & 1 & & & & & \\ \cline{2-3}
& Ca8 & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& MLC & 1 & & & MLC phosphatase upon receing signal from rho gtpase causes stress in cytoskeleton which further is depolymerised via cofilin severing the polymers & & \\ \cline{2-3} \cline{6-6}
& RhoA & 2 & & & Rho activation through & & \\ \cline{1-6}
MP3a & RhoA & & & MP3a = Ca3\&PKC\& Rho & Rho GTPase pathways are Needed for Chloride channel functional but not activation. & & \\ \cline{2-3} \cline{6-6}
& Ca3 & 1 & & & Exogenouse calcium is needed for Chloride channel activation & & \\ \cline{2-3} \cline{6-6}
& PKC & 31 & & & ref from latex & & \\ \cline{1-6}
Shrinkage & mTorC2 & 1 & 5-40 minutes & Shrinkage = mTorC2\& Ca2||Ca3\& MP3a\& MP3b & MtorC2 role in shrinkage is advised via depolymerization and MLC & & \\ \cline{2-3} \cline{6-6}
& Ca2 & 1 & & & Exogenouse calcium along with Cytosolic Ca help help in Chloride channel activation which ultimately leads to Osmolyte release after depolymerization. & & \\ \cline{2-3} \cline{6-6}
& Ca3 & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& MP3a & 1 & & & MLC is connected with the channel through actin cytoskeletal rearrangments & & \\ \cline{2-3} \cline{6-6}
& MP3b & 10 & & & & & \\ \cline{1-6}
MP3b & MP3a & 10 & As previous & MP3b = MP3a\&PKC & Shrinkage and hyperppolarization induced KCC and Cl channel leads to release of Osmolyte and taurine. & & \\ \cline{2-2}
& PKC & & & & & & \\ \cline{1-6}
MP4 & Depolimerization & & MP4 is switched off because of hypotonic environment & MP4 = MLC\& PKC\&PIP2 & When Depolimerization ends. It should turn ON till end to produce hypotonic environment to shutdown mp4 (because mp4 is deactivated by hypotonic environment) and during it’s activation when a.a are being influxed in cell along with volume and other ions. The mtorc1 senses a.a… only a.a channels in mp5 turn off and AQ channels remains open & & \\ \cline{2-2} \cline{6-6}
& MLC & & & & Depolymerization is needed to activate NKCC in MP4 & & \\ \cline{2-2} \cline{6-6}
& PKC & & & & Ref from Latex & & \\ \cline{1-6}
Swelling & MP4 & 5 & after 10 mins of mtorc1 ending & Swelling = MP4\&MP5\& Clswell\& Repolimerization & It is suggested that with the osmolyte influx there is a net influx of water for cell swelling and migration purposes. & & \\ \cline{2-3} \cline{6-6}
& MP5 & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& CSwell & 30 & & & & & \\ \cline{2-3} \cline{6-6}
& Repolimerization & 240 & & & should be till end, because its dependant on MP5 and MP4. & & \\ \cline{1-6}
RhoA & mTorC2 & 25 & 15 mins to 3 hours- Through phospho around 10 mins prior to MLC & RhoA = mTorC2|| CycD1\&!P21 & RhoA is activated through phosphorylation mediated by mTORC2. Activated rhoA directly recruits chloride intracellular channels to the membrane. & & \\ \cline{2-3} \cline{6-6}
& CycD1 & 2 & & & Rho signaling is both sufficient to induce cyclin D1 transcriptional activity, and is required for EGF to induce cyclin D1 promoter activity. Also Rho helps in the translocation of CycD complex into nucleas & & \\ \cline{2-3} \cline{6-6}
& P21 & 5 & & & P21 is reponsible to RhoA inhibition to cease the downregulation effects of RhoA on cell's cytoskeleton. & & \\ \cline{1-6}
MLC & PKC & 35 & takes 30 mins to phosphorylate and activates via Rho and Cam- Until repolimerization & MLC = PKC||CaM\& RhoA & increases the phosphorylation of MLC to activate it and it remains activated until repolimerization is done & & \\ \cline{2-3} \cline{6-6}
& CaM & 3 & & & CaM binds and activates MLCK which phosphorylates MLC for its activation & & \\ \cline{2-3} \cline{6-6}
& RhoA & 30 & & & RhoA GTPase phosphorylates the MLCKs for cytoskeleton contraction which ultimately leads to deolymerization. & & \\ \cline{1-6}
Repolimerization & PIP2 & 35 & After MLC phospho- should be closed where swelling is stopped & Repol = PIP2\& MLC\&! \mbox{Ca1-8} & PIP2 interacts with cytoskeletal proteins and help in repolimerization & & \\ \cline{2-3} \cline{6-6}
& RhoA & & & & Through the activaiton of MLC and deactivaiton of Cofilin protein. It helps in repolymerization & & \\ \cline{2-3} \cline{6-6}
& MLC & 1 & & & increases the phosphorylation of MLC to activate it and it remains activated until repolimerization is done & & \\ \cline{1-6}
Clbicarb & IP3 and PKC & & & ClSwell = RhoA\&MP4 & IP3 and PKC are the regulator of Cl-/HCO3- channel when there is excessive protonation in the cell to normalise the pH of the cell. This exchange is countered via Chloride for hyperpolarization. & & \\ \cline{2-3}
& RhoA & 10 & & & & & \\ \cline{2-3}
& MP4 & 240 & & & & & \\ \cline{1-6}
CycD1 & CaM & 1 & Basal- full time & CycDComplex = CaM\&P21 & Basal Cyclin D presence is regulated via Calcium\slash calmadulin and P21 proteins for activity and stability. & & \\ \cline{2-3}
& P21 & 1 & & & & & \\ \cline{1-6}
CycD2 & CaM & 200 & 1 hour to 4 and then starts in the middle of S till M- full time from activation & CycD\-Production = CaM\&IEG|| MAPK & Once, the IEG is activated via MAPK pathway kinases the production starts and CycD/CDK4 complex is formed for further regulation of pRb. & & \\ \cline{2-3}
& IEG & 230 & & & & & \\ \cline{2-3}
& P21 & 1 & & & & & \\ \cline{1-6}
E2F & CycD2 & 15 & 4th hours till end from activation & E2F = CycD1|| CycD\&PrB & Produced cyclin D along with basal help in partial phosphorylation of pRb. Cyclin E after helps in complete phosphorylation of the Prb. & & \\ \cline{2-3} \cline{6-6}
& CycE1 & 10 & & & & & \\ \cline{1-6}
MP5 & PLC & 50 & after 10 mins of mtorc1 ending & MP5 = PLC\&MLC|| ClSwell & Phospho lipid contects (PLA) play a role in the activation of Osmolyte channels via mechanosensitvity & & \\ \cline{2-3} \cline{6-6}
& MLC+PKC & 50 & & & MLC through Phosphorylation and lnks via cytoskeleton. While, PKC has integral role in the Taurine channel activation & & \\ \cline{2-3} \cline{6-6}
& Swelling & 210 & & & Swelling and Chloride Bi carbonate exchanger help in maintaining the charge balance of Osmolytic protein entrance. Also, with osmolyte influx there is a net influx of water for cell swelling and migration purposes. & & \\ \cline{2-3} \cline{6-6}
& Clbicarb & 0 & & & & & \\ \cline{1-6}
RHEB & AKT & 300 & around 300 mins to turn on mtorc1 & Rheb = AKT & AKT acts at TCS2 to activate it which further releases the Rheb Protein. & & \\ \cline{1-6}
mTorC1 & MAPK & 140 & after enriching with a.a it takes almost 20 mins to one hours for activation of mtorc1- As previous & MtorC1 = MAPK\& Rheb\&MP5 & Proteins of MAPK pathway downregulates mTORC1 activity by downregulating cytoplasmic amino acid content & & \\ \cline{2-3} \cline{6-6}
& Rheb & 20 & & & Rheb Activation helps mToRc1 in sensing the A.A sufficiency which then leads to the termination of the osmolytic intake along with water content. & & \\ \cline{2-3} \cline{6-6}
& MP5 & 200 & & & Through MP5 the osmolytic intake produce a causal effect on A.A sensing. & & \\ \cline{1-6}
CycE1 & mTorC1 & 1 & & CycE(Basal) = mTorC1 & Once, mTorC1 is activated to sense A.A. It further releases P21 from basal Cyclin E. This Free/Active CycE helps in complete phosphorylation of pRb. & & \\ \cline{1-6}
CycE2 & P21 & 5 & 2 hours prior to S & CycE2 (Prod) = pRb\&E2F\& p21 & PIP2 interacts with cytoskeletal proteins and help in depolimerization & & \\ \cline{2-3} \cline{6-6}
& E2F & 180 & & & the Active T.F (E2F) is responsible for Cyclin E production in bulk. & & \\ \cline{1-6}
CycE3 & P21 & 460 & At G1/S Boundary & CycE3 (Bound) = !p21\&RhoA & The Produced Cyclin bounds with p21 to stay nuetral unless it recives a signal. & & \\ \cline{1-6}
P21 & MAPK & 32 & Degrading from start and finishes at around end to free E2 & P21 = MAPK\& CycD1,2\&! RhoA & MAPK pathways help the transcription of P21 and along with basal amounts this p21 helps in the sequestration of CycD into the nucleus. & & \\ \cline{2-3} \cline{6-6}
& CycD1 & 1 & & & & & \\ \cline{2-3} \cline{6-6}
& Rho & 420 & & & RhoA has a sugnificant role in P21 degradation along with ubiquitin ligase proteins to help activate the Cyclin E for G1/S transfer. & & \\
%\hline
\end{longtable}
\end{landscape}
\end{document}